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Papers by negar ataei

Feyz Journals of Kashan University of Medical Sciences, 2013

Background: Lead exposure is involved in cardiovascular diseases, as a major cause of mortality w... more Background: Lead exposure is involved in cardiovascular diseases, as a major cause of mortality worldwide. This study aimed to provide an overview of the underlying mechanisms. Materials and Methods: The recent studies regarding Lead and cardiovascular diseases are reviewed. Electronic information resources such as Web of knowledge, PubMed, Science direct and Google scholar were used. Results: The data analysis indicated that the low level Lead exposure in long term causes a marked increase in arterial pressure by several mechanisms: an increase in the activities of angiotensin converting enzyme and kininase II, the effect on synthesis and/or release of renin, a reduction in the Nitric oxide availability and an increase in arterial resistance, the stimulatory effect on sympathetic nervous system, the alteration of adrenergic system and endothelium derived vasoregulatory factors, the dysregulation of arterial natriuretic peptide and interference with dependent signaling pathway. The other action of Lead is the promotion of oxidative stress (OS). Several studies demonstrated the association between OS and cardiovascular diseases. Lead has an effect on endothelial and vascular functions by interfering with the synthesis of some proteoglycans. Also, this metal can arouse a negative effect on fibrinolytic process and promote the growth of vascular smooth cells, which are involved in the formation of atherosclerotic plaque. Conclusion: Further research is needed to characterize the full impact of Lead exposure on cardiovascular diseases. Considering the high levels of Lead pollution and prevalence of cardiovascular diseases in Iran, the effects of Lead exposure on cardiovascular diseases need to be included in the risk assessment of Lead exposure.

Toxicology in Vitro, Apr 1, 2019

Evidences for involvement of estrogen receptor induced ERK1/2 activation in ovarian cancer cell p... more Evidences for involvement of estrogen receptor induced ERK1/2 activation in ovarian cancer cell proliferation by Cadmium Chloride, Toxicology in Vitro,

Journal of Medical Education Development, Sep 10, 2015

Razi Journal of Medical Sciences, Jul 10, 2017

Background: Cardiovascular Diseases (CVDs) are major causes of mortality worldwide. Obesity is re... more Background: Cardiovascular Diseases (CVDs) are major causes of mortality worldwide. Obesity is regarded as an independent CVDs risk factor. In this article we focus on the role of adipokines which are involved in CVDs pathogenesis. Methods: The recent studies regarding the role of adipokines such as Leptin, Resistin, TNFα, IL-6, MCP-1, Visfatin, Chemerin, Apelin, Omentin, Adiponectin and Vaspin in CVDs pathogenesis are reviewed. We searched articles in electronic information databases: Web of knowledge, pubMed, sciencedirect and Google Scholar Results: Adipose tissue is an active endocrine organ which secretes important bioactive mediators that are called adipokines. These proteins have complex function in regulation of insulin sensitivity, glucose and lipid metabolism. Adipokines are involved in cardiovascular system homeostasis. There are well recognized anti-inflammatory and cardioprotective effects of some adipokines such as Adiponectin. There is adipose tissue dysfunction in obesity state, which is represented by inflammatory cells infiltration and abnormal production of adipokines, so adipokine balance is impaired. In this condition decreased or increased levels of some adipokines are associated with incidence of cardiovascular diseases through several mechanisms such as insulin resistance, vascular calcification, fibrinolysis disturbance, increased adhesion molecules expression, increased foam cell formation, oxidative stress, vascular inflammation and endothelial dysfunction Conclusion: In physiological condition, adipokines have protective effects on cardiovascular system. Adipokines imbalance causes pathological effects on this system. Undoubtedly, further researches in this field can promise appropriate strategies for CVDs prevention, control or even treatment.

KAUMS Journal, Mar 15, 2013

Background: Aggregation of beta amyloid plaques (Aβ) in the brain is one of the hallmarks of Alzh... more Background: Aggregation of beta amyloid plaques (Aβ) in the brain is one of the hallmarks of Alzheimer's disease (AD). Recent studies have shown that the change in Cu hemostasis can cause and progress AD. Materials and Methods: The literature review and recent investigations were studied. Data were analyzed and the consistent and controversial results were compared. Results: The amyloid precursor protein (APP) has three Copper binding sites including histidine 149, 151, 147 that plays a key role in the APP stability, folding and metabolism. APP acts as a Cu chaperon and metalloprotein in the brain. When Copper binds to these histidine residues, APP structure will be stable and reduce the generation of Aβ. At low Copper status, the conversion of APP to Aβ plaques and the risk of AD can be increased. Moreover, the excessive concentration of Copper especially inorganic Copper can also interact with Aβ plaques and produce H2O2 then oxidize it and cause cross-linked Aβ. Also, Cu toxicity increases ROS in specific regions of the brain involved in AD. Conclusion: There are some challenges among the related studies that Copper is a protective and progressive factor in AD. It seems that both Copper deficiency and toxicity are involved in AD. So, the maintenance of Copper balance is necessary for treatment.

International Journal of Preventive Medicine, 2015

Background: Long-term memory is based on synaptic plasticity, a series of biochemical mechanisms ... more Background: Long-term memory is based on synaptic plasticity, a series of biochemical mechanisms include changes in structure and proteins of brain's neurons. In this article, we systematically reviewed the studies that indicate calcium/calmodulin kinase II (CaMKII) is a ubiquitous molecule among different enzymes involved in human long-term memory and the main downstream signaling pathway of long-term memory. Methods: All of the observational, case-control and review studies were considered and evaluated by the search engines PubMed, Cochrane Central Register of Controlled Trials and ScienceDirect Scopus between 1990 and February 2015. We did not carry out meta-analysis. Results: At the first search, it was fined 1015 articles which included "synaptic plasticity" OR "neuronal plasticity" OR "synaptic density" AND memory AND "molecular mechanism" AND "calcium/calmodulin-dependent protein kinase II" OR CaMKII as the keywords. A total of 335 articles were duplicates in the databases and eliminated. A total of 680 title articles were evaluated. Finally, 40 articles were selected as reference. Conclusions: The studies have shown the most important intracellular signal of long-term memory is calcium-dependent signals. Calcium linked calmodulin can activate CaMKII. After receiving information for learning and memory, CaMKII is activated by Glutamate, the most important neurotransmitter for memory-related plasticity. Glutamate activates CaMKII and it plays some important roles in synaptic plasticity modification and long-term memory.

Asian Pacific Journal of Cancer Prevention, Apr 14, 2015

Prostate cancer, with a lifetime prevalence of one in six men, is the second cause of malignancy-... more Prostate cancer, with a lifetime prevalence of one in six men, is the second cause of malignancy-related death and the most prevalent cancer in men in many countries. Nowadays, prostate cancer diagnosis is often based on the use of biomarkers, especially prostate-specific antigen (PSA) which can result in enhanced detection at earlier stage and decreasing in the number of metastatic patients. However, because of the low specificity of PSA, unnecessary biopsies and mistaken diagnoses frequently occur. Prostate cancer has various features so prognosis following diagnosis is greatly variable. There is a requirement for new prognostic biomarkers, particularly to differentiate between inactive and aggressive forms of disease, to improve clinical management of prostate cancer. Research continues into finding additional markers that may allow this goal to be attained. We here selected a group of candidate biomarkers including PSA, PSA velocity, percentage free PSA, TGFβ1, AMACR, chromogranin A, IL-6, IGFBPs, PSCA, biomarkers related to cell cycle regulation, apoptosis, PTEN, androgen receptor, cellular adhesion and angiogenesis, and also prognostic biomarkers with Genomic tests for discussion. This provides an outline of biomarkers that are presently of prognostic interest in prostate cancer investigation.

Journal of Medical Education Development, Sep 10, 2015

تحقیقات نظام سلامت, Jan 3, 2014

AJP: Cell Physiology, 2007

There is accumulating evidence that Ca2+-dependent signaling pathways regulate proliferation and ... more There is accumulating evidence that Ca2+-dependent signaling pathways regulate proliferation and migration of vascular smooth muscle (VSM) cells, contributing to the intimal accumulation of VSM that is a hallmark of many vascular diseases. In this study we investigated the role of the multifunctional serine/threonine kinase, calmodulin (CaM)-dependent protein kinase II (CaMKII), as a mediator of Ca2+ signals regulating VSM cell proliferation. Differentiated VSM cells acutely isolated from rat aortic media express primarily CaMKIIγ gene products, whereas passaged primary cultures of de-differentiated VSM cells express primarily CaMKIIδ2, a splice variant of the δ gene. Experiments examining the time course of CaMKII isoform modulation revealed the process was rapid in onset following initial dispersion and primary culture of aortic VSM with a significant increase in CaMKIIδ2 protein and a significant decrease in CaMKIIγ protein within 30 h, coinciding with the onset of DNA synthesis ...

KAUMS Journal, 2013

Background: Aggregation of beta amyloid plaques (AI²) in the brain is one of the hallmarks of Alz... more Background: Aggregation of beta amyloid plaques (AI²) in the brain is one of the hallmarks of Alzheimer's disease (AD). Recent studies have shown that the change in Cu hemostasis can cause and progress AD. Materials and Methods: The literature review and recent investigations were studied. Data were analyzed and the consistent and controversial results were compared. Results: The amyloid precursor protein (APP) has three Copper binding sites including histidine 149, 151, 147 that plays a key role in the APP stability, folding and metabolism. APP acts as a Cu chaperon and metalloprotein in the brain. When Copper binds to these histidine residues, APP structure will be stable and reduce the generation of AI². At low Copper status, the conversion of APP to AI² plaques and the risk of AD can be increased. Moreover, the excessive concentration of Copper especially inorganic Copper can also interact with AI² plaques and produce H2O2 then oxidize it and cause cross-linked AI². Also, Cu...

Razi Journal of Medical Sciences, 2017

Background: Cardiovascular Diseases (CVDs) are major causes of mortality worldwide. Obesity is re... more Background: Cardiovascular Diseases (CVDs) are major causes of mortality worldwide. Obesity is regarded as an independent CVDs risk factor. In this article we focus on the role of adipokines which are involved in CVDs pathogenesis. Methods: The recent studies regarding the role of adipokines such as Leptin, Resistin, TNFα, IL-6, MCP-1, Visfatin, Chemerin, Apelin, Omentin, Adiponectin and Vaspin in CVDs pathogenesis are reviewed. We searched articles in electronic information databases: Web of knowledge, pubMed, sciencedirect and Google Scholar Results: Adipose tissue is an active endocrine organ which secretes important bioactive mediators that are called adipokines. These proteins have complex function in regulation of insulin sensitivity, glucose and lipid metabolism. Adipokines are involved in cardiovascular system homeostasis. There are well recognized anti-inflammatory and cardioprotective effects of some adipokines such as Adiponectin. There is adipose tissue dysfunction in ob...

مجله دانشکده پزشکی اصفهان, 2013

مقدمه: سرطان پستان شایع‌ترین بدخیمی در زنان ایرانی است. مطالعات نشان داده‌اند که که سطح بالای IGF... more مقدمه: سرطان پستان شایع‌ترین بدخیمی در زنان ایرانی است. مطالعات نشان داده‌اند که که سطح بالای IGF-1 (Insulin like growth factor-1) و غلظت پایین IGFBP-3 (Insulin like growth factor binding protein 3) در خون و یا نسبت بالای IGF-1 به IGFBP-3 می‌تواند به عنوان یک عامل پیش‌آگهی از سرطان پستان به کار رود. روش‌ها: با بررسی كلیه‌ی اطلاعات موجود در Ncbi-Pubmedبین سال‌های 1987 تا 2013 ارتباط بین IGF و سرطان پستان تحت بررسی مروری قرار گرفت. یافته‌ها: از مجموع 1188 مقاله که کلیدواژه‌های مورد جستجوی ما را در بر داشت و به بررسی IGF-1 در سرطان پستان پرداخته بودند، 46 مقاله ارتباط آن را با سرطان پستان به طور مستقیم و در عنوان مقاله نشان داده بودند، 92 مقاله ارتباط IGF-1 و IGFBP-3 را با سرطان پستان بررسی كرده بودند که 9 مورد آن‌ها مقالات مروری بود. از این میان، 30 مقاله به عنوان مرجع اصلی انتخاب و بررسی شدند. نتیجه‌گیری: مطالعات نشان دادند که بیان ژن IGF-1 در افراد مبتلا به سرطان پستان در مقایسه با افراد سالم افزایش می‌یابد. IGF-1 دارای اثرات میتوژنیکی و آنتی‌آپوپتوتیکی باست و بدین ترتیب سبب افزایش...

Feyz Journals of Kashan University of Medical Sciences, 2013

Background: Lead exposure is involved in cardiovascular diseases, as a major cause of mortality w... more Background: Lead exposure is involved in cardiovascular diseases, as a major cause of mortality worldwide. This study aimed to provide an overview of the underlying mechanisms. Materials and Methods: The recent studies regarding Lead and cardiovascular diseases are reviewed. Electronic information resources such as Web of knowledge, PubMed, Science direct and Google scholar were used. Results: The data analysis indicated that the low level Lead exposure in long term causes a marked increase in arterial pressure by several mechanisms: an increase in the activities of angiotensin converting enzyme and kininase II, the effect on synthesis and/or release of renin, a reduction in the Nitric oxide availability and an increase in arterial resistance, the stimulatory effect on sympathetic nervous system, the alteration of adrenergic system and endothelium derived vasoregulatory factors, the dysregulation of arterial natriuretic peptide and interference with dependent signaling pathway. The ...

Background and Aims: LDH5 (lactate dehydrogenase 5) is an isoenzyme of LDH that converts pyruvate... more Background and Aims: LDH5 (lactate dehydrogenase 5) is an isoenzyme of LDH that converts pyruvate to lactate under anaerobic conditions to energy production. LDH5 abundantly expresses in some tumors, versus adjacent normal tissues. It has been proposed as a new tumor marker that increases in some cancers. Bioinformatics analysis of LDH5 and comparison with LDH1 that is predominant isoenzyme in normal tissues can help to design its inhibitors and Methods: The data have been obtained by online analysis at bioinformatics websites like EXPASY, NCBI,BRANDA, NCBI. Alignment, PDB, uniprot,SWISS PDB WIEVER and JMOL software Results: LDH5 composes four M polypeptides, expresses by A gene contains 13830 bp located on chromosome 11p15.4. it has 6 variants that variant 1 is predominate. LDH1 compose four H polypeptides and expresses by B gene with 22515 bp located on chromosome 12p12.2/12.1. it has 2 variants that both of them encode the same proteins. Their similarity in DNA, mRNA and protein is 100%, 85% and 76% respectively. LDH5 and LDH1 have 332 and 334 amino acids respectively. Both of isoenzymes have 5 types of sites. 2 dimer interface sites and 1 NAD and 1 substrate binding site in both of them is the same but There are 10 acetylation and 2 phosphorylation sites in LDH5 and 7acetylation, 3 phosphorylation sites in LDH1. Substrate binding site residues in LDH1 and LDH5 are quite similar and respectively include Gln100/101, Arg106/107, Asn138/139, Arg169/170, His193/194, Ala238/239, and Thr248/249. Also all of amino acids of their NAD binding site is the same except 67th amino acid that in LDH5 is Histidine and in LDH1 is Glutamine. Conclusions: Understanding about Bioinformatics differences of LDH5 as a new tumor marker candidate with LDH1 that express in normal tissue may help to cancer research.

Research in Pharmaceutical Sciences

Cadmium (Cd), a ubiquitous environmental and occupational pollutant, acts as a metalloestrogen to... more Cadmium (Cd), a ubiquitous environmental and occupational pollutant, acts as a metalloestrogen to induce cell proliferation. It is suggested that Cd may also contribute to the development of estrogen-related cancers like ovarian cancer which is the most lethal cancer in women. Furthermore, it was shown that melatonin has antiproliferative effect on estradiol (E2)-induced proliferation. The aim of the present study was to evaluate whether melatonin inhibits Cd-induced proliferation in ovarian cancer cell lines and also whether Cd and melatonin can modulate estrogen receptor α (ERα) expression. OVCAR3 and SKOV3 human ovarian cancer cell lines were treated with CdCl 2 (1-100 nM) and melatonin (1 µM) for 48 h. Cell proliferation evaluation was carried out by bromodeoxyuridine (BrdU) incorporation assay. ERα expression was detected by western blotting method 24 h after cell treatment. The results were demonstrated that Cd increased proliferation of ovarian cancer cell lines in a dose dependent manner. Melatonin inhibited Cd-induced proliferation of OVCAR3 and SKOV3 cell lines. Moreover, CdCl 2 significantly increased ERα expression in both OVCAR3 and SKOV3 cell lines compared to control. Melatonin significantly inhibited Cd inducing effect on ERα expression of OVCAR3 and SKOV3 cell. In conclusion, due to the proliferative effect on ovarian cancer cell lines, Cd could play an important role in the etiology of ovarian cancer by inducing cells ERα expression. Furthermore, melatonin has the protective role on Cd-induced cell proliferation by inhibition of ERα expression.

Feyz Journals of Kashan University of Medical Sciences, 2013

Background: Lead exposure is involved in cardiovascular diseases, as a major cause of mortality w... more Background: Lead exposure is involved in cardiovascular diseases, as a major cause of mortality worldwide. This study aimed to provide an overview of the underlying mechanisms. Materials and Methods: The recent studies regarding Lead and cardiovascular diseases are reviewed. Electronic information resources such as Web of knowledge, PubMed, Science direct and Google scholar were used. Results: The data analysis indicated that the low level Lead exposure in long term causes a marked increase in arterial pressure by several mechanisms: an increase in the activities of angiotensin converting enzyme and kininase II, the effect on synthesis and/or release of renin, a reduction in the Nitric oxide availability and an increase in arterial resistance, the stimulatory effect on sympathetic nervous system, the alteration of adrenergic system and endothelium derived vasoregulatory factors, the dysregulation of arterial natriuretic peptide and interference with dependent signaling pathway. The other action of Lead is the promotion of oxidative stress (OS). Several studies demonstrated the association between OS and cardiovascular diseases. Lead has an effect on endothelial and vascular functions by interfering with the synthesis of some proteoglycans. Also, this metal can arouse a negative effect on fibrinolytic process and promote the growth of vascular smooth cells, which are involved in the formation of atherosclerotic plaque. Conclusion: Further research is needed to characterize the full impact of Lead exposure on cardiovascular diseases. Considering the high levels of Lead pollution and prevalence of cardiovascular diseases in Iran, the effects of Lead exposure on cardiovascular diseases need to be included in the risk assessment of Lead exposure.

Toxicology in Vitro, Apr 1, 2019

Evidences for involvement of estrogen receptor induced ERK1/2 activation in ovarian cancer cell p... more Evidences for involvement of estrogen receptor induced ERK1/2 activation in ovarian cancer cell proliferation by Cadmium Chloride, Toxicology in Vitro,

Journal of Medical Education Development, Sep 10, 2015

Razi Journal of Medical Sciences, Jul 10, 2017

Background: Cardiovascular Diseases (CVDs) are major causes of mortality worldwide. Obesity is re... more Background: Cardiovascular Diseases (CVDs) are major causes of mortality worldwide. Obesity is regarded as an independent CVDs risk factor. In this article we focus on the role of adipokines which are involved in CVDs pathogenesis. Methods: The recent studies regarding the role of adipokines such as Leptin, Resistin, TNFα, IL-6, MCP-1, Visfatin, Chemerin, Apelin, Omentin, Adiponectin and Vaspin in CVDs pathogenesis are reviewed. We searched articles in electronic information databases: Web of knowledge, pubMed, sciencedirect and Google Scholar Results: Adipose tissue is an active endocrine organ which secretes important bioactive mediators that are called adipokines. These proteins have complex function in regulation of insulin sensitivity, glucose and lipid metabolism. Adipokines are involved in cardiovascular system homeostasis. There are well recognized anti-inflammatory and cardioprotective effects of some adipokines such as Adiponectin. There is adipose tissue dysfunction in obesity state, which is represented by inflammatory cells infiltration and abnormal production of adipokines, so adipokine balance is impaired. In this condition decreased or increased levels of some adipokines are associated with incidence of cardiovascular diseases through several mechanisms such as insulin resistance, vascular calcification, fibrinolysis disturbance, increased adhesion molecules expression, increased foam cell formation, oxidative stress, vascular inflammation and endothelial dysfunction Conclusion: In physiological condition, adipokines have protective effects on cardiovascular system. Adipokines imbalance causes pathological effects on this system. Undoubtedly, further researches in this field can promise appropriate strategies for CVDs prevention, control or even treatment.

KAUMS Journal, Mar 15, 2013

Background: Aggregation of beta amyloid plaques (Aβ) in the brain is one of the hallmarks of Alzh... more Background: Aggregation of beta amyloid plaques (Aβ) in the brain is one of the hallmarks of Alzheimer's disease (AD). Recent studies have shown that the change in Cu hemostasis can cause and progress AD. Materials and Methods: The literature review and recent investigations were studied. Data were analyzed and the consistent and controversial results were compared. Results: The amyloid precursor protein (APP) has three Copper binding sites including histidine 149, 151, 147 that plays a key role in the APP stability, folding and metabolism. APP acts as a Cu chaperon and metalloprotein in the brain. When Copper binds to these histidine residues, APP structure will be stable and reduce the generation of Aβ. At low Copper status, the conversion of APP to Aβ plaques and the risk of AD can be increased. Moreover, the excessive concentration of Copper especially inorganic Copper can also interact with Aβ plaques and produce H2O2 then oxidize it and cause cross-linked Aβ. Also, Cu toxicity increases ROS in specific regions of the brain involved in AD. Conclusion: There are some challenges among the related studies that Copper is a protective and progressive factor in AD. It seems that both Copper deficiency and toxicity are involved in AD. So, the maintenance of Copper balance is necessary for treatment.

International Journal of Preventive Medicine, 2015

Background: Long-term memory is based on synaptic plasticity, a series of biochemical mechanisms ... more Background: Long-term memory is based on synaptic plasticity, a series of biochemical mechanisms include changes in structure and proteins of brain's neurons. In this article, we systematically reviewed the studies that indicate calcium/calmodulin kinase II (CaMKII) is a ubiquitous molecule among different enzymes involved in human long-term memory and the main downstream signaling pathway of long-term memory. Methods: All of the observational, case-control and review studies were considered and evaluated by the search engines PubMed, Cochrane Central Register of Controlled Trials and ScienceDirect Scopus between 1990 and February 2015. We did not carry out meta-analysis. Results: At the first search, it was fined 1015 articles which included "synaptic plasticity" OR "neuronal plasticity" OR "synaptic density" AND memory AND "molecular mechanism" AND "calcium/calmodulin-dependent protein kinase II" OR CaMKII as the keywords. A total of 335 articles were duplicates in the databases and eliminated. A total of 680 title articles were evaluated. Finally, 40 articles were selected as reference. Conclusions: The studies have shown the most important intracellular signal of long-term memory is calcium-dependent signals. Calcium linked calmodulin can activate CaMKII. After receiving information for learning and memory, CaMKII is activated by Glutamate, the most important neurotransmitter for memory-related plasticity. Glutamate activates CaMKII and it plays some important roles in synaptic plasticity modification and long-term memory.

Asian Pacific Journal of Cancer Prevention, Apr 14, 2015

Prostate cancer, with a lifetime prevalence of one in six men, is the second cause of malignancy-... more Prostate cancer, with a lifetime prevalence of one in six men, is the second cause of malignancy-related death and the most prevalent cancer in men in many countries. Nowadays, prostate cancer diagnosis is often based on the use of biomarkers, especially prostate-specific antigen (PSA) which can result in enhanced detection at earlier stage and decreasing in the number of metastatic patients. However, because of the low specificity of PSA, unnecessary biopsies and mistaken diagnoses frequently occur. Prostate cancer has various features so prognosis following diagnosis is greatly variable. There is a requirement for new prognostic biomarkers, particularly to differentiate between inactive and aggressive forms of disease, to improve clinical management of prostate cancer. Research continues into finding additional markers that may allow this goal to be attained. We here selected a group of candidate biomarkers including PSA, PSA velocity, percentage free PSA, TGFβ1, AMACR, chromogranin A, IL-6, IGFBPs, PSCA, biomarkers related to cell cycle regulation, apoptosis, PTEN, androgen receptor, cellular adhesion and angiogenesis, and also prognostic biomarkers with Genomic tests for discussion. This provides an outline of biomarkers that are presently of prognostic interest in prostate cancer investigation.

Journal of Medical Education Development, Sep 10, 2015

تحقیقات نظام سلامت, Jan 3, 2014

AJP: Cell Physiology, 2007

There is accumulating evidence that Ca2+-dependent signaling pathways regulate proliferation and ... more There is accumulating evidence that Ca2+-dependent signaling pathways regulate proliferation and migration of vascular smooth muscle (VSM) cells, contributing to the intimal accumulation of VSM that is a hallmark of many vascular diseases. In this study we investigated the role of the multifunctional serine/threonine kinase, calmodulin (CaM)-dependent protein kinase II (CaMKII), as a mediator of Ca2+ signals regulating VSM cell proliferation. Differentiated VSM cells acutely isolated from rat aortic media express primarily CaMKIIγ gene products, whereas passaged primary cultures of de-differentiated VSM cells express primarily CaMKIIδ2, a splice variant of the δ gene. Experiments examining the time course of CaMKII isoform modulation revealed the process was rapid in onset following initial dispersion and primary culture of aortic VSM with a significant increase in CaMKIIδ2 protein and a significant decrease in CaMKIIγ protein within 30 h, coinciding with the onset of DNA synthesis ...

KAUMS Journal, 2013

Background: Aggregation of beta amyloid plaques (AI²) in the brain is one of the hallmarks of Alz... more Background: Aggregation of beta amyloid plaques (AI²) in the brain is one of the hallmarks of Alzheimer's disease (AD). Recent studies have shown that the change in Cu hemostasis can cause and progress AD. Materials and Methods: The literature review and recent investigations were studied. Data were analyzed and the consistent and controversial results were compared. Results: The amyloid precursor protein (APP) has three Copper binding sites including histidine 149, 151, 147 that plays a key role in the APP stability, folding and metabolism. APP acts as a Cu chaperon and metalloprotein in the brain. When Copper binds to these histidine residues, APP structure will be stable and reduce the generation of AI². At low Copper status, the conversion of APP to AI² plaques and the risk of AD can be increased. Moreover, the excessive concentration of Copper especially inorganic Copper can also interact with AI² plaques and produce H2O2 then oxidize it and cause cross-linked AI². Also, Cu...

Razi Journal of Medical Sciences, 2017

Background: Cardiovascular Diseases (CVDs) are major causes of mortality worldwide. Obesity is re... more Background: Cardiovascular Diseases (CVDs) are major causes of mortality worldwide. Obesity is regarded as an independent CVDs risk factor. In this article we focus on the role of adipokines which are involved in CVDs pathogenesis. Methods: The recent studies regarding the role of adipokines such as Leptin, Resistin, TNFα, IL-6, MCP-1, Visfatin, Chemerin, Apelin, Omentin, Adiponectin and Vaspin in CVDs pathogenesis are reviewed. We searched articles in electronic information databases: Web of knowledge, pubMed, sciencedirect and Google Scholar Results: Adipose tissue is an active endocrine organ which secretes important bioactive mediators that are called adipokines. These proteins have complex function in regulation of insulin sensitivity, glucose and lipid metabolism. Adipokines are involved in cardiovascular system homeostasis. There are well recognized anti-inflammatory and cardioprotective effects of some adipokines such as Adiponectin. There is adipose tissue dysfunction in ob...

مجله دانشکده پزشکی اصفهان, 2013

مقدمه: سرطان پستان شایع‌ترین بدخیمی در زنان ایرانی است. مطالعات نشان داده‌اند که که سطح بالای IGF... more مقدمه: سرطان پستان شایع‌ترین بدخیمی در زنان ایرانی است. مطالعات نشان داده‌اند که که سطح بالای IGF-1 (Insulin like growth factor-1) و غلظت پایین IGFBP-3 (Insulin like growth factor binding protein 3) در خون و یا نسبت بالای IGF-1 به IGFBP-3 می‌تواند به عنوان یک عامل پیش‌آگهی از سرطان پستان به کار رود. روش‌ها: با بررسی كلیه‌ی اطلاعات موجود در Ncbi-Pubmedبین سال‌های 1987 تا 2013 ارتباط بین IGF و سرطان پستان تحت بررسی مروری قرار گرفت. یافته‌ها: از مجموع 1188 مقاله که کلیدواژه‌های مورد جستجوی ما را در بر داشت و به بررسی IGF-1 در سرطان پستان پرداخته بودند، 46 مقاله ارتباط آن را با سرطان پستان به طور مستقیم و در عنوان مقاله نشان داده بودند، 92 مقاله ارتباط IGF-1 و IGFBP-3 را با سرطان پستان بررسی كرده بودند که 9 مورد آن‌ها مقالات مروری بود. از این میان، 30 مقاله به عنوان مرجع اصلی انتخاب و بررسی شدند. نتیجه‌گیری: مطالعات نشان دادند که بیان ژن IGF-1 در افراد مبتلا به سرطان پستان در مقایسه با افراد سالم افزایش می‌یابد. IGF-1 دارای اثرات میتوژنیکی و آنتی‌آپوپتوتیکی باست و بدین ترتیب سبب افزایش...

Feyz Journals of Kashan University of Medical Sciences, 2013

Background: Lead exposure is involved in cardiovascular diseases, as a major cause of mortality w... more Background: Lead exposure is involved in cardiovascular diseases, as a major cause of mortality worldwide. This study aimed to provide an overview of the underlying mechanisms. Materials and Methods: The recent studies regarding Lead and cardiovascular diseases are reviewed. Electronic information resources such as Web of knowledge, PubMed, Science direct and Google scholar were used. Results: The data analysis indicated that the low level Lead exposure in long term causes a marked increase in arterial pressure by several mechanisms: an increase in the activities of angiotensin converting enzyme and kininase II, the effect on synthesis and/or release of renin, a reduction in the Nitric oxide availability and an increase in arterial resistance, the stimulatory effect on sympathetic nervous system, the alteration of adrenergic system and endothelium derived vasoregulatory factors, the dysregulation of arterial natriuretic peptide and interference with dependent signaling pathway. The ...

Background and Aims: LDH5 (lactate dehydrogenase 5) is an isoenzyme of LDH that converts pyruvate... more Background and Aims: LDH5 (lactate dehydrogenase 5) is an isoenzyme of LDH that converts pyruvate to lactate under anaerobic conditions to energy production. LDH5 abundantly expresses in some tumors, versus adjacent normal tissues. It has been proposed as a new tumor marker that increases in some cancers. Bioinformatics analysis of LDH5 and comparison with LDH1 that is predominant isoenzyme in normal tissues can help to design its inhibitors and Methods: The data have been obtained by online analysis at bioinformatics websites like EXPASY, NCBI,BRANDA, NCBI. Alignment, PDB, uniprot,SWISS PDB WIEVER and JMOL software Results: LDH5 composes four M polypeptides, expresses by A gene contains 13830 bp located on chromosome 11p15.4. it has 6 variants that variant 1 is predominate. LDH1 compose four H polypeptides and expresses by B gene with 22515 bp located on chromosome 12p12.2/12.1. it has 2 variants that both of them encode the same proteins. Their similarity in DNA, mRNA and protein is 100%, 85% and 76% respectively. LDH5 and LDH1 have 332 and 334 amino acids respectively. Both of isoenzymes have 5 types of sites. 2 dimer interface sites and 1 NAD and 1 substrate binding site in both of them is the same but There are 10 acetylation and 2 phosphorylation sites in LDH5 and 7acetylation, 3 phosphorylation sites in LDH1. Substrate binding site residues in LDH1 and LDH5 are quite similar and respectively include Gln100/101, Arg106/107, Asn138/139, Arg169/170, His193/194, Ala238/239, and Thr248/249. Also all of amino acids of their NAD binding site is the same except 67th amino acid that in LDH5 is Histidine and in LDH1 is Glutamine. Conclusions: Understanding about Bioinformatics differences of LDH5 as a new tumor marker candidate with LDH1 that express in normal tissue may help to cancer research.

Research in Pharmaceutical Sciences

Cadmium (Cd), a ubiquitous environmental and occupational pollutant, acts as a metalloestrogen to... more Cadmium (Cd), a ubiquitous environmental and occupational pollutant, acts as a metalloestrogen to induce cell proliferation. It is suggested that Cd may also contribute to the development of estrogen-related cancers like ovarian cancer which is the most lethal cancer in women. Furthermore, it was shown that melatonin has antiproliferative effect on estradiol (E2)-induced proliferation. The aim of the present study was to evaluate whether melatonin inhibits Cd-induced proliferation in ovarian cancer cell lines and also whether Cd and melatonin can modulate estrogen receptor α (ERα) expression. OVCAR3 and SKOV3 human ovarian cancer cell lines were treated with CdCl 2 (1-100 nM) and melatonin (1 µM) for 48 h. Cell proliferation evaluation was carried out by bromodeoxyuridine (BrdU) incorporation assay. ERα expression was detected by western blotting method 24 h after cell treatment. The results were demonstrated that Cd increased proliferation of ovarian cancer cell lines in a dose dependent manner. Melatonin inhibited Cd-induced proliferation of OVCAR3 and SKOV3 cell lines. Moreover, CdCl 2 significantly increased ERα expression in both OVCAR3 and SKOV3 cell lines compared to control. Melatonin significantly inhibited Cd inducing effect on ERα expression of OVCAR3 and SKOV3 cell. In conclusion, due to the proliferative effect on ovarian cancer cell lines, Cd could play an important role in the etiology of ovarian cancer by inducing cells ERα expression. Furthermore, melatonin has the protective role on Cd-induced cell proliferation by inhibition of ERα expression.