Ricardo Marques | Universidade da Beira Interior (original) (raw)

Research Papers by Ricardo Marques

Molecular and Cellular Biochemistry, 2008

Biochemical Pharmacology, 2015

The development of prostate cancer (PCa) is intimately associated with the hormonal environment, ... more The development of prostate cancer (PCa) is intimately associated with the hormonal environment, and the sex steroids estrogens have been implicated in prostate malignancy. However, if some studies identified estrogens as causative agents of PCa, others indicated that these steroids have a protective role counteracting prostate overgrowth. The tyrosine kinase receptor c-KIT and its ligand, the stem cell factor (SCF), have been associated with the control of cell proliferation/apoptosis and prostate carcinogenesis, and studies show that estrogens regulate their expression in different tissues, though, in the case of prostate this remains unknown. The present study aims to evaluate the role of 17β-estradiol (E2) in regulating the expression of SCF/c-KIT in human prostate cell lines and rat prostate, and to investigate the consequent effects on prostate cell proliferation and apoptosis. qPCR, Western Blot, and immuno(cito)histochemistry analysis showed that E2-treatment decreased the expression of SCF and c-KIT both in human prostate cells and rat prostate. Furthermore, the diminished expression of SCF/c-KIT was underpinned by the diminished prostate weight and reduced proliferation index. On the other hand, the results of TUNEL labelling, the increased activity of caspase-3, and the augmented expression of caspase-8 and Fas system in the prostate of E2-treated animals indicated augmented apoptosis in response to E2. The obtained results demonstrated that E2 down-regulated the expression of SCF/c-KIT system in prostate cells, which was associated with antiproliferative and proapoptotic effects. Moreover, these findings support the protective role of estrogens in PCa and open new perspectives on the application of estrogen-based therapies.

Transgenic research, Jan 9, 2015

Regucalcin (RGN) is a calcium-binding protein underexpressed in human prostate cancer cases, and ... more Regucalcin (RGN) is a calcium-binding protein underexpressed in human prostate cancer cases, and it has been associated with the suppression of cell proliferation and the regulation of several metabolic pathways. On the other hand, it is known that the metabolic reprogramming with augmented glycolytic metabolism and enhanced proliferative capability is a characteristic of prostate cancer cells. The present study investigated the influence of RGN on the glycolytic metabolism of rat prostate by comparing transgenic adult animals overexpressing RGN (Tg-RGN) with their wild-type counterparts. Glucose consumption was significantly decreased in the prostate of Tg-RGN animals relatively to wild-type, and accompanied by the diminished expression of glucose transporter 3 and glycolytic enzyme phosphofructokinase. Also, prostates of Tg-RGN animals displayed lower lactate levels, which resulted from the diminished expression/activity of lactate dehydrogenase. The expression of the monocarboxyl...

Translational Research, 2015

Regucalcin (RGN) is a calcium (Ca(2+))-binding protein that displays a characteristic downregulat... more Regucalcin (RGN) is a calcium (Ca(2+))-binding protein that displays a characteristic downregulated expression with aging in several tissues. Besides its role in regulating intracellular Ca(2+) homeostasis, RGN has been associated with the control of oxidative stress, cell proliferation, and apoptosis. Thus, the diminished expression of RGN with aging may contribute to the age-associated deterioration of cell function. In the present study, we hypothesized that the maintenance of high expression levels of RGN may prevent age-related alterations in the processes mentioned previously. First, we confirmed that RGN expression is significantly diminished in the prostate of 8-, 9-, 12-, and 24-months wild-type rats. Then, the effect of aging on lipid peroxidation, antioxidant defenses, cell proliferation, and apoptosis in the prostate of wild-type controls and transgenic rats overexpressing RGN (Tg-RGN) was investigated. The activity of glutathione and the antioxidant capacity were increased in Tg-RGN rats in response to the age-associated increase in thiobarbituric acid reactive substances levels, an effect not seen in wild type. Overexpression of RGN also counteracted the effect of aging increasing prostate cell proliferation. In contrast to wild-type animals, the prostate weight of Tg-RGN did not change with aging and was underpinned by the diminished expression of stem cell factor and c-kit, and increased expression of p53. In addition, aged Tg-RGN animals displayed increased expression (activity) of apoptosis regulators, therefore not showing the age-induced resistance to apoptosis observed in wild type. Altogether, these findings indicate the protective role of RGN against the development of age-related pathologies, such as, for example, prostate cancer.

The international journal of biochemistry & cell biology, 2012

Prostate cancer (PCa) progresses from an early stage, confined to prostate, to a more aggressive ... more Prostate cancer (PCa) progresses from an early stage, confined to prostate, to a more aggressive metastasized cancer related with loss of androgen responsiveness. Although, it has been recognized that PCa cells have unique metabolic features, their glycolytic profile in androgen-dependent and androgen-independent stages of disease is much less known. Hence, the main purpose of this study was to compare glucose metabolism in androgen-responsive (LNCaP) and androgen-nonresponsive (PC3) PCa cells. Cell culture medium was collected and differences in glucose consumption and, lactate and alanine production were measured using Proton Nuclear Magnetic Resonance ((1)H NMR) spectra analysis. The mRNA and protein expression of glucose transporters (GLUT1 and GLUT3), phosphofructokinase 1 (PFK1), lactate dehydrogenase (LDH) and monocarboxylate transporter (MCT4) were determined by real-time PCR and Western Blot, respectively. The obtained results demonstrate that androgen-responsive (LNCaP) an...

Experimental Cell Research, 2015

Regucalcin (RGN) is a calcium-binding protein, which has been shown to be underexpressed in cance... more Regucalcin (RGN) is a calcium-binding protein, which has been shown to be underexpressed in cancer cases. This study aimed to determine the association of RGN expression with clinicopathological parameters of human breast cancer. In addition, the role of RGN in malignancy of mammary gland using transgenic rats overexpressing the protein (Tg-RGN) was investigated. Wild-type (Wt) and Tg-RGN rats were treated with 7,12-dimethylbenz[α]anthracene (DMBA). Carcinogen-induced tumors were histologically classified and the Ki67 proliferation index was estimated. Immunohistochemistry analysis showed that RGN immunoreactivity was negatively correlated with the histological grade of breast infiltrating ductal carcinoma suggesting that progression of breast cancer is associated with loss of RGN. Tg-RGN rats displayed lower incidence of carcinogen-induced mammary gland tumors, as well as lower incidence of invasive forms. Moreover, higher proliferation was observed in non-invasive tumors of Wt animals comparatively with Tg-RGN. Overexpression of RGN was associated with diminished expression of cell-cycle inhibitors and increased expression of apoptosis inducers. Augmented activity of apoptosis effector caspase-3 was found in the mammary gland of Tg-RGN. RGN overexpression protected from carcinogen-induced mammary gland tumor development and was linked with reduced proliferation and increased apoptosis. These findings indicated the protective role of RGN in the carcinogenesis of mammary gland.

Yamaguchi and, although classified as a calcium (Ca 2+ )binding protein, it does not contain the ... more Yamaguchi and, although classified as a calcium (Ca 2+ )binding protein, it does not contain the typical eF-hand Ca 2+ -binding motif . The overall structure of RGN protein contains 24 β-strands forming 6 β-sheets able to bind diverse divalent cations (Ca 2+ , Mg 2+ , Mn 2+ and Zn 2+ ) . The RGN ability to bind Ca 2+ was recently confirmed by X-ray diffraction studies which have allowed the resolving of the crystal structure of human RGN protein bound to Ca 2+ or Zn 2+ cations. Although Ca 2+ and Zn 2+ ions bind to the same amino acid residues forming a unique metal binding site in a nearly identical coordination, an very much higher level of dissociation constant is documented for Ca 2+ which could be relevant under non-physiological conditions, whereas elevated Ca 2+ levels can occur .

Papers by Ricardo Marques

Medical Oncology, 2015

Androgens have been associated with the development of normal breast, and their role in mammary g... more Androgens have been associated with the development of normal breast, and their role in mammary gland carcinogenesis has also been described. Several studies reported that androgens inhibit breast cancer cell growth, whereas others linked their action with the modulation of calcium (Ca 2?) pumps, Ca 2? channels and Ca 2?binding proteins. Also, it is known that deregulated Ca 2? homeostasis has been implicated in the pathophysiology of breast. The L-type Ca 2? channels (LTCCs) were found to be up-regulated in colon, colorectal and prostate cancer, but their presence in breast tissues remains uncharacterized. On the other hand, regucalcin (RGN) is a Ca 2?binding protein involved in the control of mammary gland cell proliferation, which has been identified as an androgen target gene in distinct tissues except breast. This study aimed to confirm the expression and activity of LTCCs in human breast cancer cells and investigate the effect of androgens in regulating the expression of a 1C subunit (Ca v 1.2) of LTCCs and Ca 2?-binding protein RGN. PCR, Western blot, immunofluorescence and electrophysiological experiments demonstrated the expression and activity of Ca v 1.2 subunit in MCF-7 cells. The MCF-7 cells were treated with 1, 10 or 100 nM of 5a-dihydrotestosterone (DHT) for 24-72 h. The obtained results showed that 1 nM DHT up-regulated the expression of Ca v 1.2 subunit while diminishing RGN protein levels, which was underpinned by reduced cell viability. These findings first confirmed the presence of LTCCs in breast cancer cells and opened new perspectives for the development of therapeutic approaches targeting Ca 2? signaling. Keywords 5a-Dihydrotestosterone Á Ca v 1.2 Á DHT Á L-type calcium channels Á MCF-7 cells Á Regucalcin

Journal of Cancer Research and Clinical Oncology, 2015

Conclusions The results obtained establish androgens as modulators of glycolytic metabolism in PC... more Conclusions The results obtained establish androgens as modulators of glycolytic metabolism in PCa cells by stimulating glucose consumption, as well as the production and export of lactate, which may represent a crucial issuedriven prostate tumor development. These findings also highlight the importance of PCa therapies targeting AR and metabolism-related proteins.

Conception of a dissertation requires a personal work of reflection, research and inspiration. It... more Conception of a dissertation requires a personal work of reflection, research and inspiration. It is not merely an individualistic work, it results from several contributions to the construction of incentive, will and support for its development. For this reason, I want to thank and dedicate to all that allowed and helped me on this project. First of all, I would like to express my deepest gratitude to my supervisor, Professor Sílvia Socorro, for the opportunity she gave me to develop this study and for the unconditional support, guidance and help during my academic journey. I also acknowledge to my co-supervisor, Professor Cláudio Maia, for all his availability and help. I would also like to thank to Professor Ignacio Verde for providing us L-type calcium channel (α 1C subunit) primers. Moreover, I would like to thank to all my group colleagues, especially to Ricardo Marques, Inês Gomes, Sara Correia, Cátia Vaz, Luís Rato and Daniel Rodrigues, for all the advices, teaching and support. Principally, their friendship and joy was truly important to face all the difficulties during the development of this project. I would also like to thank all my friends, especially to Ana Chegão, Andreia Ramos, Joana Varge, Carlos Gaspar and Ana Rita Magalhães, for all the good times shared, advices and patience during my academic life. Queria agradecer, do fundo do meu coração, aos meus pais por todo o amor, apoio, carinho e confiança incondicionais que sempre me deram. Agradeço-lhes por tudo o que sou hoje! Sem eles nada disto seria possível. Um especial obrigado à minha irmã, Patrícia, por todo o amor, carinho e amizade que sempre me demonstrou. I could not end these acknowledgements without a special thanks to my boyfriend, Joel, for all his love, unconditional support, advices, care, patience and understanding during the good and the bad days. To all of you… Thank you! Androgens in breast cancer cells physiology: a connection with calcium homeostasis? vi Androgens in breast cancer cells physiology: a connection with calcium homeostasis? vii

Prostate cancer (PCa) onset and development requires a sequence of genetic changes and additional... more Prostate cancer (PCa) onset and development requires a sequence of genetic changes and additional metabolic adaptations to ensure survival of the modified cells and to finally achieve a malignant phenotype. This concept may be associated with the “Warburg phenomenon”, which consists of an increased glycolytic capacity and reduced mitochondrial oxidative phosphorylation, maintained even in the presence of high oxygen concentrations. It has been proposed that this alteration may be a metabolic mechanism of tumor cells to survive and growth under hypoxic conditions through the modulation of key enzymes and transporters involved in glycolytic metabolic pathways. PCa progression is characterized by a transition from an androgen-dependent to an androgen-independent phenotype, which corresponds to early and advanced stages of PCa respectively, and an increase of glucose uptake and consumption is required for rapid proliferation of androgen-dependent cells. In addition, androgen-responsive ...

$Research paper thumbnail of Paradoxical and contradictory effects of imatinib in two cell line models of hormone-refractory prostate cancer$

The Prostate, 2015

BACKGROUND. Imatinib mesylate is a chemotherapeutic drug that inhibits the tyrosine kinase activi... more BACKGROUND. Imatinib mesylate is a chemotherapeutic drug that inhibits the tyrosine kinase activity of c-KIT and has been successfully used to treat leukemias and some solid tumors. However, its application for treatment of hormone-refractory prostate cancer (HRPC) has shown modest effectiveness and did not follow the outcomes in cultured cells or animal models. Moreover, the molecular pathways by which imatinib induces cytotoxicity in prostate cancer cells are poorly characterized. METHODS. Two cell line models of HRPC (DU145 and PC3) were exposed to 20 mM of imatinib for 6-72 hr. MTS assay was used to assess cell viability during the course of experiment. Gene expression analysis of c-KIT, cell-cycle and apoptosis regulators, and angiogenic factors was determined by means of real-time PCR, western blot, and/or immunocytochemistry. The enzymatic activity of the apoptosis effector, caspase-3, was determined by a colorimetric assay. RESULTS. Imatinib significantly decreased the viability of DU145 cells but paradoxically augmented the viability of PC3 cells. DU145 cells displayed diminished expression of anti-apoptotic Bcl-2 protein and augmented levels of caspase-8 and-9, as well as, increased enzymatic activity of caspase-3 in response to imatinib. No differences existed on the expression levels of apoptosis-related proteins in PC3 cells treated with imatinib, though the activity of caspase-3 was decreased. The mRNA levels of angiogenic factor VEGF were decreased in DU145-treated cells, whereas an opposite effect was seen in PC3. In addition, it was shown that DU145 and PC3 cells present a differential expression of c-KIT protein variants. CONCLUSION. DU145 and PC3 cells displayed a contradictory behavior in response to imatinib, which was underpinned by a distinct expression pattern (or activity) of target regulators of cell-cycle, apoptosis, and angiogenesis. The paradoxical effect of imatinib in PC3 cells may be related with the differential expression of c-KIT protein variants. Moreover, the present findings helped to understand the discrepancies in the efficacy of imatinib as therapeutic option in HRPC.

The Prostate, 2014

Regucalcin (RGN) is a calcium (Ca(2+) )-binding protein underexpressed in prostate adenocarcinoma... more Regucalcin (RGN) is a calcium (Ca(2+) )-binding protein underexpressed in prostate adenocarcinoma comparatively to non-neoplastic prostate or benign prostate hyperplasia cases. Moreover, RGN expression is negatively associated with the cellular differentiation of prostate adenocarcinoma, suggesting that loss of RGN may be associated with tumor onset and progression. However, the RGN actions over the control of prostate cell growth have not been investigated. Androgens are implicated in the promotion of prostate cell proliferation, thus we studied the in vivo effect of androgens on RGN expression in rat prostate. The role of RGN modulating cell proliferation and apoptotic pathways in rat prostate was investigated using transgenic animals (Tg-RGN) overexpressing the protein. In vivo stimulation with 5α-dihydrotestosterone (DHT) down-regulated RGN expression in rat prostate. Cell proliferation index and prostate weight were reduced in Tg-RGN, which was concomitant with altered expressi...

Endocrine Abstracts, 2014

Prostate cancer (PCa) is an endocrine tumor that presents distinct metabolic features associated ... more Prostate cancer (PCa) is an endocrine tumor that presents distinct metabolic features associated with neoplastic development, namely in the transition from the androgendependent to the androgen-independent phenotype that characterizes advanced stages of prostate cancer. Recently, we have found that LNCaP (androgen-responsive) and PC3 (androgen-nonresponsive) PCa cells present distinct glycolytic metabolism profiles in consequence of altered gene expression and/or activity of glycolytic enzymes and transporters. Therefore, this study was designed aiming to examine the effect of androgens on gene expression of glucose transporters and glycolytic enzymes in androgenresponsive PCa cells. LNCaP cells were treated with 10 nM of 5α-dihydrotestosterone (DHT) for 12, 24, and 48 h. Glucose consumption and lactate production were determined spectrophotometrically using commercial kits. Expression of glucose transporters (GLUT1 and GLUT3), phosphofructokinase 1 (PFK1), lactate dehydrogenase (LDH) and monocarboxylate transporter (MCT4) mRNA and protein was analyzed by real-time PCR and Western Blot, respectively. LDH enzymatic activity also was determined. The obtained results demonstrated that androgens stimulation diminished the expression of both GLUT1 and GLUT3, and increased PFK levels. Also, the expression of LDH and MCT4 was diminished in LNCaP cells in the presence of DHT, which was concomitant with decreased enzymatic activity of LDH. In addition, we verified that androgenic regulation of genes associated with glycolytic metabolism underlies altered glucose consumption and lactate production in LNCaP cells. These findings demonstrated that androgens are modulators of glycolytic metabolism in PCa cells, which may represent a relevant aspect driven prostate tumor development. 16th European Congress of Endocrinology

Molecular and Cellular Biochemistry, 2007

Sildenafil citrate (Viagra) is a potent and specific inhibitor of cyclic guanosine monophosphate ... more Sildenafil citrate (Viagra) is a potent and specific inhibitor of cyclic guanosine monophosphate (cGMP)specific phosphodiesterase type 5 (PDE5), which exhibits cardioprotective action against ischemia/reperfusion injury in intact and isolated heart. The mechanism of its cardioprotective action is not completely understood, but some results suggested that sildenafil exerts cardioprotection through the opening of mitochondrial ATP-sensitive K + channels (mitoK ATP). However, the impact of sildenafil citrate per se on isolated heart mitochondrial function is unknown. The goal of this study was to investigate the influence of the compound on mitochondrial function (bioenergetics, Ca 2+-induced mitochondrial permeability transition, and hydrogen peroxide (H 2 O 2) generation) in an attempt to correlate its known actions with effects on heart mitochondria. It was observed that sildenafil citrate concentrations of up to 50 lM did not significantly affect glutamate/malate-supported respiration in states 2, 3, 4, oligomycin-inhibited state 3, and uncoupled respiration. The respiratory control ratio (RCR), the ADP to oxygen ratio (ADP/O), the transmembrane potential (DW), the phosphorylation rate, and the membrane permeability to H + , K + and Ca 2+ were not affected either. However, sildenafil citrate decreased H 2 O 2 generation by mitochondria respiring glutamate/malate, and also decreased the formation of superoxide radical (O 2 •-) generated in a hypoxantine/xantine oxidase system. It was concluded that sildenafil citrate concentrations of up to 50 lM do not affect either rat heart mitochondrial bioenergetics or Ca 2+induced mitochondrial permeability transition, but it depresses H 2 O 2 generation by acting as a superoxide dismutase (SOD)-mimetic. By preventing reactive oxygen species (ROS) generation, sildenafil citrate may preserve heart mitochondrial function.

European Journal of Cancer, 2012

Introduction: Programmed Cell Death 4 (PDCD4) is a tumour suppressor protein that is important in... more Introduction: Programmed Cell Death 4 (PDCD4) is a tumour suppressor protein that is important in translational control. It binds and inhibits eukaryotic Initiation Factor 4A1 (eIF4A1), a helicase unwinding 5 UTR secondary structures. PDCD4 appears to function in different ways depending on cell type and genetic background and, therefore, it is important to study its role in a context-dependent manner. This project focuses on understanding global and message-specific translation regulation by PDCD4 and eIF4A1, and phenotypes induced by those interactions in breast cancer. Material and Method: Immunohistochemical analysis of PDCD4 and eIF4A1 expression was performed on a set of 3,605 cases of archival breast tumours (SEARCH). Transient knock-downs of PDCD4 and eIF4A1 were obtained using siRNA. Polysome fractionation was performed on sucrose gradients, and total, subpolysomal and polysomal RNA was collected from control, PDCD4 and eIF4A1 knock-down cells, and analysed on gene expression microarray, followed by differential gene expression and pathway enrichment analysis. PDCD4 and eIF4A1 levels were assayed by Western blotting. Stable PDCD4 knock-down and over-expression cell lines were generated using lentiviral infections, and growth and migratory properties were assayed. Results and Discussion: In the patient cohort studied, PDCD4 expression is strongly predictive of survival in estrogen receptor positive breast cancer patients. PDCD4 resides in both nuclear and cytoplasmic compartments. Nuclear PDCD4 correlates negatively with grade, stage, tumour size and lymph node status, and the proliferation marker Ki67. It positively correlates with the Luminal A tumour subtype and Bcl-2. In contrast, eIF4A1 is predictive of poor outcome in estrogen receptor negative tumours. PDCD4 levels differ across breast cancer cell lines and increase with confluency. Transient knock-down of PDCD4 in MCF7 exerts few phenotypic effects, whereas knock-down of eIF4A1 causes morphological changes and decrease in cell growth. Stable PDCD4 over-expression results in slower growth phenotype. Transient PDCD4 knock-down yields very few differentially expressed genes, consistent with the very high levels of eIF4A1 expressed by this cell line. In contrast, eIF4A1 knock-down has a very pronounced effect on the polysome profile and affects many genes involved in cell adhesion, cytoskeleton remodelling, apoptosis, development, cell cycle, translation and metabolism. Conclusion: Here we show that PDCD4 and eIF4A1 can differentially predict survival depending on breast cancer subtype. Moreover, knock-downs of these molecules in MCF7 affect the expression of different sets of genes, while only eIF4A1 knock-down induces an obvious phenotype in cell culture. We propose a model to explain how dysregulation of these key translational regulators contributes to the malignant phenotype in breast cancer. 177 Effect of Androgens on the Expression of Ca2+-binding Protein, Regucalcin, and Ca2+-channels in MCF-7 Cells

European Journal of Cancer, 2012

Background: Regucalcin (RGN) is a calcium (Ca 2+)-binding protein, also known as Senescence marke... more Background: Regucalcin (RGN) is a calcium (Ca 2+)-binding protein, also known as Senescence marker protein-30 (SMP30) by its characteristic downregulated expression along with aging process. RGN plays a role as Ca 2+ homeostasis regulator and has been shown to catalyse an important step in L-ascorbic acid biosynthesis being also associated with protection against oxidative stress. In addition, in vitro overexpression studies have been indicating that RGN has suppressive effects on cell proliferation and apoptosis. Moreover, hepatocytes from SMP30 knockout mice are highly susceptible to tumor necrosis factor-a and actinomicyn D induced-apoptosis. Recently, we reported a diminished expression of RGN in human prostate cancer cases which correlates with cellular differentiation of prostate adenocarcinoma. In the present study we analyzed the expression of cell-cycle and apoptosis regulators in the prostate of transgenic rats overexpressing RGN in comparison with their wild-type counterparts. Material and Methods: Sprague Dawley rats overexpressing RGN (Tg-RGN) were obtained from Japan SLC, Inc. Whole prostates (n = 7 for each group) were collected from Tg-RGN and wild-type 3 month-old animals, and longitudinally divided for mRNA and protein extraction. Expression of cell-cycle and apoptosis regulators was determined by means of real-time PCR and Western Blot. Results and Discussion: Tg-RGN rats showed altered prostatic expression of Bcl-2, BAX, caspase 9 and caspase 3, when compared with wild-type animals. Also, the expression of oncogenes, H-ras and c-myc, and that of tumor suppressor gene p53 was modified in Tg-RGN rats. Chk2 and p21 expression was not significantly changed in the prostate of Tg-RGN rats. Cellular homeostasis is maintained by the establishment of a tight equilibrium between cell death, survival and proliferation. The altered patterns of above mentioned proteins in the prostate of animals overexpressing RGN, suggest it may play a role in the control of apoptosis and proliferation of prostate cells. Conclusion: RGN seems to play a role in cell death/survival balance of prostate cells and therefore may be involved in prostate tumor development and/or progression.

Molecular and Cellular Biochemistry, 2008

Biochemical Pharmacology, 2015

Transgenic research, Jan 9, 2015

Translational Research, 2015

The international journal of biochemistry & cell biology, 2012

Experimental Cell Research, 2015

Medical Oncology, 2015

Journal of Cancer Research and Clinical Oncology, 2015

$Research paper thumbnail of Paradoxical and contradictory effects of imatinib in two cell line models of hormone-refractory prostate cancer$

The Prostate, 2015

The Prostate, 2014

Endocrine Abstracts, 2014

Molecular and Cellular Biochemistry, 2007

European Journal of Cancer, 2012

Cellular and Molecular Life Sciences, 2013

Experimental Cell Research, 2015

Microwave and Optical Technology Letters, 2005

In this paper, a compact and narrowband microstrip band-pass structure based on complementary spl... more In this paper, a compact and narrowband microstrip band-pass structure based on complementary split-ring resonators (CSRRs) etched in the back metal level (ground plane) is presented. Specifically, the structure is a two-stage CSRR-based device, where a series gap is etched in the output CSRR stage and two shunt stubs are added in the input cell. By these means we obtain a narrow and quite symmetric band-pass structure. A prototype device with 2% fractional bandwidth has been designed and fabricated for operation at the S-band. The dimensions of the device are as small as 14.6 × 11 mm, while high-frequency selectivity is achieved at both band edges due to the presence of two transmission zeros. To demonstrate the possibility to control the bandwidth over a narrow band, a wider (10% bandwidth) filter has been also designed and fabricated. These structures can be of interest for application in narrow band-pass filters where miniaturization and compatibility with planar technologies are key issues. © 2005 Wiley Periodicals, Inc. Microwave Opt Technol Lett 46: 508–512, 2005; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/mop.21031