Ischemic acute renal failure induces the expression of a wide range of nephrogenic proteins - PubMed (original) (raw)
. 2006 Apr;290(4):R861-70.
doi: 10.1152/ajpregu.00384.2005. Epub 2005 Nov 10.
Affiliations
- PMID: 16284088
- DOI: 10.1152/ajpregu.00384.2005
Free article
Ischemic acute renal failure induces the expression of a wide range of nephrogenic proteins
Sandra Villanueva et al. Am J Physiol Regul Integr Comp Physiol. 2006 Apr.
Free article
Abstract
Ischemia-induced acute renal failure (ARF) is a disorder with high morbidity and mortality. ARF is characterized by a regeneration phase, yet its molecular basis is still under study. Changes in gene expression have been reported in ARF, and some of these genes are specific for nephrogenic processes. We tested the hypothesis that the regeneration process developed after ischemia-induced ARF can be characterized by the reexpression of important regulatory proteins of kidney development. The distribution pattern and levels of nephrogenic proteins in rat kidneys after ischemia were studied by immunohistochemistry and immunoblot analysis. Ischemic damage was assessed by conventional morphology, serum creatinine, and the apoptotic markers terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) and caspase 3. The hypoxia levels induced by ischemia were assessed by specific markers: hypoxia induced factor (HIF)-1alpha and 2-pimonidazole. In kidneys with ARF, an important initial damage was observed through periodic acid Schiff staining, by the induction of damage markers alpha-smooth muscle actin (alpha-SMA) and macrophages (ED-1) and by apoptosis induction. In agreement with diminishing renal damage at the initial reparation phase, the expression of the mesenchymal proteins vimentin, neural cell adhesion molecules (Ncam), and the epithelial markers, Pax-2, Noggin, and basic fibroblast growth factor was observed; after, in a second phase, the tubular markers bone morphogen protein 7, Engrailed, and Lim-1, as well as the transcription factors Smad and p-Smad, were observed. Additionally, the endothelial markers VEGF and Tie-2 were induced at the initial and middle stages of regeneration phase, respectively. The expression of these proteins was restricted in time and space, as well as spatially and temporally. Because all of these proteins are important in maintaining a functional kidney, these results suggest that during the regeneration process after induced hypoxia, these nephrogenic proteins can be reexpressed in a similar fashion to that observed during development, thus restoring mature kidney function.
Similar articles
- bFGF induces an earlier expression of nephrogenic proteins after ischemic acute renal failure.
Villanueva S, Cespedes C, Gonzalez A, Vio CP. Villanueva S, et al. Am J Physiol Regul Integr Comp Physiol. 2006 Dec;291(6):R1677-87. doi: 10.1152/ajpregu.00023.2006. Epub 2006 Jul 27. Am J Physiol Regul Integr Comp Physiol. 2006. PMID: 16873559 - Inhibition of bFGF-receptor type 2 increases kidney damage and suppresses nephrogenic protein expression after ischemic acute renal failure.
Villanueva S, Cespedes C, Gonzalez AA, Roessler E, Vio CP. Villanueva S, et al. Am J Physiol Regul Integr Comp Physiol. 2008 Mar;294(3):R819-28. doi: 10.1152/ajpregu.00273.2007. Epub 2008 Jan 9. Am J Physiol Regul Integr Comp Physiol. 2008. PMID: 18184769 - Effect of ischemic acute renal damage on the expression of COX-2 and oxidative stress-related elements in rat kidney.
Villanueva S, Céspedes C, González AA, Vio CP, Velarde V. Villanueva S, et al. Am J Physiol Renal Physiol. 2007 May;292(5):F1364-71. doi: 10.1152/ajprenal.00344.2006. Epub 2007 Jan 23. Am J Physiol Renal Physiol. 2007. PMID: 17244895 - Gene regulation in regeneration after acute kidney injury.
Beamish JA, Watts JA, Dressler GR. Beamish JA, et al. J Biol Chem. 2024 Aug;300(8):107520. doi: 10.1016/j.jbc.2024.107520. Epub 2024 Jun 29. J Biol Chem. 2024. PMID: 38950862 Free PMC article. Review. - Gene expression in nephrotoxic and ischemic acute renal failure.
Safirstein R. Safirstein R. J Am Soc Nephrol. 1994 Jan;4(7):1387-95. doi: 10.1681/ASN.V471387. J Am Soc Nephrol. 1994. PMID: 8161720 Review.
Cited by
- Bi-functional KIT-PR1P peptides combine with VEGF to protect ischemic kidney in rats by targeting to Kim-1.
Zhou R, Liu H, Hou X, Liu Q, Sun S, Li X, Cao W, Nie W, Shi C, Chen W. Zhou R, et al. Regen Ther. 2023 Dec 28;25:162-173. doi: 10.1016/j.reth.2023.12.014. eCollection 2024 Mar. Regen Ther. 2023. PMID: 38178930 Free PMC article. - Functioning and mechanisms of PTMs in renal diseases.
Liu Z, Yang J, Du M, Xin W. Liu Z, et al. Front Pharmacol. 2023 Nov 21;14:1238706. doi: 10.3389/fphar.2023.1238706. eCollection 2023. Front Pharmacol. 2023. PMID: 38074159 Free PMC article. Review. - Insights into Repeated Renal Injury Using RNA-Seq with Two New RPTEC Cell Lines.
Merrick BA, Martin NP, Brooks AM, Foley JF, Dunlap PE, Ramaiahgari S, Fannin RD, Gerrish KE. Merrick BA, et al. Int J Mol Sci. 2023 Sep 18;24(18):14228. doi: 10.3390/ijms241814228. Int J Mol Sci. 2023. PMID: 37762531 Free PMC article. - FGF2 Alleviates Microvascular Ischemia-Reperfusion Injury by KLF2-mediated Ferroptosis Inhibition and Antioxidant Responses.
Chen F, Zhan J, Liu M, Mamun AA, Huang S, Tao Y, Zhao J, Zhang Y, Xu Y, He Z, Du S, Lu W, Li X, Chen Z, Xiao J. Chen F, et al. Int J Biol Sci. 2023 Aug 21;19(13):4340-4359. doi: 10.7150/ijbs.85692. eCollection 2023. Int J Biol Sci. 2023. PMID: 37705747 Free PMC article. - Advances and potential of regenerative medicine in pediatric nephrology.
Slaats GG, Chen J, Levtchenko E, Verhaar MC, Arcolino FO. Slaats GG, et al. Pediatr Nephrol. 2024 Feb;39(2):383-395. doi: 10.1007/s00467-023-06039-0. Epub 2023 Jul 3. Pediatr Nephrol. 2024. PMID: 37400705 Free PMC article. Review.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Other Literature Sources
Research Materials
Miscellaneous