ArticlePloS one2013
Transgelin Up-Regulation in Obstructive Nephropathy.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- Unveiling the role of transgelin as a prognostic and therapeutic target in kidney fibrosis via a proteomic approach.Experimental & molecular medicine · 2024Article
- Sitagliptin protects renal glomerular endothelial cells against high glucose-induced dysfunction and injury.Bioengineered · 2022Article
- Transgelin-2 in Multiple Myeloma: A New Marker of Renal Impairment?Molecules (Basel, Switzerland) · 2021Article
- Puromycin aminonucleoside-induced podocyte injury is ameliorated by the Smad3 inhibitor SIS3.FEBS open bio · 2020Article
- Thioredoxin-interacting protein deficiency ameliorates kidney inflammation and fibrosis in mice with unilateral ureteral obstruction.Laboratory investigation; a journal of technical methods and pathology · 2018Article
- The transition of smooth muscle cells from a contractile to a migratory, phagocytic phenotype: direct demonstration of phenotypic modulation.The Journal of physiology · 2016Article
- Whole-transcriptome analysis of UUO mouse model of renal fibrosis reveals new molecular players in kidney diseases.Scientific reports · 2016Article
- The glomerular parietal epithelial cell's responses are influenced by SM22 alpha levels.BMC nephrology · 2014Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fibrosis is a complex and multifactorial process, affecting the structure and compromising the function of several organs. Among those, renal fibrosis is an important pathological change, eventually leading to renal failure. Proteomic analysis of the renal parenchyma in the well-established rat model of unilateral ureteral obstruction (UUO model) suggested that transgelin was up-regulated during the development of fibrosis. Transgelin up-regulation was confirmed both at the protein and at the mRNA level. It was observed that at early stages of fibrosis transgelin was mainly expressed in the interstitial compartment and, more specifically, in cells surrounding the glomeruli. Subsequently, it was confirmed that transgelin expressing cells were activated fibroblasts, based on their extensive co-expression of α-SMA and their complete lack of co-distribution with markers of other cell types (endothelial, epithelial and cells of the immune system). These periglomerular fibroblasts exhibited staining for transgelin mainly cytoplasmic but occasionally nuclear as well. In addition, transgelin expression in periglomerular fibroblasts was absent in renal fibrosis developed in a hypertensive model, compared to the UUO model. Promoter analysis indicated that there are several conserved motifs for transcription factor binding. Among those, Kruppel-like factor 6 was found to be up-regulated in transgelin positive periglomerular activated fibroblasts, suggesting a possible involvement in the mechanism of transgelin up-regulation. These data strongly suggest that transgelin is up-regulated in the obstructive nephropathy and could be used as a novel marker for renal fibrosis in the future.
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