Role of myofibroblasts and collagen type IV in patients of IgA nephropathy as markers of renal dysfunction

Bakshi, Arti; Chhabra, Seema; Joshi, Kusum; Sakhuja,

doi:10.4103/0971-4065.62098

Cited by 9 publications

(10 citation statements)

References 11 publications

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“…[2021] In response to tissue injury, renal interstitial fibroblasts and tubular epithelial cells undergo an activation process to become α-SMA-positive myofibroblast and produce abundant extracellular matrix. [22] A variety of cytokines involve in this phenotypic activation, in which TGF-β is the prime stimulator, as shown in previous studies. [23] The influence of other cytokines depends on regulating the generation of TGF-β.…”

Section: Discussionmentioning

confidence: 77%

Protection of rhein on IgA nephropathy mediated by inhibition of fibronectin expression in rats

Peng

Zeng

et al. 2013

Indian J Pharmacol

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Objective:To investigate the protective effects of rhein on IgA nephropathy (IgAN) in the rat model.Materials and Methods:Twenty-eight female sprague dawley rats were divided randomly into four groups, namely control, IgAN, rhein-prevented and rhein-treated. The pathologic changes on renal tissue were observed by the H and E, staining and the amount of urinary red blood cells and 24-h urinary protein excretion were measured. The glomerular deposition of immune globulin A (IgA) was measured by immunofluorescence staining. Fibronectin (FN) and α-smooth muscle actin (α-SMA) expression on renal tissue were measured via immunohistochemistry.Results:The model of IgAN was established according to Bovine serum albumin-Lipopolysaccharide-Carbon tetrachloride protocol, which was evidenced by histological structural lesions of glomeruli, IgA deposition and urinary measurement. Histological examination of kidney sections from both rhein-prevented group and rhein-treated group showed that glomerular hypertrophy, mesangial expansion, excessive extracellular matrix, and renal capsule dilation were markedly ameliorated compared with IgAN group. Moreover, rhein treatment significantly reduced IgA deposition in glomerulus, the volume of urinary red blood cells and 24-h urinary protein excretion. More importantly, increased FN expression in IgAN was back to normal level in rhein-prevented and rhein-treated group, which was along with the reduction of α-SMA expression in renal tissues.Conclusions:These findings indicate that rhein prevents the development of glomerulosclerosis and halts the progression of IgAN via inhibition of FN and α-SMA expression.

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Section: Discussionmentioning

confidence: 77%

Protection of rhein on IgA nephropathy mediated by inhibition of fibronectin expression in rats

Peng

Zeng

et al. 2013

Indian J Pharmacol

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“…IL1RN is involved in autoinflammatory disease ( 24 ) and may contribute to the risk of IgAN ( 25 , 26 ). COL4A2 is a member of the collagen type IV family that may be effective as a marker of renal dysfunction ( 27 ). Furthermore, IL1RN and COL4A2 were enriched in a number of inflammation-associated biological processes such as the negative regulation of the IL1-mediated signaling pathway and negative regulation of heterotypic cell-cell adhesion.…”

Section: Discussionmentioning

confidence: 99%

Identification of potential biomarkers and therapeutic targets for human IgA nephropathy and hypertensive nephropathy by bioinformatics analysis

Cui

Liu

Cui

et al. 2017

Molecular Medicine Reports

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In order to further elucidate the potential correlations and treatments of IgA nephropathy (IgAN) and hypertensive nephropathy (HT), bioinformatics analysis of IgAN and HT was performed. The mRNA expression profiles of human renal biopsy samples from patients with IgAN, patients with HT and pre-transplant healthy living controls (LD) were downloaded from the Gene Expression Omnibus database. Then, the differentially expressed genes (DEGs) were identified and functions of DEGs were analyzed. Finally, the regulatory networks containing DEGs and related-transcription factors (TFs) were constructed using Cytoscape software. When compared with the LD group, 134 and 188 DEGs were obtained in the IgAN and HT groups, respectively. A total of 39 genes were altered in the HT group when compared with the IgAN group. In addition, 66 genes were shared in the IgAN and HT groups when compared with the LD group, 6 of which [early growth response 1, activating transcription factor 3, nuclear receptor subfamily 4 group A member 2 (NR4A2), NR4A1, v-maf avian musculoaponeurotic fibrosarcoma oncogene homolog F and Kruppel like factor 6] were identified as TFs. In addition, DEGs including interleukin (IL) 1 receptor antagonist, collagen type 4 α2 chain, IL8, FBJ murine osteosarcoma viral oncogene homolog and somatostatin were enriched in a number of inflammation-associated biological processes, and DEGs including structural maintenance of chromosomes protein 3, v-crk avian sarcoma virus CT10 oncogene homolog and myosin 6 were enriched in non-inflammation-associated biological processes. Therefore, the differentially expressed TF genes and the genes associated with inflammation may be effective as potential therapeutic targets for IgAN and HT.

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“…16,17 α-Smooth muscle actin (α-SMA), as a specific marker for EMT, takes part in the development and progression of RIF. 16,18 Of all the cytokines and growth factors involved, transforming growth factor (TGF)-β1 plays the most important role, and the increased expression of TGF-β1 is closely correlated with the development of RIF. 19,20 TGF-β1 is known to be one of the major mediators which leads to RIF by inducing the production of α-SMA and ECM (Col-IV and FN) in the renal interstitium.…”

Section: Introductionmentioning

confidence: 99%

Association of PAX2 with Cell Apoptosis in Unilateral Ureteral Obstruction Rats

et al. 2012

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Renal interstitial fibrosis (RIF) is the final common pathway for chronic kidney disease. Cell apoptosis is a critical detrimental event that leads to renal fibrosis. Paired box 2 (PAX2) plays a major role in the development of the kidney. This study was performed to investigate whether PAX2 was associated with cell apoptosis in the progression of RIF in unilateral ureteral obstruction (UUO) rats. Eighty Wistar male rats were divided into two groups randomly: sham operation group (SHO) and model group subjected to UUO (GU), n = 40, respectively. The model was established by left ureteral ligation. Renal tissues were collected 14 and 28 days after surgery. Protein expressions of PAX2, transforming growth factor-β1 (TGF-β1), α-smooth muscle actin (α-SMA), collagen-IV (Col-IV), fibronectin (FN), and caspase-3 were detected using immunohistochemical analysis; mRNA expression of PAX2 in renal tissue was detected by real-time reverse transcription polymerase chain reaction; and RIF index and cell apoptosis index in renal interstitium were also calculated. When compared with those in the SHO group, expressions of PAX2 (protein and mRNA) were markedly increased in the GU group (each p < 0.01). Protein expressions of TGF-β1, α-SMA, Col-IV, FN, and caspase-3 and RIF index and cell apoptosis index in the GU group were remarkably increased when compared with those in the SHO group (each p < 0.01). The protein expression of PAX2 was positively correlated with the protein expressions of TGF-β1, α-SMA, Col-IV, FN, and caspase-3 and with RIF index and cell apoptosis index (all p < 0.01). The apoptotic cell in our observation was mainly derived from renal tubular epithelial cells. In conclusion, the increased expression of PAX2 is associated with cell apoptosis in the progression of RIF in UUO rats, suggesting that PAX2 is a potentially therapeutic target for prevention of RIF.

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Role of myofibroblasts and collagen type IV in patients of IgA nephropathy as markers of renal dysfunction

Cited by 9 publications

References 11 publications

Protection of rhein on IgA nephropathy mediated by inhibition of fibronectin expression in rats

Protection of rhein on IgA nephropathy mediated by inhibition of fibronectin expression in rats

Identification of potential biomarkers and therapeutic targets for human IgA nephropathy and hypertensive nephropathy by bioinformatics analysis

Association of PAX2 with Cell Apoptosis in Unilateral Ureteral Obstruction Rats

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