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Epidermal Growth Factor Receptor Activation is Essential for Kidney Fibrosis Development

ABSTRACT: We found that EGFR expression increased in interstitial myofibroblasts in human and mouse fibrotic kidneys. Selective EGFR deletion in the fibroblast/pericyte population inhibited interstitial fibrosis in response to unilateral ureteral obstruction, ischemia or nephrotoxins. We used single-nucleus RNA sequencing analysis to demonstrate the role of EGFR activation in UUO model.

ORGANISM(S): Mus musculus

PROVIDER: GSE244839 | GEO | 2023/11/02

REPOSITORIES: GEO

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miR-132 mediates renal fibrosis: miRNA profiling of foxd1-derivative interstital cells derived from murine fibrotic kidneys compared to healthy kidneys

Project description:Chronic kidney disease is associated with progressive renal fibrosis, where perivascular cells give rise to the majority of Î±-SMA positive myofibroblasts. We sought to identify pericytic miRNAs that could serve as a target to decrease myofibroblast formation. We induced kidney fibrosis in FoxD1-GC;Z/Red-mice by unilateral ureteral obstruction (UUO) followed by FACS sorting of dsRed-positive FoxD1-derivative cells and miRNA profiling. MiR-132 selectively increased 21-fold during pericyte-to-myofibroblast formation whereas miR-132 was only 2.5-fold up in total kidney lysates (both in UUO and ischemia-reperfusion injury). MiR-132 silencing in UUO decreased collagen deposition (35%) and tubular apoptosis. Immunohistochemistry, western blot and qRT-PCR confirmed a similar decrease in interstitial Î±-SMA+ cells. Pathway analysis identified a rate-limiting role for miR-132 in myofibroblast proliferation that was confirmed in vitro. Indeed, antagomir-132 treated mice displayed a reduction in the number of proliferating, ki67+ interstitial myofibroblasts. Interestingly, this was selective for the interstitial compartment and did not impair the reparative proliferation of tubular epithelial cells, as evidenced by an increase in ki67+ epithelial cells, as well as increased (p-)RB1, Cyclin-A and decreased RASA1, p21 levels in kidney lysates. Taken together, silencing miR-132 counteracts the progression of renal fibrosis by selectively decreasing myofibroblast proliferation and could potentially serve as a novel antifibrotic therapy. Total RNA obtained from FACS sorted mouse FoxD1-derivative interstitial cells from healthy or fibrotic kidneys

2016-02-16 | E-GEOD-76549 | biostudies-arrayexpress

miR-132 mediates renal fibrosis: Genome-wide analysis of gene expression in foxd1-derivative interstital cells derived from fibrotic kidneys from mice treated with antagomir-132 or scramblemir

Project description:Chronic kidney disease is associated with progressive renal fibrosis, where perivascular cells give rise to the majority of Î±-SMA positive myofibroblasts. We sought to identify pericytic miRNAs that could serve as a target to decrease myofibroblast formation. We induced kidney fibrosis in FoxD1-GC;Z/Red-mice by unilateral ureteral obstruction (UUO) followed by FACS sorting of dsRed-positive FoxD1-derivative cells and miRNA profiling. MiR-132 selectively increased 21-fold during pericyte-to-myofibroblast formation whereas miR-132 was only 2.5-fold up in total kidney lysates (both in UUO and ischemia-reperfusion injury). MiR-132 silencing in UUO decreased collagen deposition (35%) and tubular apoptosis. Immunohistochemistry, western blot and qRT-PCR confirmed a similar decrease in interstitial Î±-SMA+ cells. Pathway analysis identified a rate-limiting role for miR-132 in myofibroblast proliferation that was confirmed in vitro. Indeed, antagomir-132 treated mice displayed a reduction in the number of proliferating, ki67+ interstitial myofibroblasts. Interestingly, this was selective for the interstitial compartment and did not impair the reparative proliferation of tubular epithelial cells, as evidenced by an increase in ki67+ epithelial cells, as well as increased (p-)RB1, Cyclin-A and decreased RASA1, p21 levels in kidney lysates. Taken together, silencing miR-132 counteracts the progression of renal fibrosis by selectively decreasing myofibroblast proliferation and could potentially serve as a novel antifibrotic therapy. Total RNA obtained from FACS sorted mouse renal FoxD1-derivatve interstitial cells from mice that were treated with antagomir-132 or scramblemir and underwent UUO (n=4)

2016-02-16 | E-GEOD-76548 | biostudies-arrayexpress

miR-132 mediates renal fibrosis: miRNA profiling of foxd1-derivative interstital cells derived from murine fibrotic kidneys compared to healthy kidneys

Project description:Chronic kidney disease is associated with progressive renal fibrosis, where perivascular cells give rise to the majority of α-SMA positive myofibroblasts. We sought to identify pericytic miRNAs that could serve as a target to decrease myofibroblast formation. We induced kidney fibrosis in FoxD1-GC;Z/Red-mice by unilateral ureteral obstruction (UUO) followed by FACS sorting of dsRed-positive FoxD1-derivative cells and miRNA profiling. MiR-132 selectively increased 21-fold during pericyte-to-myofibroblast formation whereas miR-132 was only 2.5-fold up in total kidney lysates (both in UUO and ischemia-reperfusion injury). MiR-132 silencing in UUO decreased collagen deposition (35%) and tubular apoptosis. Immunohistochemistry, western blot and qRT-PCR confirmed a similar decrease in interstitial α-SMA+ cells. Pathway analysis identified a rate-limiting role for miR-132 in myofibroblast proliferation that was confirmed in vitro. Indeed, antagomir-132 treated mice displayed a reduction in the number of proliferating, ki67+ interstitial myofibroblasts. Interestingly, this was selective for the interstitial compartment and did not impair the reparative proliferation of tubular epithelial cells, as evidenced by an increase in ki67+ epithelial cells, as well as increased (p-)RB1, Cyclin-A and decreased RASA1, p21 levels in kidney lysates. Taken together, silencing miR-132 counteracts the progression of renal fibrosis by selectively decreasing myofibroblast proliferation and could potentially serve as a novel antifibrotic therapy.

2016-02-16 | GSE76549 | GEO

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2014-03-01 | E-GEOD-50439 | biostudies-arrayexpress

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Project description:Gene array of kidney tissue of wild type and Notch-3 knockout mice was performed following unilateral ureteral obstruction (UUO).

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2017-01-26 | E-MTAB-4984 | biostudies-arrayexpress

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2022-07-20 | GSE174289 | GEO

Effect of Hirudin,Curcumin or Buyang Huanwu Formulas Exposure on Gene Expression of UUO rats

Project description:We performed RNA-Seq analysis to investigate the gene expression patterns in the kidneys of rats with unilateral ureteral obstruction (UUO) treated with hirudin, curcumin or Buyang Huanwu Formula(BHF).

2021-08-06 | GSE181380 | GEO

Transcriptional profiles of kidneys that underwent reversible UUO model using model mice for erythropoietin-deficiency anemia (ISAM)

Project description:We have established a novel mouse model for postnatal erythropoietin (Epo)-deficiency anaemia, designated ISAM (inherited super anemic mouse) using a transgenic complementation rescue technique. To identify responsible signals for myofibroblastic transformation of Renal Erythropoietin-producing cells (REPs), we examined the mRNA expression profile of whole ISAM kidneys that underwent reversible UUO model. Unilateral ureteral obstruction (UUO)-induced gene expression changes were analyzed. Three UUO-treated samples (Clip), three reversed UUO kidneys (ClipR-14), and two sham-treated and one untreated samples were compared.

2013-03-20 | E-GEOD-45304 | biostudies-arrayexpress

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