OASIS overexpression in murine podocyte cell line
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ABSTRACT:
PROVIDER: PRJNA851269 | ENA |
REPOSITORIES: ENA
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Project description:Podocyte injury is involved in the onset and progression of various kidney diseases. We previously demonstrated that the transcription factor, old astrocyte specifically induced substance (OASIS) in myofibroblasts, contributes to kidney fibrosis, as a novel role of OASIS in the kidneys. Importantly, we found that OASIS is also expressed in podocytes; however, the pathophysiological significance of OASIS in podocytes remains unknown. Upon lipopolysaccharide (LPS) treatment, there is an increase in OASIS in murine podocytes. Enhanced serum creatinine levels and tubular injury, but not albuminuria and podocyte injury, are attenuated upon podocyte-restricted OASIS knockout in LPS-treated mice, as well as diabetic mice. The protective effects of podocyte-specific OASIS deficiency on tubular injury are mediated by protein kinase C iota (PRKCI/PKCι), which is negatively regulated by OASIS in podocytes. Furthermore, podocyte-restricted OASIS transgenic mice show tubular injury and tubulointerstitial fibrosis, with severe albuminuria and podocyte degeneration. Finally, there is an increase in OASIS-positive podocytes in the glomeruli of patients with minimal change nephrotic syndrome and diabetic nephropathy. Taken together, OASIS in podocytes contributes to podocyte and/or tubular injury, in part through decreased PRKCI. The induction of OASIS in podocytes is a critical event for the disturbance of kidney homeostasis.
2022-06-22 | GSE206525 | GEO
Project description:Human podocyte cell line mRNA-seq
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Project description:Investigation of whole genome gene expression level changes in OASIS KO calvaria compared to wild-type calvaria. To gain further insight into the potential mechanisms underlying the defective bone formation in OASIS KO mice, we compared the gene expression in calvaria between WT and OASIS KO mice using a microarray.
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Project description:The change of mRNA expression in murine immortalized podocyte were analyzed after miR-26a silencing. These results provide a basical information of molecular pathology in podocyte biology.
2014-10-01 | GSE51210 | GEO
Project description:The change of mRNA expression in murine immortalized podocyte were analyzed after miR-26a silencing. These results provide a basical information of molecular pathology in podocyte biology. Mouse podocytes immortalized by temperature sensitive SV40 were used. Podocyte cultures grown at 33 °C were trypsinized and then cultured with RPMI-1640 without antibiotics in 24-well plates at 60–70% confluence for 2 days. On day 3, an anti-miR negative control (40 pmol) or the miR-26a miRNA inhibitor (40 pmol) was transfected to podocytes. The cells were analyzed after culturing for 24 hour.
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Project description:Podocytes are essential cells of the renal blood filter. They structurally compose the renal blood filter by interdigitating with neighboring podocytes by the means of a modified adherens junction, the slit membrane. In podocyte injury, loss of podocytes is a common feature. Podocyte loss could be mediated by the cleavage of podocyte cell adhesion molecules through the A Disintegrin and Metalloproteinase 10 (ADAM10). Here we show that ADAM10 is highly abundant at the site of blood filtration, namely at podocyte foot processes. Podocyte-expressed ADAM10 is not required for the development of the renal filter but plays a major role in podocyte injury. Following antibody-mediated injury, ADAM10 is upregulated in humans and mice. ADAM10 activity results in the cleavage of cell-cell adhesion molecules. This cleavage paves the way for an activation of the injury related Wnt/-catenin signaling pathway and for podocyte loss. We therefore conclude that ADAM10-mediated ectodomain shedding of injury-related cadherins drives podocyte injury. As part of this project, we have analyzed the membrane proteome of murin podocytes to evaluate the abundance of membrane bound proteases.
2021-02-19 | PXD022213 | Pride
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