ArticleBMC nephrology2016
RhoA deficiency disrupts podocyte cytoskeleton and induces podocyte apoptosis by inhibiting YAP/dendrin signal.
Article in BMC nephrology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 32 citations in OpenAlex.
- Proximity-based proteomics (BioID) uncovers the Rho GTPase interactome in kidney podocytes.Frontiers in cell and developmental biology · 2025Article
- New Insights into the Pleiotropic Actions of Dipeptidyl Peptidase-4 Inhibitors Beyond Glycaemic Control.TouchREVIEWS in endocrinology · 2024Review
- Swollen Feet: Considering the Paradoxical Roles of Interleukins in Nephrotic Syndrome.Biomedicines · 2024Review
- A preliminary study of the miRNA restitution effect on CNV-induced miRNA downregulation in CAKUT.BMC genomics · 2024Article
- Cytoskeleton Rearrangement in Podocytopathies: An Update.International journal of molecular sciences · 2024Review
- Effects and mechanism of Rictor interference in podocyte injury induced by high glucose.Experimental and therapeutic medicine · 2023Article
- A YAP/TAZ-ARHGAP29-RhoA Signaling Axis Regulates Podocyte Protrusions and Integrin Adhesions.Cells · 2023Article
- Hippo/YAP signaling pathway: a new therapeutic target for diabetes mellitus and vascular complications.Therapeutic advances in endocrinology and metabolism · 2023Review
- Rho GTPases in kidney physiology and diseases.Small GTPases · 2022Article
- Integrin β3 overexpression contributes to podocyte injury through inhibiting RhoA/YAP signaling pathway.Bioengineered · 2021Article
- Exosomal microRNA-16-5p from human urine-derived stem cells ameliorates diabetic nephropathy through protection of podocyte.Journal of cellular and molecular medicine · 2021Article
- Review
- Cholesterol activates the Wnt/PCP-YAP signaling in SOAT1-targeted treatment of colon cancer.Cell death discovery · 2021Article
- Protective effects of DPP-4 inhibitor on podocyte injury in glomerular diseases.BMC nephrology · 2020Article
- Modulation of proteomic and inflammatory signals by Bradykinin in podocytes.Journal of advanced research · 2020Article
- Yes-associated protein regulates podocyte cell cycle re-entry and dedifferentiation in adriamycin-induced nephropathy.Cell death & disease · 2019Article
- The motor protein Myo1c regulates transforming growth factor-β-signaling and fibrosis in podocytes.Kidney international · 2019Article
- Role of mTOR signaling in the regulation of high glucose-induced podocyte injury.Experimental and therapeutic medicine · 2019Article
- Expression of DENDRIN in several glomerular diseases and correlation to pathological parameters and renal failure - preliminary study.Diagnostic pathology · 2018Article
- Similar Biophysical Abnormalities in Glomeruli and Podocytes from Two Distinct Models.Journal of the American Society of Nephrology : JASN · 2018Article
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Authors and funding
22 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPodocyte apoptosis is a major mechanism that leads to proteinuria in many kidney diseases. However, the concert mechanisms that cause podocyte apoptosis in these kidney diseases are not fully understood. RhoA is one of Rho GTPases that has been well studied and plays a key role in regulating cytoskeletal architecture. Previous study showed that insufficient RhoA could result in rat aortic smooth muscle cell apoptosis. However, whether RhoA is involved in podocyte apoptosis remains unknown.
methodsCulture podocytes were treated with LPS, ADR or siRNA for 48 h before harvest. Subcellular immunoblotting, qRT-PCR, immunofluorescence and flow cytometry were used to exam the expression and function of RhoA or YAP in podocytes.
resultsWe found that the expression of RhoA and its activity were significantly decreased in LPS or ADR-injured podocytes, accompanying loss of stress fibers and increased cell apoptosis. Knocking down RhoA or its downstream effector mDia expression by siRNA also caused loss of stress fibers and podocyte apoptosis. Moreover, our results further demonstrated that RhoA deficiency could reduce the mRNA and protein expression of YAP, which had been regarded as an anti-apoptosis protein in podocyte. Silenced dendrin expression significantly abolished RhoA, mDia or YAP deficiency-induced podocyte apoptosis.
conclusionRhoA deficiency could disrupt podocyte cytoskeleton and induce podocyte apoptosis by inhibiting YAP/dendrin signal. RhoA/mDia/YAP/dendrin signal pathway may potentially play an important role in regulating podocyte apoptosis. Maintaining necessary RhoA would be one potent way to prevent proteinuria kidney diseases.
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