ArticleScientific reports2019
Coro2b, a podocyte protein downregulated in human diabetic nephropathy, is involved in the development of protamine sulphate-induced foot process effacement.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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7 citing papers in PubMed, 11 citations in OpenAlex.
- Role of the UHRF1-KLHL6-CORO2B axis in obesity-related insulin resistance.Journal of diabetes investigation · 2026Article
- Investigation of psychosocial stress and DNA methylation in genes related to immune response, metabolism, and calcium signaling among African American and White middle-aged adults.Environmental epigenetics · 2026Article
- Actin Cytoskeleton and Integrin Components Are Interdependent for Slit Diaphragm Maintenance inCells · 2024Article
- Candidate Genes and Gene Networks Change with Age in Japanese Black Cattle by Blood Transcriptome Analysis.Genes · 2023Article
- Shared Patterns of Gene Expression and Protein Evolution Associated with Adaptation to Desert Environments in Rodents.Genome biology and evolution · 2022Article
- KCNQ1OT1 inhibition alleviates high glucose-induced podocyte injury by adsorbing miR-23b-3p and regulating Sema3A.Clinical and experimental nephrology · 2022Article
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9 authors at 6 institutions in 1 country.
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Abstract
Podocytes have an important role in the pathogenesis of diabetic nephropathy (DN). Podocyte foot process effacement, mediated largely by the actin-based cytoskeleton of foot processes, is commonly detected in DN and is believed to be a key pathogenic event in the development of proteinuria. In this study, we identified coronin 2b (Coro2b), a member of known actin-regulating proteins, the coronins, as a highly podocyte-enriched molecule located at the cytoplasmic side of the apical plasma membrane. Studies in human renal biopsies show that glomerular Coro2b expression is significantly down-regulated in patients with DN. Studies in knockout mice indicate that Coro2b is not required for the development or maintenance of the glomerular filtration barrier. Moreover, inactivation of Coro2b specifically in podocytes does not affect the outcome of nephropathy in a streptozotocin-induced diabetes model. However, Coro2b seems to modulate the reorganization of foot processes under pathological conditions as Coro2b knockout podocytes are partially protected from protamine sulfate perfusion-induced foot process effacement. Taken together, our study suggests a role for Coro2b in the pathogenesis of glomerulopathies. Further studies regarding the involvement of Coro2b in podocyte health and diseases are warranted.
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