ArticleNephron2015
TGFβ-Induced Actin Cytoskeleton Rearrangement in Podocytes Is Associated with Compensatory Adaptation of Mitochondrial Energy Metabolism.
Article in Nephron, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 17 citations in OpenAlex.
- Klotho prevents transforming growth factor-β2-induced senescent-like morphological changes in the retinal pigment epithelium.Cell death & disease · 2023Article
- PTEN-induced kinase 1 deficiency alters albumin permeability and insulin signaling in podocytes.Journal of molecular medicine (Berlin, Germany) · 2022Article
- Rapid manipulation of mitochondrial morphology in a living cell with iCMM.Cell reports methods · 2021Article
- Podocyte Glucocorticoid Receptors Are Essential for Glomerular Endothelial Cell Homeostasis in Diabetes Mellitus.Journal of the American Heart Association · 2021Article
- Features of Cytokine Storm Identified by Distinguishing Clinical Manifestations in COVID-19.Frontiers in public health · 2021Article
- The diabetic microenvironment causes mitochondrial oxidative stress in glomerular endothelial cells and pathological crosstalk with podocytes.Cell communication and signaling : CCS · 2020Article
- Endothelin receptor-A mediates degradation of the glomerular endothelial surface layer via pathologic crosstalk between activated podocytes and glomerular endothelial cells.Kidney international · 2019Article
- Healthy diet is associated with gene expression in blood: the Framingham Heart Study.The American journal of clinical nutrition · 2019Article
- Glomerular Endothelial Cell Stress and Cross-Talk With Podocytes in Early [corrected] Diabetic Kidney Disease.Frontiers in medicine · 2018Review
- Glomerular Endothelial Mitochondrial Dysfunction Is Essential and Characteristic of Diabetic Kidney Disease Susceptibility.Diabetes · 2017Article
- mir-218-2 promotes glioblastomas growth, invasion and drug resistance by targeting CDC27.Oncotarget · 2017Article
- Shift in Focus-To Explore the Role of the Endothelium in Kidney Disease.HSOA journal of nephrology & renal therapy · 2016Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
BACKGROUND/
aimsIn podocytes, the overexpression of TGFβ ligands and receptors during glomerulosclerosis could be a causal factor for injury induction and perpetuation in glomerular tufts. Mitochondrial dysfunction and oxidative stress are emerging as potential therapeutic targets in glomerular injury, and TGFβ has been shown to modulate mitochondrial metabolism in different cell types. This study aims at investigating the role of TGFβ in podocyte energy metabolism and cytoskeleton dynamics.
methodsMitochondrial function and cytoskeleton dynamics were analyzed in TGFβ-treated WT and Smad2/3 double KO podocytes.
resultsTGFβ treatment in podocytes induced a significant Smad-dependent increase of mitochondrial oxygen consumption rate (OCR). ATP content was unchanged and increased respiration was not associated with increased mitochondrial mass. Increased cellular reactive oxygen species induced by Smad-mediated TGFβ signaling were reverted by NADPH oxidase inhibitor apocynin. TGFβ treatment did not induce mitochondrial oxidative stress, and Smad2/3-dependent TGFβ signaling and increased mitochondrial OCR were found to be associated with actin cytoskeleton dynamics. The role of motor proteins myosin II and dynamin in TGFβ-induced actin polymerization was demonstrated by specific inhibition, resulting in actin stabilization and normalization of mitochondrial OCR.
conclusionTGFβ-induced rearrangements of actin cytoskeleton are controlled by Smad2/3 signaling pathways and coupled with the activation of mitochondrial ATP synthesis as bioenergetic adaptation to ATP consumption by ATP- and GTP-dependent motor proteins, myosin II and dynamin.
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