ArticleCellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology2011
Reversal by growth hormone of homocysteine-induced epithelial-to-mesenchymal transition through membrane raft-redox signaling in podocytes.
Article in Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 28 citations in OpenAlex.
- The Use of Kidney Biomarkers, Nephrin and KIM-1, for the Detection of Early Glomerular and Tubular Damage in Patients with Acromegaly: A Case-Control Pilot Study.Diseases (Basel, Switzerland) · 2024Article
- Catalpol inhibits HHcy-induced EndMT in endothelial cells by modulating ROS/NF-κB signaling.BMC cardiovascular disorders · 2024Article
- Redox Signaling in Chronic Kidney Disease-Associated Cachexia.Antioxidants (Basel, Switzerland) · 2023Review
- Tripterygium glycoside suppresses epithelial‑to‑mesenchymal transition of diabetic kidney disease podocytes by targeting autophagy through the mTOR/Twist1 pathway.Molecular medicine reports · 2021Article
- Renal effects of growth hormone in health and in kidney disease.Pediatric nephrology (Berlin, Germany) · 2021Article
- Control of lysosomal TRPML1 channel activity and exosome release by acid ceramidase in mouse podocytes.American journal of physiology. Cell physiology · 2019Article
- Article
- Inhibition of pannexin-1 channel activity by adiponectin in podocytes: Role of acid ceramidase activation.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2018Article
- The wnt/β-catenin signaling pathway participates in rhein ameliorating kidney injury in DN mice.Molecular and cellular biochemistry · 2016Article
- Role of NADPH Oxidase in Metabolic Disease-Related Renal Injury: An Update.Oxidative medicine and cellular longevity · 2016Review
- (Pro)renin receptor regulates autophagy and apoptosis in podocytes exposed to high glucose.American journal of physiology. Endocrinology and metabolism · 2015Article
- Coronary endothelial dysfunction induced by nucleotide oligomerization domain-like receptor protein with pyrin domain containing 3 inflammasome activation during hypercholesterolemia: beyond inflammation.Antioxidants & redox signaling · 2015Article
- Stem cell conditioned culture media attenuated albumin-induced epithelial-mesenchymal transition in renal tubular cells.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2015Article
- Overexpression of miR-34c inhibits high glucose-induced apoptosis in podocytes by targeting Notch signaling pathways.International journal of clinical and experimental pathology · 2015Article
- Enhanced epithelial-to-mesenchymal transition associated with lysosome dysfunction in podocytes: role of p62/Sequestosome 1 as a signaling hub.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2015Article
- Inhibition of hyperhomocysteinemia-induced inflammasome activation and glomerular sclerosis by NLRP3 gene deletion.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2014Article
- High glucose induces podocyte injury via enhanced (pro)renin receptor-Wnt-β-catenin-snail signaling pathway.PloS one · 2014Article
- Protective role of growth hormone against hyperhomocysteinemia-induced glomerular injury.Naunyn-Schmiedeberg's archives of pharmacology · 2013Article
- Hypoxia-inducible factor prolyl-hydroxylase-2 mediates transforming growth factor beta 1-induced epithelial-mesenchymal transition in renal tubular cells.Biochimica et biophysica acta · 2013Article
- Role of NADPH oxidase-mediated reactive oxygen species in podocyte injury.BioMed research international · 2013Review
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Epithelial-to-Mesenchymal Transition (EMT) is an important pathogenic mechanism mediating glomerular injury or sclerosis in a variety of renal and systemic diseases such as hyperhomocysteinemia (hHcys). The present study was designed to test whether Hcys-induced EMT in podocytes is reversed by growth hormone (GH), a hormone regulating cell differentiation and growth and to explore the cellular and molecular mechanism mediating its action. It was found that Hcys induced significant EMT in podocytes, as shown by marked decreases in slit diaphragm-associated protein P-cadherin and zonula occludens-1 as epithelial markers and by dramatic increases in the expression of mesenchymal markers, fibroblast specific protein-1 and α-smooth muscle actin, which were detected by all examinations via immunocytochemistry, real time RT-PCR and Western blot analysis. When podocytes were treated with GH at 25 ng/mL, however, Hcys failed to induce podocyte EMT. Using electromagnetic spin resonance spectrometry, Hcys-induced superoxide (O(2).(-)) production via NADPH oxidase was found to be significantly inhibited by GH (66%). Functionally, GH was shown to substantially inhibit Hcys-induced increases in the permeability of podocyte monolayers and to block the decrease in podocin expression in these cells. In addition, NADPH oxidase subunit, gp91(phox) and GH receptors aggregated in membrane raft clusters, which produced O(2).(-) in response to Hcys and could be blocked by GH, membrane raft disruptors filipin and MCD or NADPH oxidase inhibitor, apocynin. It is concluded that Hcys-induced podocyte EMT is associated with transmembrane membrane raft-redox signaling and that GH reverses this Hcys-induced EMT protecting podocytes from functional disturbance.
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Registered trials
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