ArticleJournal of cellular physiology2018
IL-6 increases podocyte motility via MLC-mediated focal adhesion impairment and cytoskeleton disassembly.
Article in Journal of cellular physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed.
- SETD7 exacerbates diabetic nephropathy through activating ACell & bioscience · 2025Article
- Pharmacological Blockade of the Adenosine ACells · 2024Article
- Swollen Feet: Considering the Paradoxical Roles of Interleukins in Nephrotic Syndrome.Biomedicines · 2024Review
- IL-6 and diabetic kidney disease.Frontiers in immunology · 2024Review
- The influence of calcitriol and methylprednisolone on podocytes function in minimal change disease in vitro model.Scientific reports · 2023Article
- Loss of S1P Lyase Expression in Human Podocytes Causes a Reduction in Nephrin Expression That Involves PKCδ Activation.International journal of molecular sciences · 2023Article
- Glomerular cell cross talk in diabetic kidney diseases.Journal of diabetes · 2022Review
- Suppressor of cytokine signalling 3 (SOCS3) expressed in podocytes attenuates glomerulonephritis and suppresses autoantibody production in an imiquimod-induced lupus model.Lupus science & medicine · 2021Article
- Dragon's Blood Regulates Rac1-WAVE2-Arp2/3 Signaling Pathway to Protect Rat Intestinal Epithelial Barrier Dysfunction Induced by Simulated Microgravity.International journal of molecular sciences · 2021Article
- MAD2B-mediated cell cycle reentry of podocytes is involved in the pathogenesis of FSGS.International journal of biological sciences · 2021Article
- Lysophosphatidic Acid and IL-6 Trans-signaling Interact via YAP/TAZ and STAT3 Signaling Pathways in Human Trabecular Meshwork Cells.Investigative ophthalmology & visual science · 2020Article
- A Novel Role of Interleukin-6 as a Regulatory Factor of Inflammation-Associated Deterioration in Osteoblast Arrangement.International journal of molecular sciences · 2020Article
- Review
- Exploring protective effect ofChinese medicine · 2020Article
- Motility of human renal cells is disturbed by infection with pathogenic hantaviruses.BMC infectious diseases · 2018Article
- Dietary cysteamine hydrochloride protects against oxidation, inflammation, and mucosal barrier disruption of broiler chickens challenged with Clostridium perfringens.Journal of animal science · 2018Article
- IL-6 increases podocyte motility via MLC-mediated focal adhesion impairment and cytoskeleton disassembly.Journal of cellular physiology · 2018Article
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13 authors.
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No grant is acknowledged in the PubMed record.
Abstract
The disturbance of podocyte motility is an essential pathogenic mechanisms of foot process effacement during proteinuric diseases, and myosin light chain (MLC) is a pivotal component in regulating the motility of podocytes. Inflammatory cytokine interleukin-6 (IL-6) has been reported to induce podocyte abnormalities by various mechanisms, however, whether aberrant cell motility contributes to the IL-6-induced podocyte injury remains unknown. Here, by wound healing, transwell, and cell migration assays, we confirmed that IL-6 accelerates the motility of podocyte. Simultaneously, the phosphorylation of MLC is elevated along with perturbed focal adhesion (FAs) and cytoskeleton. Next, via genetic and pharmacologic interruption of MLC or its phosphorylation we revealed that the activation of MLC is implicated in IL-6-mediated podocyte hypermotility as well as the disassembly of FAs and F-actin. By using stattic, an inhibitor for STAT3 phosphorylation, we uncovered that STAT3 activation is the upstream event for MLC phosphorylation and the following aberrant motility of podocytes. Additionally, we found that calcitriol markedly attenuates podocyte hypermotility via blocking STAT3-MLC. In conclusion, our study demonstrated that IL-6 interrupts FAs dynamic, cytoskeleton organization, and eventually leads to podocyte hypermotility via STAT3/MLC, whereas calcitriol exerts its protective role by inhibiting this pathway. These findings enrich the mechanisms accounting for IL-6-mediated podocyte injury from the standpoint of cell motility and provide a novel therapeutic target for podocyte disorders.
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