ArticleDrug design, development and therapy2015
High glucose inhibits ClC-2 chloride channels and attenuates cell migration of rat keratinocytes.
Article in Drug design, development and therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 15 citations in OpenAlex.
- Regulatory and disruptive variants in the CLCN2 gene are associated with modified skin color pattern phenotypes in the corn snake.Genome biology · 2025Article
- Human In Vitro Skin Models for Wound Healing and Wound Healing Disorders.Biomedicines · 2023Review
- Identification and validation of a signature involving voltage-gated chloride ion channel genes for prediction of prostate cancer recurrence.Frontiers in endocrinology · 2022Article
- In focus in HCB.Histochemistry and cell biology · 2021Article
- The calcium-activated chloride channel-associated protein rCLCA2 is expressed throughout rat epidermis, facilitates apoptosis and is downmodulated by UVB.Histochemistry and cell biology · 2021Article
- High Glucose Suppresses Keratinocyte Migration Through the Inhibition of p38 MAPK/Autophagy Pathway.Frontiers in physiology · 2019Article
- NPPB modulates apoptosis, proliferation, migration and extracellular matrix synthesis of conjunctival fibroblasts by inhibiting PI3K/AKT signaling.International journal of molecular medicine · 2018Article
- Research and progress on ClC‑2 (Review).Molecular medicine reports · 2017Review
- BLT2 expression improves skin integrity and protects from alterations caused by hyperglycemia in type 2 diabetes.Dermato-endocrinology · 2017Article
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- The CLC-2 Chloride Channel Modulates ECM Synthesis, Differentiation, and Migration of Human Conjunctival Fibroblasts via the PI3K/Akt Signaling Pathway.International journal of molecular sciences · 2016Article
- Dendritic epidermal T cells facilitate wound healing in diabetic mice.American journal of translational research · 2016Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAccumulating evidence has demonstrated that migration of keratinocytes is critical to wound epithelialization, and defects of this function result in chronic delayed-healing wounds in diabetes mellitus patients, and the migration has been proved to be associated with volume-activated chloride channels. The aim of the study is to investigate the effects of high glucose (HG, 25 mM) on ClC-2 chloride channels and cell migration of keratinocytes.
methodsNewborn Sprague Dawley rats were used to isolate and culture the keratinocyte in this study. Immunofluorescence assay, real-time polymerase chain reaction, and Western blot assay were used to examine the expression of ClC-2 protein or mRNA. Scratch wound assay was used to measure the migratory ability of keratinocytes. Transwell cell migration assay was used to measure the invasion and migration of keratinocytes. Recombinant lentivirus vectors were established and transducted to keratinocytes. Whole-cell patch clamp was used to perform the electrophysiological studies.
resultsWe found that the expression of ClC-2 was significantly inhibited when keratinocytes were exposed to a HG (25 mM) medium, accompanied by the decline of volume-activated Cl(-) current (I Cl,vol), migration potential, and phosphorylated PI3K as compared to control group. When knockdown of ClC-2 by RNAi or pretreatment with wortmannin, similar results were observed, including I Cl,vol and migration keratinocytes were inhibited.
conclusionOur study proved that HG inhibited ClC-2 chloride channels and attenuated cell migration of rat keratinocytes via inhibiting PI3K signaling.
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