ArticleMolecular medicine reports2018
Upregulation of connexin43 by glucose deprivation in H9c2 cells via the extracellular signal‑regulated kinase/mitogen‑activated protein kinase signaling pathway.
Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 5 citations in OpenAlex.
- Connexins and Glucose Metabolism in Cancer.International journal of molecular sciences · 2022Review
- Connexin 43 hyper-phosphorylation at serine 282 triggers apoptosis in rat cardiomyocytes via activation of mitochondrial apoptotic pathway.Acta pharmacologica Sinica · 2022Article
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5 authors at 2 institutions in 1 country.
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Abstract
Cardiac connexin43 (Cx43) serves an essential role in maintaining the functional integrity of the heart. The present study investigated the effect of glucose deprivation (GD) on Cx43 protein expression levels in H9c2 cells, and demonstrated that following 2 h GD, Cx43 protein expression levels in H9c2 cells increased by ~68%. In addition, GD activated the extracellular signal‑regulated kinase (ERK)/mitogen‑activated protein kinase (MAPK) signaling pathway, which regulated the expression levels of cardiac Cx43. A MAPK inhibitor and U0126, an ERK inhibitor, abolished the effects of GD on Cx43 expression levels. Under GD, the protein expression levels of Beclin‑1, p62 and LC3 were augmented, and were decreased in the presence of ERK inhibitor or siRNA‑ERK. In addition, H9c2 cells exposed to GD exhibited marked increase in LDH release and decreased MTT reduction activity, all of which were not significantly reversed by U0126 treatment. Therefore, the ERK/MAPK signaling pathway may be involved in elevating cardiac Cx43 expression levels under GD in H9c2 cells.
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