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Updated: Oct 12, 2025

Perturbing Endothelial Biomechanics via Connexin 43 Structural Disruption
Published on: October 4, 2019
Data on Connexin 43 hemichannels regulation of cellular redox in lens
Yumeng Quan1,2, Yu Du1, Changrui Wu1
1Department of Biochemistry and Structural Biology, University of Texas Health Science Center, 7703 Floyd Curl Drive, San Antonio, TX 78229-3900, USA.
Abstract:
This article describes a dataset that is related to the research paper "Connexin hemichannels regulate redox potential via metabolite exchange and protect lens against cellular oxidative damage". Growing evidence demonstrates that oxidative stress is a key event in cataract formation. Hemichannels (HCs) formed by Connexin (Cx) 43, a Cx subtype only present in the epithelium of lens tissue, mediate the exchange of small molecules between the intracellular and extracellular environments, including redox-related metabolic molecules, such as glutathione (GSH) and reactive oxygen species (ROS). Here, we used a Cx43 heterozygous mouse model, Cx43E2 antibody (a specific Cx43 HC blocker), and knocked down Cx43 expression by siRNA in human lens epithelial HLE-B3 cells to assess the oxidative response of Cx43 HCs to H2O2 and UVB radiation. Western blot analysis of heterozygous Cx43-null (Cx43+/-) mouse lenses showed the haploinsufficiency of Cx43 protein. We further assessed anti-oxidative gene expression in response to H2O2 and UVB radiation treatment in the Cx43-deficient lens epithelial cells. This dataset will be useful for understanding the critical role of Cx43 HCs in maintaining redox homeostasis in the lens under oxidative stress.
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