The role of Connexin 46 promoter in lens and other hypoxic tissues

• Type of Material: Article
• Authors: Samuel Molina, Emory University; Dolores J. Takemoto, Kansas State University
• Language: English
• Date: 2012-03-01
• Publisher: Taylor & Francis Open
• Publication Version: Final Published Version
• Copyright Statement: © 2012 Landes Bioscience.
• License: Creative Commons Attribution-Noncommercial 3.0 Unported
• Final Published Version (URL): http://dx.doi.org/10.4161/cib.18715
• Title of Journal or Parent Work: Communicative and Integrative Biology
• ISSN: 1942-0889
• Volume: 5
• Issue: 2
• Start Page: 114
• End Page: 117
• Grant/Funding Information: NIH R01-EY13421 to D.J.T.; Kansas State University Research Foundation Doctoral Scholarship to S.A.M.
• Keywords: Connexin 43; xenografts; Connexin 46; tumors; hypoxia; connexin promoter; cellular differentiation; lens
• Research Categories: Engineering, Biomedical; Chemistry, Biochemistry

Abstract

Gap junctions are multimeric membrane protein channels that connect the cytoplasm of one cell to another. Much information about connexins regards electrophysiology and channel function but relatively little information is known about non-channel functions of connexins. Lens connexins, Cx43, Cx46 and Cx50, have been extensively studied for their role in lens homeostasis. Connexins allow the movement of small metabolically relevant molecules and ions between cells and this action in the lens prevents cataract formation. Interruption of Cx46 channel function leads to cataract formation due to dysregulation of lens homeostasis. The loss of Cx46 upregulates Cx43 in lens cell culture and suppresses tumor growth in breast and retinoblastoma tumor xenografts. Upregulation of Cx46 in hypoxic tissues has been noted and may be due in part to the effects of hypoxia and HIF activators. Here, we report that the Cx46 promoter is regulated by hypoxia and also offer speculation about the role of Cx46 in lens differentiation and solid tumor growth.