Strongly decreased gap junctional permeability to inositol 1,4,5-trisphosphate in connexin32 deficient hepatocytes

42Citations
Citations of this article
11Readers
Mendeley users who have this article in their library.

Abstract

Livers from connexin32 (Cx32) deficient mice have been shown to be defective in hormonally induced glucose mobilization. In order to determine whether this effect is due to decreased diffusion of the second messenger inositol 1,4,5-trisphosphate (IP3) between hepatocytes, we injected iontophoretically different amounts of IP3 in Fura-2 loaded hepatocyte doublets (i.e. cell pairs) from wild type or Cx32 deficient mice. Whereas 84% of wild type hepatocytes showed an intercellular Ca2+ wave spreading from the injected cell to the neighboring cell, only 25% of Cx32 deficient hepatocyte doublets did so. The amount of IP3 necessary to induce an intercellular Ca2+ wave in Cx32 deficient hepatocyte doublets was estimated to be about 25-fold higher than in wild type doublets. This confirms the notion that the low hormonally or electrically induced glucose mobilization found in Cx32 deficient livers relative to wild type livers is due to largely hindered diffusion of IP3 between Cx32 deficient hepatocytes. Copyright (C) 2000 Federation of European Biochemical Societies.

Cite

CITATION STYLE

APA

Niessen, H., & Willecke, K. (2000). Strongly decreased gap junctional permeability to inositol 1,4,5-trisphosphate in connexin32 deficient hepatocytes. FEBS Letters, 466(1), 112–114. https://doi.org/10.1016/S0014-5793(99)01770-6

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free