Prospect Of Selective Inhibition Of The Gap Protein Connexin43

967 Words Nov 24th, 2015 4 Pages
Title of paper: Selective Connexin43 Inhibition Prevents Isoproterenol-Induced Arrhythmias and Lethality in Muscular Dystrophy Mice

Authors: J. Patrick Gonzalez1, Jayalakshmi Ramachandran2, Lai-Hua Xie1, Jorge E. Contreras2 & Diego Fraidenraich1
Author Affiliations: Department of Cell Biology and Molecular Medicine, Rutgers Biomedical and Health Sciences, New Jersey Medical School, Newark, NJ USA.

Journal Reference:

Section A

This research paper examines the prospect of selective inhibition of the gap protein connexin43. Duchenne Muscular dystrophy is caused by an X-linked mutation and it is the most frequent and severe form of muscular dystrophy. This research used WT, mdx and mdx:utr mice and samples of human DMD heart tissue. The authors analyzed the correlation between the protein connexin43 and arrhythmias that lead to further cardiac pathology. The mice and Human DMD heart tissues show altered and numerous Cx43 localization and expression in the cardiomyocytes. When exposed to isoproterenol, which is a product similar to adrenaline, both mdx and mdx:utr mice suffered from arrhythmias and died within the span of one hour to 24 while the WT mice exposed to the same treatment showed none of these signs. The research showed that administering Gap 26 or Gap 19 mimetic peptides in a preemptive manner that inhibits Cx43 was 90% successful with mdx mice when it came to the Isoproterenol challenge. The inhibitors did not have the same effect on the mdx:utr mice due to…

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