|TITLE||Prof. Jong Sun KANG & Ha Na CHO Demonstrate the Role of Cdon in Cardiac Function and Remodeling|
Cdon is expressed and predominantly localized at intercalated disk in both mice and human hearts. Cdon−/− mice develop cardiac dysfunction and fibrosis with altered expression of remodeling genes. Cdon deficiency causes aberrant localization and function of gap junction protein connexin 43, correlating with hyperactivated Wnt signaling. Blocking of Wnt signaling in Cdon-depleted cardiomyocytes attenuates aberrant intercellular coupling. Conversely, Wnt activator causes aberrant activation of gap junction with decreased Cdon levels, suggestive of a feedback mechanism. This data suggests that Cdon is required for the control of Wnt signaling to prevent cardiac remodeling.
The research, supported by the Ministry of Science, ICT and Future Planning, as a part of a project supporting the cultivation of future researchers, as well as to increase performance, was conducted mostly by Ph.D. program students; Myung Ho JUNG (advising professor: Jong Sun KANG) and Hyun Ji KIM (advising professor: Ha Na CHO).
This study was published in one of the world’s most renowned scientific research papers Proceedings of the National Academy of Sciences as of Feb. 2nd with the subject title “Cdon deficiency causes cardiac remodeling through hyperactivation of WNT/β-catenin signaling”.
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