JDP2 and ATF3 deficiencies dampen maladaptive cardiac remodeling and preserve cardiac function

PloS One
R KalfonA Aronheim

Abstract

c-Jun dimerization protein (JDP2) and Activating Transcription Factor 3 (ATF3) are closely related basic leucine zipper proteins. Transgenic mice with cardiac expression of either JDP2 or ATF3 showed maladaptive remodeling and cardiac dysfunction. Surprisingly, JDP2 knockout (KO) did not protect the heart following transverse aortic constriction (TAC). Instead, the JDP2 KO mice performed worse than their wild type (WT) counterparts. To test whether the maladaptive cardiac remodeling observed in the JDP2 KO mice is due to ATF3, ATF3 was removed in the context of JDP2 deficiency, referred as double KO mice (dKO). Mice were challenged by TAC, and followed by detailed physiological, pathological and molecular analyses. dKO mice displayed no apparent differences from WT mice under unstressed condition, except a moderate better performance in dKO male mice. Importantly, following TAC the dKO hearts showed low fibrosis levels, reduced inflammatory and hypertrophic gene expression and a significantly preserved cardiac function as compared with their WT counterparts in both genders. Consistent with these data, removing ATF3 resumed p38 activation in the JDP2 KO mice which correlates with the beneficial cardiac function. Collectively, mi...Continue Reading

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Citations

Jun 2, 2020·Circulation·Shimrit AvrahamAmi Aronheim
May 1, 2021·International Journal of Molecular Sciences·Gerhild EulerMariana S Parahuleva

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Methods Mentioned

BETA
PCR
Fluorescence

Software Mentioned

GraphPad Prism
Image Pro Plus

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