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Articles by Jian-Ping Jin
Total Records ( 2 ) for Jian-Ping Jin
  Qi-Quan Huang , M. Moazzem Hossain , Kaichun Wu , Kakoli Parai , Richard M. Pope and Jian-Ping Jin
  The actin cytoskeleton plays a major role in cell motility that is essential for the function of phagocytes. Calponin is an actin-associated regulatory protein. Here we report the finding of significant levels of the h2 isoform of calponin in peripheral blood cells of myeloid lineage. To study the functional significance, h2-calponin gene (Cnn2) interrupted mice were constructed. Germ line transmission of the Cnn2-flox-neo allele was obtained in chimeras from two independent clones of targeted embryonic stem cells. The insertion of the neoR cassette into intron 2 of the Cnn2 gene resulted in a significant knockdown of h2-calponin expression. Removing the frt-flanked neoR cassette by FLP1 recombinase rescued the knockdown effect. Cre recombinase-induced deletion of the loxP-flanked exon 2 eliminated the expression of h2-calponin protein. H2-calponin-free mice showed reduced numbers of peripheral blood neutrophils and monocytes. H2-calponin-free macrophages demonstrated a higher rate of proliferation and faster migration than that of h2-calponin-positive cells, consistent with a faster diapedesis of peripheral monocytes and neutrophils. H2-calponin-free macrophages showed reduced spreading in adhesion culture together with decreased tropomyosin in the actin cytoskeleton. The lack of h2-calponin also significantly increased macrophage phagocytotic activity, suggesting a novel mechanism to regulate phagocyte functions.
  Han-Zhong Feng , Min Chen , Lee S. Weinstein and Jian-Ping Jin
  Although β-adrenergic stimuli are essential for myocardial contractility, β-blockers have a proven beneficial effect on the treatment of heart failure, but the mechanism is not fully understood. The stimulatory G protein α-subunit (Gsα) couples the β-adrenoreceptor to adenylyl cyclase and the intracellular cAMP response. In a mouse model of conditional Gsα deficiency in the cardiac muscle (Gsα-DF), we demonstrated heart failure phenotypes accompanied by increases in the level of a truncated cardiac troponin I (cTnI-ND) from restricted removal of the cTnI-specific N-terminal extension. To investigate the functional significance of the increase of cTnI-ND in Gsα-DF cardiac muscle, we generated double transgenic mice to overexpress cTnI-ND in Gsα-DF hearts. The overexpression of cTnI-ND in Gsα-DF failing hearts increased relaxation velocity and left ventricular end diastolic volume to produce higher left ventricle maximum pressure and stroke volume. Supporting the hypothesis that up-regulation of cTnI-ND is a compensatory rather than a destructive myocardial response to impaired β-adrenergic signaling, the aberrant expression of β-myosin heavy chain in adult Gsα-DF but not control mouse hearts was reversed by cTnI overexpression. These data indicate that the up-regulation of cTnI-ND may partially compensate for the cardiac inefficiency in impaired β-adrenergic signaling.
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