UROTENSIN Ⅱ INHIBITED THE PROLIFERATION OF CARDIAC SIDE POPULATION CELLS IN PRESSURE OVERLOAD MICE B

来源 :第九届海峡两岸心血管科学研讨会暨首届台湾南部国际心脑血管科学研讨会 | 被引量 : 0次 | 上传用户:zhmwq
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Cardiac side population cells (CSPs) are promising cell resource for the regeneration in diseased heart as intrinsic cardiac stem cells.However the relative low ratio of CSPs in the heart limited the ability of CSPs to repair heart and improve cardiac function effectively under pathophysiological condition.Which factors limiting the proliferation of CSPs in diseased heart are unclear.Here, we show that urotensin Ⅱ (UⅡ) regulates the proliferation of CSPs by c-Jun N-terminal kinase (JNK) and low density lipoprotein receptor-related protein 6 (LRP6) signaling during pressure overload.Pressure overload grealty upregulated UⅡ level in plasma, UⅡ receptor (UT) antagonist, urantide, promoted CSPs proliferation and improved cardiac dysfunction during chronic pressure overload.In cultured CSPs subjected to mechanical stretch (MS), UⅡ significantly inhibited the proliferation by UT.Nanofluidic proteomic immunoassay (NIA) showed it is the JNK activation, but not the extracellular signal-regulated kinas (ERK) activation, that involved in the UⅡ-inhibited-proliferation of CSPs during pressure overload.
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