Junjie Xiao1, Jin Li1, Tianzao Xu1, Dongcao Lv1, Bo Shen2, Yang Song3, Jiahong Xu4. 1. Regeneration Lab and Experimental Center of Life Sciences, Shanghai University Shanghai 200444, China ; Shanghai Key Laboratory of Bio-Energy Crops, School of Life Science, Shanghai University Shanghai 200444, China. 2. Shanghai Entry-Exit Inspection and Quarantine Bureau Shanghai 200135, China. 3. Tongji University School of Medicine Shanghai 200065, China. 4. Department of Cardiology, Shanghai Tongji Hospital, Tongji University School of Medicine Shanghai 200065, China.
Abstract
OBJECTIVE: Cardiac hypertrophy is a compensatory response of the heart to maintain its pumping capacity. Cardiac hypertrophy can be divided into pathological hypertrophy and physiological hypertrophy. The major forms of physiological hypertrophy include developing in response to developmental maturation, exercise, and pregnancy, which is adaptive and beneficial. Exercise has well-known beneficial cardiovascular effects and has recently been shown to be protective for myocardial ischemia-reperfusion injury. However, there are conflicting reports for the cardiac protective effects of pregnancy-induced hypertrophy. In the present study, we investigated the effects of pregnancy-induced physiological hypertrophy in cardiac ischemia-reperfusion injury and if cardiac progenitor cells were activated during pregnancy. METHODS: Physiological hypertrophy was induced in pregnancy and the mRNA levels of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) were determined by real-time polymerase chain reactions (RT-PCRs) analysis. Triphenyltetrazolium chloride staining was used to determine the cardiac ischemia-reperfusion injury. c-Kit and Nkx2.5 levels were determined by RT-PCRs, western blot and immunofluorescent staining. RESULTS: Heart weight (HW) and the ratio of HW to tibia length were increased while mRNA levels of ANP and BNP remained unchanged. Pregnancy-induced physiological hypertrophy protected against cardiac ischemia-reperfusion injury. In pregnancy, c-Kit positive cardiac progenitor cells were activated. CONCLUSION: This study presents that pregnancy-induced physiological hypertrophy activates cardiac progenitor cells and thereafter protects against cardiac ischemia-reperfusion injury.
OBJECTIVE:Cardiac hypertrophy is a compensatory response of the heart to maintain its pumping capacity. Cardiac hypertrophy can be divided into pathological hypertrophy and physiological hypertrophy. The major forms of physiological hypertrophy include developing in response to developmental maturation, exercise, and pregnancy, which is adaptive and beneficial. Exercise has well-known beneficial cardiovascular effects and has recently been shown to be protective for myocardial ischemia-reperfusion injury. However, there are conflicting reports for the cardiac protective effects of pregnancy-induced hypertrophy. In the present study, we investigated the effects of pregnancy-induced physiological hypertrophy in cardiac ischemia-reperfusion injury and if cardiac progenitor cells were activated during pregnancy. METHODS: Physiological hypertrophy was induced in pregnancy and the mRNA levels of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) were determined by real-time polymerase chain reactions (RT-PCRs) analysis. Triphenyltetrazolium chloride staining was used to determine the cardiac ischemia-reperfusion injury. c-Kit and Nkx2.5 levels were determined by RT-PCRs, western blot and immunofluorescent staining. RESULTS: Heart weight (HW) and the ratio of HW to tibia length were increased while mRNA levels of ANP and BNP remained unchanged. Pregnancy-induced physiological hypertrophy protected against cardiac ischemia-reperfusion injury. In pregnancy, c-Kit positive cardiac progenitor cells were activated. CONCLUSION: This study presents that pregnancy-induced physiological hypertrophy activates cardiac progenitor cells and thereafter protects against cardiac ischemia-reperfusion injury.
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