Specific inhibition of HDAC4 in cardiac progenitor cells enhances myocardial repairs.
نویسندگان
چکیده
We have recently shown that in vivo inhibition of histone deacetylase (HDAC) stimulates endogenous myocardial regeneration in infarcted hearts (Zhang L et al. J Pharmacol Exp Ther 341: 285-293, 2012). Furthermore, our observation demonstrates that HDAC inhibition promotes cardiogenesis, which is associated with HDAC4 reduction. However, it remains unknown as to whether specific inhibition of HDAC4 modulates cardiac stem cells (CSCs) to facilitate myocardial repair and to preserve cardiac performance. c-kit(+) CSCs were isolated from adult mouse hearts and were transfected with HDAC4 siRNA to knockdown HDAC4 of c-kit(+) CSCs. The transfection of HDAC4 siRNA caused a marked reduction of HDAC4 mRNA and proteins in c-kit(+) CSCs. Mouse myocardial infarction (MI) was created to assess the effect of HDAC4 inhibition in c-kit(+) CSCs on myocardial regeneration in vivo when cells were introduced into MI hearts. Transplantation of HDAC4 siRNA-treated c-kit(+) CSCs into MI hearts improved ventricular function, attenuated ventricular remodeling, and promoted CSC-derived regeneration and neovascularization. Furthermore, Ki67 and BrdU positively proliferative myocytes increased in MI hearts receiving HDAC4 siRNA-treated c-kit(+) CSCs compared with MI hearts engrafted with control siRNA-treated c-kit(+) CSCs. In addition, compared with MI hearts engrafted with control adenoviral GFP-infected c-kit(+) CSCs, MI hearts receiving adenoviral HDAC4-infected c-kit(+) CSCs exhibited attenuated cardiac functional recovery, CSC-derived regeneration, and neovascularization, which was accompanied with adverse ventricular remodeling and decrease in Ki67 and BrdU positively proliferative myocytes. HDAC4 inhibition facilitated c-kit(+) CSCs into the differentiation into cardiac lineage commitments in vitro, while HDAC4 overexpression attenuated c-kit(+) CSC-derived cardiogenesis. Our results indicate that HDAC4 inhibition promotes CSC-derived cardiac regeneration and improves the restoration of cardiac function.
منابع مشابه
INHIBITION OF WNT3A DIMINISHED ANGIOGENIC DIFFERENTIATION CAPACITY OF RAT CARDIAC PROGENITOR CELLS
Background & Aims: Myocardial infarction is a leading cause of human mortality in industrialized and developing societies. Limited restorative ability of of cardiomyocytes after ischemic changes can causes extensive damage lead to prominent chronic heart failure. At present, the application of certain drugs is touted as one of the main available approaches to inhibit the spread of the lesion an...
متن کاملNogo receptor blockade enhances subventricular zone’s stem cells proliferation and differentiation in demyelination context
Introduction: Nogo-A and Nogo receptor (NgR) are expressed in the subventricular zone (SVZ) stem cells. NgR plays critical inhibitory roles in axonal regeneration and remyelination. However, the role of NgR in SVZ niche behaviors in demyelination context is still uncertain. Here we investigated the effects of NgR inhibition on SVZ niche reaction in a local model of demyelination in adult mouse ...
متن کاملAre Stem Cells the next Therapeutic Tool for Heart Repair?
Cardiovascular disease remains the leading cause of morbidity and mortality in the United States and Europe. In recent years, the understanding that regenerative processes exist at the level of the myocardium, has placed stem cell research at center stage in cardiology. A stem cell is a cell that has the ability to divide (self replicate) for indefinite periods often throughout the life of the ...
متن کاملPlGF Repairs Myocardial Ischemia through Mechanisms of Angiogenesis, Cardioprotection and Recruitment of Myo-Angiogenic Competent Marrow Progenitors
RATIONALE Despite preclinical success in regenerating and revascularizing the infarcted heart using angiogenic growth factors or bone marrow (BM) cells, recent clinical trials have revealed less benefit from these therapies than expected. OBJECTIVE We explored the therapeutic potential of myocardial gene therapy of placental growth factor (PlGF), a VEGF-related angiogenic growth factor, with ...
متن کاملSarcoplasmic reticulum Ca2+‐induced Ca2+ release regulates class IIa HDAC localization in mouse embryonic cardiomyocytes
In embryonic cardiomyocytes, sarcoplasmic reticulum (SR)-derived Ca2+ release is required to induce Ca2+ oscillations for contraction and to control cardiac development through Ca2+ -activated pathways. Here, our aim was to study how SR Ca2+ release regulates cytosolic and nuclear Ca2+ distribution and the subsequent effects on the Ca2+ -dependent localization of class IIa histone deacetylases ...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید
ثبت ناماگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید
ورودعنوان ژورنال:
- American journal of physiology. Cell physiology
دوره 307 4 شماره
صفحات -
تاریخ انتشار 2014