PMID- 29773102 OWN - NLM STAT- MEDLINE DCOM- 20181127 LR - 20181127 IS - 1007-8738 (Print) IS - 1007-8738 (Linking) VI - 34 IP - 3 DP - 2018 Mar TI - [Over-expression of BDNF inhibits angiotensin II-induced apoptosis of cardiomyocytes in SD rats]. PG - 218-224 AB - Objective To investigate the role and molecular mechanism of brain-derived neurotrophic factor (BDNF) against the process of cardiomyocyte hypertrophy and apoptosis. Methods Cardiomyocyte hypertrophy were estabolished by angiotensin II (Ang II) in neonatal cardiomyocytes in vitro and incomplete ligature of abdominal aorta of SD rats in vivo. BDNF over-expressing recombinant vector pcDNA5-BDNF was transfected into cardiomyocytes by liposomes. Immunofluorescence staining was used to detect the effect of BDNF transfection on the surface area of myocardial cells. The effect of BDNF transfection on the apoptosis of cardiomyocytes was assayed by flow cytometry. Real-time fluorescent quantitative PCR was performed to detect the effect of over-expression of BDNF on the expressions of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) mRNAs in cardiomyocytes. Western blot assay was used to observe the changes of BDNF, ANP and BNP, calmodulin kinase 2 (CaMK2) and phosphorylated calmodulin kinase 2 (p-CaMK2), calcineurin (CaN), p-CaN, nuclear factor of activated T cells 3 (NFATC3) and p-NFATC3 protein expressions in the myocardial tissues and cardiomyocytes. Results The expression of BDNF protein increased significantly in cardiac hypertrophy animal and cell models in a time-dependent manner. Compared with the untransfected control cardiomyocytes, the surface area of cardiomyocytes, the rate of apoptosis, the levels of ANP and BNP mRNA and protein expression, the levels of p-CaMK2 and CaN protein in the BDNF over-expressed cardiomyocytes were remarkably reduced, while the level of p-NFATC3 protein rose significantly. Conclusion BDNF inhibits the apoptosis of cardiomyocytes induced by Ang II, and it plays the role by inhibiting CaMK2 and CaN signaling pathways. FAU - Cao, Jingli AU - Cao J AD - Department of Cardiovascular Medicine, Graduate School of Medical University of Tianjin, Tianjing 300070; Department of Cardiovascular Medicine, Tianjin Haibin People's Hospital, Tianjing 300280, China. FAU - Wu, Yingfeng AU - Wu Y AD - Department of Cardiovascular Medicine, Tianjin Haibin People's Hospital, Tianjing 300280, China. *Corresponding author, E-mail: longxiaofeng88@sina.com. FAU - Liu, Geming AU - Liu G AD - Department of Cardiovascular Medicine, Tianjin Haibin People's Hospital, Tianjing 300280, China. FAU - Li, Zhenlong AU - Li Z AD - Department of Cardiovascular Medicine, Tianjin Haibin People's Hospital, Tianjing 300280, China. LA - chi PT - Journal Article PL - China TA - Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi JT - Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology JID - 101139110 RN - 0 (Brain-Derived Neurotrophic Factor) RN - 11128-99-7 (Angiotensin II) RN - 114471-18-0 (Natriuretic Peptide, Brain) RN - 85637-73-6 (Atrial Natriuretic Factor) RN - EC 2.7.11.17 (Calcium-Calmodulin-Dependent Protein Kinase Type 2) RN - EC 2.7.11.17 (Camk2a protein, rat) RN - EC 3.1.3.16 (Calcineurin) SB - IM MH - Angiotensin II/*metabolism MH - Animals MH - *Apoptosis MH - Atrial Natriuretic Factor/genetics/metabolism MH - Brain-Derived Neurotrophic Factor/*genetics/metabolism MH - Calcineurin/genetics/metabolism MH - Calcium-Calmodulin-Dependent Protein Kinase Type 2/genetics/metabolism MH - Cells, Cultured MH - Male MH - Myocytes, Cardiac/cytology/*metabolism MH - Natriuretic Peptide, Brain/genetics/metabolism MH - Phosphorylation MH - Rats MH - Rats, Sprague-Dawley MH - Signal Transduction EDAT- 2018/05/19 06:00 MHDA- 2018/11/28 06:00 CRDT- 2018/05/19 06:00 PHST- 2018/05/19 06:00 [entrez] PHST- 2018/05/19 06:00 [pubmed] PHST- 2018/11/28 06:00 [medline] PST - ppublish SO - Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi. 2018 Mar;34(3):218-224.