title: Infrasound exposure induces apoptosis of rat cardiac myocytes by regulating the expression of apoptosis-related proteins.
abstract: It has been reported that exposure to infrasound causes cardiac dysfunction. Allowing for the key role of apoptosis in the pathogenesis of cardiovascular diseases, the objective of this study was to investigate the apoptotic effects of infrasound. Cardiac myocytes cultured from neonatal rats were exposed to infrasound of 5 Hz at 130 dB. The apoptosis was determined by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling. Also, the expression levels of a series of apoptosis-related proteins were detected. As a result, infrasound induced apoptosis of cultured rat cardiac myocytes in a time-dependant manner. The expression of proapoptotic proteins such as Bax, caspase-3, caspase-8, caspase-9, and FAS was significantly up-regulated, with concomitant down-regulated expression of antiapoptotic proteins such as Bcl-x, and the inhibitory apoptosis proteins family proteins including XIAP, cIAP-1, and cIAP-2. The expression of poly (ADP-ribose) polymerase and β-catenin, which are the substrate proteins of caspase-3, was significantly decreased. In conclusion, infrasound is an apoptotic inducer of cardiac myocytes.
authors.affiliation: Department of Cardiology, Third Hospital, Nanchang, Jiangxi, China.
authors.forename: Zhao-Hui
authors.initials: ZH
authors.lastname: Pei
authors.forename: Bao-Ying
authors.initials: BY
authors.lastname: Chen
authors.forename: Ru
authors.initials: R
authors.lastname: Tie
authors.forename: Hai-Feng
authors.initials: HF
authors.lastname: Zhang
authors.forename: Ge
authors.initials: G
authors.lastname: Zhao
authors.forename: Ping
authors.initials: P
authors.lastname: Qu
authors.forename: Xiao-Xing
authors.initials: XX
authors.lastname: Zhu
authors.forename: Miao-Zhang
authors.initials: MZ
authors.lastname: Zhu
authors.forename: Jun
authors.initials: J
authors.lastname: Yu
mesh_terms: D000161:Acoustic Stimulation / Q000009:adverse effects* / Q000379:methods; D000818:Animals; D000831:Animals, Newborn; D017209:Apoptosis / Q000502:physiology*; D000075747:Baculoviral IAP Repeat-Containing 3 Protein; D020169:Caspases / Q000378:metabolism*; D002478:Cells, Cultured; D015870:Gene Expression; D051034:Inhibitor of Apoptosis Proteins / Q000235:genetics / Q000378:metabolism; D032383:Myocytes, Cardiac / Q000378:metabolism / Q000473:pathology*; D011065:Poly(ADP-ribose) Polymerases / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D015854:Up-Regulation; D051636:X-Linked Inhibitor of Apoptosis Protein / Q000235:genetics / Q000378:metabolism; D051028:bcl-2-Associated X Protein / Q000378:metabolism; D051020:bcl-X Protein / Q000378:metabolism; D051176:beta Catenin / Q000378:metabolism; D019014:fas Receptor / Q000235:genetics* / Q000378:metabolism
chemical_list: C494828:Bax protein, rat; C494813:Bcl2l1 protein, rat; C495268:Ctnnb1 protein, rat; C491898:Fas protein, rat; D051034:Inhibitor of Apoptosis Proteins; D012333:RNA, Messenger; D051636:X-Linked Inhibitor of Apoptosis Protein; D051028:bcl-2-Associated X Protein; D051020:bcl-X Protein; D051176:beta Catenin; D019014:fas Receptor; D000075747:Baculoviral IAP Repeat-Containing 3 Protein; C494836:Birc3 protein, rat; D011065:Poly(ADP-ribose) Polymerases; D020169:Caspases