title: Cardiac telocytes were decreased during myocardial infarction and their therapeutic effects for ischaemic heart in rat.
abstract: Recently, cardiac telocytes were found in the myocardium. However, the functional role of cardiac telocytes and possible changes in the cardiac telocyte population during myocardial infarction in the myocardium are not known. In this study, the role of the recently identified cardiac telocytes in myocardial infarction (MI) was investigated. Cardiac telocytes were distributed longitudinally and within the cross network of the myocardium, which was impaired during MI. Cardiac telocytes in the infarction zone were undetectable from approximately 4 days to 4 weeks after an experimental coronary occlusion was used to induce MI. Although cardiac telocytes in the non-ischaemic area of the ischaemic heart experienced cell death, the cell density increased approximately 2 weeks after experimental coronary occlusion. The cell density was then maintained at a level similar to that observed 1-4 days after left anterior descending coronary artery (LAD)-ligation, but was still lower than normal after 2 weeks. We also found that simultaneous transplantation of cardiac telocytes in the infarcted and border zones of the heart decreased the infarction size and improved myocardial function. These data indicate that cardiac telocytes, their secreted factors and microvesicles, and the microenvironment may be structurally and functionally important for maintenance of the physiological integrity of the myocardium. Rebuilding the cardiac telocyte network in the infarcted zone following MI may be beneficial for functional regeneration of the infarcted myocardium.
authors.affiliation: Key Laboratory for Regenerative Medicine, Ministry of Education, Ji Nan University, Guangzhou, China.
authors.forename: Baoyin
authors.initials: B
authors.lastname: Zhao
authors.forename: Shang
authors.initials: S
authors.lastname: Chen
authors.forename: Juanjuan
authors.initials: J
authors.lastname: Liu
authors.forename: Ziqiang
authors.initials: Z
authors.lastname: Yuan
authors.forename: Xufeng
authors.initials: X
authors.lastname: Qi
authors.forename: Junwen
authors.initials: J
authors.lastname: Qin
authors.forename: Xin
authors.initials: X
authors.lastname: Zheng
authors.forename: Xiaotao
authors.initials: X
authors.lastname: Shen
authors.forename: Yanhong
authors.initials: Y
authors.lastname: Yu
authors.forename: Thomas J
authors.initials: TJ
authors.lastname: Qnin
authors.forename: John Yeuk-Hon
authors.initials: JY
authors.lastname: Chan
authors.forename: Dongqing
authors.initials: D
authors.lastname: Cai
mesh_terms: D000818:Animals; D002452:Cell Count; D016923:Cell Death; D060833:Cellular Microenvironment; D054059:Coronary Occlusion / Q000150:complications; D005260:Female; D007273:Injections, Intramuscular; D009203:Myocardial Infarction / Q000209:etiology / Q000473:pathology* / Q000628:therapy*; D009206:Myocardium / Q000473:pathology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012038:Regeneration / Q000502:physiology*; D017154:Stromal Cells / Q000166:cytology* / Q000502:physiology / Q000637:transplantation