Long noncoding RNA upregulated in hypothermia treated cardiomyocytes protects against myocardial infarction through improving mitochondrial function

• Published in: International journal of cardiology Vol. 266; pp. 213 - 217
• Main Authors: Zhang, Jian, Yu, Liming, Xu, Yinli, Liu, Yu, Li, Zhi, Xue, Xiaodong, Wan, Song, Wang, Huishan
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 01.09.2018
• Subjects: Animals; Cell Line; Humans; Hypothermia; Hypothermia - metabolism; LncRNA; Mitochondria - drug effects; Mitochondria - physiology; Myocardial infarction; Myocardial Infarction - metabolism; Myocardial Infarction - prevention & control; Myocytes, Cardiac - drug effects; Myocytes, Cardiac - metabolism; Rats; RNA, Long Noncoding - biosynthesis; RNA, Long Noncoding - pharmacology; RNA, Long Noncoding - therapeutic use; Up-Regulation - drug effects; Up-Regulation - physiology; Myocardial infarction; LncRNA; Hypothermia
• ISSN: 0167-5273; 1874-1754
• DOI: 10.1016/j.ijcard.2017.12.097

Myocardial infarction (MI) is one of the most common causes of cardiac morbidity and mortality. Many evidences suggest that hypothermia have a more pronounced impact as an adjunctive therapy for MI to reduce infarct size. However, the function of long non-coding RNAs (lncRNA) in therapeutic hypothermia for MI remains poorly understood. In this study, we investigated the expression of lncRNA-UIHTC (upregulated in hypothermia treated cardiomyocytes, NONHSAT094064) in ischemic heart tissues. To investigate its function, overexpression of UIHTC was performed by adeno-associated virus vectors after MI model in rat. lncRNA-UIHTC was upregulated in ischemic or injury cardiomyocytes. Overexpression of lncRNA-UIHTC in peri-infarction attenuated cardiac dysfunction in vivo. Mechanistically, lncRNA-UIHTC enhanced the mitochondrial function via upregulation of PGC1α. Moreover, when we knocked down PGC1α, the mitochondrial maximal oxygen consumption and ATP levels enhanced by overexpression of UIHTC were nearly completely restored. Altogether we have provided a new mechanism whereby hypothermia protected heart against ischemic via lncRNA-UIHTC. The UIHTC provided a new potential therapeutic target for MI but prevented the complications of hypothermia. •lncRNA-UIHTC (upregulated in hypothermia treated cardiomyocytes) was up-regulated in cardiomyocytes during hypothermia.•lncRNA-UIHTC promoted cardiomyocytes survive in response to ischemic or ROS.•lncRNA-UIHTC protects cardiomyocytes against MI through enhancing mitochondrial function.