• Jeong Rang Park, Jong Hwa Ahn, Myeong Hee Jung, Jin Hyun Kim, Min Gyu Kang, Kye Hwan Kim, Jeong Yoon Jang, Hyun Woong Park, Jin-Sin Koh, Seok-Jae Hwang, Yongwhi Park, Young-Hoon Jeong, Choong Hwan Kwak, and Jin-Yong Hwang.
• Division of Cardiology, Department of Internal Medicine, Gyeongsang National University School of Medicine and Gyeongsang National University Hospital, Republic of Korea.
• Intern. Med. 2022 Jan 15; 61 (2): 151-158.

AbstractObjective Human microRNA-185 (miR-185) has been reported to act as a regulator of fibrosis and angiogenesis in cancer. However, miR-185 has not been investigated in patients with ST-segment elevation myocardial infarction (STEMI). We hypothesized that the changes in miR-185 levels in STEMI patients are related to the processes of myocardial healing and remodeling. Methods Between January 2011 and December 2013, 145 patients with STEMI (65.9±11.6 years old; 41 women) were enrolled. Initial and discharge serum samples collected from 20 patients with STEMI and mixed sera from 8 healthy controls were analyzed by a microarray. A quantitative reverse transcription polymerase chain reaction (RT-qPCR) analysis of miR-185 was performed in all 145 patients. The correlation between the miR-185 levels and the clinical, laboratory, angiographic, and echocardiographic parameters was analyzed. Results The microarray analysis revealed a biphasic pattern in miR-185 levels, with an initial decrease followed by an increase at discharge. The miR-185 levels at discharge were significantly correlated with the troponin-I, CK-MB, and area under the curve of CK-MB levels. There was a positive correlation between the transforming growth factor-β and miR-185 levels at discharge (ρ=0.242, p=0.026). A high wall motion score index and a low ejection fraction, as measured by echocardiography, and high B-type natriuretic peptide level at one month after STEMI were related to high miR-185 levels. Conclusion Our results showed that elevated miR-185 levels at the late stage of STEMI were related to a large amount of myocardial injury and adverse remodeling.

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