Diagnostic Utility and Pathogenic Role of Circulating MicroRNAs in Vasospastic Angina.

diagnosis microRNA pathogenesis vasospastic angina

Journal

Journal of clinical medicine
ISSN: 2077-0383
Titre abrégé: J Clin Med
Pays: Switzerland
ID NLM: 101606588

Informations de publication

Date de publication:
02 May 2020
Historique:
received: 02 04 2020
revised: 26 04 2020
accepted: 27 04 2020
entrez: 7 5 2020
pubmed: 7 5 2020
medline: 7 5 2020
Statut: epublish

Résumé

We investigated the diagnostic value and pathophysiological role of circulating microRNA (miR) in vasospastic angina (VA). We enrolled patients who underwent coronary angiography for chest pain to explore the miR's diagnostic utility. In addition, we investigated the role of miRs in regulating endothelial nitric oxide synthase (eNOS) expression in human coronary artery endothelial cells (hCAECs). Among the 121 patients, 46 were diagnosed with VA (VA group), 26 with insignificant coronary lesions (ICL group), and 49 with atherothrombotic angina (AA group). The VA group showed a significantly higher expression of miR-17-5p, miR-92a-3p, and miR-126-3p than the ICL group. In contrast, miR-221-3p and miR-222-3p were upregulated in the AA group compared to the VA group, and all levels of miR-17-5p, miR-92a-3p, miR-126-3p, miR-145-5p, miR-221-3p, and miR-222-3p differed between the AA group and the ICL group. In the hCAECs, transfection with mimics (pre-miR) of miR-17-5p, miR-92a-3p, and miR-126-3p was associated with eNOS suppression. Additionally, transfection with inhibitors (anti-miR) of miR-92a-3p significantly rescued the eNOS suppression induced by lipopolysaccharide. In conclusion, the circulating miRs not only proved to have diagnostic utility, but also contributed to pathogenesis by eNOS regulation.

Identifiants

pubmed: 32370169
pii: jcm9051313
doi: 10.3390/jcm9051313
pmc: PMC7290712
pii:
doi:

Types de publication

Journal Article

Langues

eng

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Auteurs

Chan Soon Park (CS)

Graduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology, Daejeon 34141, Korea.

Inho Kim (I)

Department of Microbiology and Immunology, Seoul National University College of Medicine, Seoul 03080, Korea.
Department of Internal Medicine, Seoul National University Hospital, Seoul 03080, Korea.

Gyu Chul Oh (GC)

Department of Internal Medicine, Seoul National University Hospital, Seoul 03080, Korea.

Jung-Kyu Han (JK)

Department of Internal Medicine, Seoul National University Hospital, Seoul 03080, Korea.

Han-Mo Yang (HM)

Department of Internal Medicine, Seoul National University Hospital, Seoul 03080, Korea.

Kyung Woo Park (KW)

Department of Internal Medicine, Seoul National University Hospital, Seoul 03080, Korea.

Hyun-Jai Cho (HJ)

Department of Internal Medicine, Seoul National University Hospital, Seoul 03080, Korea.

Hyun-Jae Kang (HJ)

Department of Internal Medicine, Seoul National University Hospital, Seoul 03080, Korea.
Department of Internal Medicine, Seoul National University College of Medicine; Seoul 03080, Korea.

Bon-Kwon Koo (BK)

Department of Internal Medicine, Seoul National University Hospital, Seoul 03080, Korea.
Department of Internal Medicine, Seoul National University College of Medicine; Seoul 03080, Korea.

Woo-Young Chung (WY)

Department of Internal Medicine, Seoul National University College of Medicine; Seoul 03080, Korea.
Department of Internal Medicine, Seoul Metropolitan Government Seoul National University Boramae Medical Center, Seoul 07061, Korea.

Seil Oh (S)

Department of Internal Medicine, Seoul National University Hospital, Seoul 03080, Korea.
Department of Internal Medicine, Seoul National University College of Medicine; Seoul 03080, Korea.

Hae-Young Lee (HY)

Department of Internal Medicine, Seoul National University Hospital, Seoul 03080, Korea.
Department of Internal Medicine, Seoul National University College of Medicine; Seoul 03080, Korea.

Classifications MeSH