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Identifying Involvement of H19-miR-675-3p-IGF1R and H19-miR-200a-PDCD4 in Treating Pulmonary Hypertension with Melatonin.
Mol Ther Nucleic Acids 2018; 13:44-54MT

Abstract

Non-coding RNAs play an important role in the pathogenesis of pulmonary arterial hypertension (PAH). The aim of this study was to characterize the therapeutic role of melatonin as well as the underlying molecular mechanism (its effects on the expression of H19 and its downstream signaling pathways) in the treatment of PAH. Real-time PCR and western blot analysis were performed to evaluate the expression of H19, miR-200a, miR-675, insulin-like growth factor-1 receptor (IGF1R), and programmed cell death 4 (PDCD4). The value of systolic pulmonary artery pressure (SPAP) and the ratio of medial thickening in the monocrotaline (MCT) group were increased, whereas the melatonin treatment could decrease these values to some extent. The weights of RV (right ventricle), LV (left ventricle) + IVS (interventricular septal), and RV/(LV + IVS) in the MCT group were much higher than those in the MCT + melatonin and control groups. In addition, the expression of H19, miR-675, IGF1R mRNA, and IGF1R protein in the MCT group was the highest, whereas their expression in the control group was the lowest. The expression of miR-200, PDCD4 mRNA, and PDCD4 protein in the MCT group was the lowest, whereas their expression in the control group was the highest. Furthermore, H19 directly suppressed the expression of miR-200a, whereas miR-675-3p and miR-200a directly inhibited the expression of IGF1R and PDCD4, respectively. Finally, melatonin treatment inhibited cell proliferation; upregulated the expression of H19, miR-675-3p, and PDCD4; and downregulated the expression of miR-200a and IGF1R. This study demonstrated the role of H19-miR-675-3p-IGF1R- and H19-miR-200a-PDCD4-signaling pathways in the melatonin treatment of PAH.

Authors+Show Affiliations

Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Anhui Medical University, Hefei 230022, China.Hefei Prevention and Treatment Center for Occupational Diseases, Hefei 230022, China.Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Anhui Medical University, Hefei 230022, China.Department of Oncology, The First Affiliated Hospital of Anhui Medical University, Hefei 230022, China.Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Anhui Medical University, Hefei 230022, China.Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Anhui Medical University, Hefei 230022, China.Division of Pulmonary/Critical Care Medicine, Cedars Sinai Medical Center, Los Angeles, CA 90015, USA.The First Clinical College of Anhui Medical University, Hefei 230032, China.The First Clinical College of Anhui Medical University, Hefei 230032, China.Department of Respiratory Medicine, Ningbo First Hospital, Ningbo 315000, China. Electronic address: caochaoningbo@126.com.Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Anhui Medical University, Hefei 230022, China. Electronic address: guanghefei@hotmail.com.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

30240970

Citation

Wang, Ran, et al. "Identifying Involvement of H19-miR-675-3p-IGF1R and H19-miR-200a-PDCD4 in Treating Pulmonary Hypertension With Melatonin." Molecular Therapy. Nucleic Acids, vol. 13, 2018, pp. 44-54.
Wang R, Zhou S, Wu P, et al. Identifying Involvement of H19-miR-675-3p-IGF1R and H19-miR-200a-PDCD4 in Treating Pulmonary Hypertension with Melatonin. Mol Ther Nucleic Acids. 2018;13:44-54.
Wang, R., Zhou, S., Wu, P., Li, M., Ding, X., Sun, L., ... Fei, G. (2018). Identifying Involvement of H19-miR-675-3p-IGF1R and H19-miR-200a-PDCD4 in Treating Pulmonary Hypertension with Melatonin. Molecular Therapy. Nucleic Acids, 13, pp. 44-54. doi:10.1016/j.omtn.2018.08.015.
Wang R, et al. Identifying Involvement of H19-miR-675-3p-IGF1R and H19-miR-200a-PDCD4 in Treating Pulmonary Hypertension With Melatonin. Mol Ther Nucleic Acids. 2018 Dec 7;13:44-54. PubMed PMID: 30240970.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Identifying Involvement of H19-miR-675-3p-IGF1R and H19-miR-200a-PDCD4 in Treating Pulmonary Hypertension with Melatonin. AU - Wang,Ran, AU - Zhou,Sijing, AU - Wu,Peipei, AU - Li,Min, AU - Ding,Xing, AU - Sun,Li, AU - Xu,Xuan, AU - Zhou,Xuexin, AU - Zhou,Luqian, AU - Cao,Chao, AU - Fei,Guanghe, Y1 - 2018/08/24/ PY - 2018/04/20/received PY - 2018/08/10/revised PY - 2018/08/18/accepted PY - 2018/9/22/pubmed PY - 2018/9/22/medline PY - 2018/9/22/entrez KW - H19 KW - apoptosis KW - melatonin KW - miR-200a KW - miR-675 KW - pulmonary arterial hypertension SP - 44 EP - 54 JF - Molecular therapy. Nucleic acids JO - Mol Ther Nucleic Acids VL - 13 N2 - Non-coding RNAs play an important role in the pathogenesis of pulmonary arterial hypertension (PAH). The aim of this study was to characterize the therapeutic role of melatonin as well as the underlying molecular mechanism (its effects on the expression of H19 and its downstream signaling pathways) in the treatment of PAH. Real-time PCR and western blot analysis were performed to evaluate the expression of H19, miR-200a, miR-675, insulin-like growth factor-1 receptor (IGF1R), and programmed cell death 4 (PDCD4). The value of systolic pulmonary artery pressure (SPAP) and the ratio of medial thickening in the monocrotaline (MCT) group were increased, whereas the melatonin treatment could decrease these values to some extent. The weights of RV (right ventricle), LV (left ventricle) + IVS (interventricular septal), and RV/(LV + IVS) in the MCT group were much higher than those in the MCT + melatonin and control groups. In addition, the expression of H19, miR-675, IGF1R mRNA, and IGF1R protein in the MCT group was the highest, whereas their expression in the control group was the lowest. The expression of miR-200, PDCD4 mRNA, and PDCD4 protein in the MCT group was the lowest, whereas their expression in the control group was the highest. Furthermore, H19 directly suppressed the expression of miR-200a, whereas miR-675-3p and miR-200a directly inhibited the expression of IGF1R and PDCD4, respectively. Finally, melatonin treatment inhibited cell proliferation; upregulated the expression of H19, miR-675-3p, and PDCD4; and downregulated the expression of miR-200a and IGF1R. This study demonstrated the role of H19-miR-675-3p-IGF1R- and H19-miR-200a-PDCD4-signaling pathways in the melatonin treatment of PAH. SN - 2162-2531 UR - https://www.unboundmedicine.com/medline/citation/30240970/Identifying_Involvement_of_H19_miR_675_3p_IGF1R_and_H19_miR_200a_PDCD4_in_Treating_Pulmonary_Hypertension_with_Melatonin_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S2162-2531(18)30230-0 DB - PRIME DP - Unbound Medicine ER -