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Inhibiting microRNA-144 abates oxidative stress and reduces apoptosis in hearts of streptozotocin-induced diabetic mice.
Cardiovasc Pathol 2015 Nov-Dec; 24(6):375-81CP

Abstract

INTRODUCTION

Hyperglycemia-induced reactive oxygen species (ROS) generation contributes to the development of diabetic cardiomyopathy. However, little is known about the role of microRNAs in the regulation of ROS formation and myocardial apoptosis in streptozotocin (STZ)-induced diabetic mice.

METHODS AND RESULTS

It was observed that microRNA-144 (miR-144) level was lower in heart tissues of STZ-induced diabetic mice. High glucose exposure also reduced miR-144 levels in cultured cardiomyocytes. Moreover, miR-144 modulated high glucose-induced oxidative stress in cultured cardiomyocytes by directly targeting nuclear factor-erythroid 2-related factor 2 (Nrf2), which was a central regulator of cellular response to oxidative stress. The miR-144 mimics aggravated high glucose-induced ROS formation and apoptosis in cardiomyocytes, which could be attenuated by treatment with Dh404, an activator of Nrf2. Meanwhile, inhibition of miR-144 suppressed ROS formation and apoptosis induced by high glucose in cultured cardiomyocytes. What was more important is that reduced myocardial oxidative stress and apoptosis and improved cardiac function were identified in STZ-induced diabetic mice when treated with miR-144 antagomir.

CONCLUSION

Although miR-144 cannot explain the increased oxidative stress in STZ, therapeutic interventions directed at decreasing miR-144 may help to decrease oxidative stress in these hearts. Inhibition of miR-144 might have clinical potential to abate oxidative stress as well as to reduce cardiomyocyte apoptosis and improve cardiac function in diabetic cardiomyopathy.

Authors+Show Affiliations

Department of Cardiovasology, Changhai Hospital, Second Military Medical University, Shanghai, China.Department of Cardiovasology, Changhai Hospital, Second Military Medical University, Shanghai, China.Department of Cardiovasology, Changhai Hospital, Second Military Medical University, Shanghai, China.Department of Cardiovasology, Changhai Hospital, Second Military Medical University, Shanghai, China.Department of Cardiovasology, Changhai Hospital, Second Military Medical University, Shanghai, China.Department of Cardiovasology, Changhai Hospital, Second Military Medical University, Shanghai, China. Electronic address: xianxianz2010@163.com.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

26164195

Citation

Yu, Manli, et al. "Inhibiting microRNA-144 Abates Oxidative Stress and Reduces Apoptosis in Hearts of Streptozotocin-induced Diabetic Mice." Cardiovascular Pathology : the Official Journal of the Society for Cardiovascular Pathology, vol. 24, no. 6, 2015, pp. 375-81.
Yu M, Liu Y, Zhang B, et al. Inhibiting microRNA-144 abates oxidative stress and reduces apoptosis in hearts of streptozotocin-induced diabetic mice. Cardiovasc Pathol. 2015;24(6):375-81.
Yu, M., Liu, Y., Zhang, B., Shi, Y., Cui, L., & Zhao, X. (2015). Inhibiting microRNA-144 abates oxidative stress and reduces apoptosis in hearts of streptozotocin-induced diabetic mice. Cardiovascular Pathology : the Official Journal of the Society for Cardiovascular Pathology, 24(6), pp. 375-81. doi:10.1016/j.carpath.2015.06.003.
Yu M, et al. Inhibiting microRNA-144 Abates Oxidative Stress and Reduces Apoptosis in Hearts of Streptozotocin-induced Diabetic Mice. Cardiovasc Pathol. 2015;24(6):375-81. PubMed PMID: 26164195.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Inhibiting microRNA-144 abates oxidative stress and reduces apoptosis in hearts of streptozotocin-induced diabetic mice. AU - Yu,Manli, AU - Liu,Yu, AU - Zhang,Bili, AU - Shi,Yicheng, AU - Cui,Ling, AU - Zhao,Xianxian, Y1 - 2015/06/19/ PY - 2015/04/01/received PY - 2015/06/16/revised PY - 2015/06/17/accepted PY - 2015/7/13/entrez PY - 2015/7/15/pubmed PY - 2016/8/23/medline KW - Diabetic cardiomyopathy KW - MicroRNA-144 KW - Nuclear factor-erythroid 2-related factor 2 KW - Oxidative stress KW - Streptozotocin SP - 375 EP - 81 JF - Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology JO - Cardiovasc. Pathol. VL - 24 IS - 6 N2 - INTRODUCTION: Hyperglycemia-induced reactive oxygen species (ROS) generation contributes to the development of diabetic cardiomyopathy. However, little is known about the role of microRNAs in the regulation of ROS formation and myocardial apoptosis in streptozotocin (STZ)-induced diabetic mice. METHODS AND RESULTS: It was observed that microRNA-144 (miR-144) level was lower in heart tissues of STZ-induced diabetic mice. High glucose exposure also reduced miR-144 levels in cultured cardiomyocytes. Moreover, miR-144 modulated high glucose-induced oxidative stress in cultured cardiomyocytes by directly targeting nuclear factor-erythroid 2-related factor 2 (Nrf2), which was a central regulator of cellular response to oxidative stress. The miR-144 mimics aggravated high glucose-induced ROS formation and apoptosis in cardiomyocytes, which could be attenuated by treatment with Dh404, an activator of Nrf2. Meanwhile, inhibition of miR-144 suppressed ROS formation and apoptosis induced by high glucose in cultured cardiomyocytes. What was more important is that reduced myocardial oxidative stress and apoptosis and improved cardiac function were identified in STZ-induced diabetic mice when treated with miR-144 antagomir. CONCLUSION: Although miR-144 cannot explain the increased oxidative stress in STZ, therapeutic interventions directed at decreasing miR-144 may help to decrease oxidative stress in these hearts. Inhibition of miR-144 might have clinical potential to abate oxidative stress as well as to reduce cardiomyocyte apoptosis and improve cardiac function in diabetic cardiomyopathy. SN - 1879-1336 UR - https://www.unboundmedicine.com/medline/citation/26164195/Inhibiting_microRNA_144_abates_oxidative_stress_and_reduces_apoptosis_in_hearts_of_streptozotocin_induced_diabetic_mice_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1054-8807(15)00077-0 DB - PRIME DP - Unbound Medicine ER -