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Effect of PKC inhibitor on experimental autoimmune myocarditis in Lewis rats.
Oncotarget. 2017 Aug 15; 8(33):54187-54198.O

Abstract

Myocarditis is a major cause of sudden, unexpected death in young people. However, it is still one of the most challenging diseases to treat in cardiology. In the present study, we showed that both expression level and activity of PKC-α were up-regulated in the rat heart of experimental autoimmune myocarditis (EAM). Intraperitoneal administration of PKC inhibitor (Ro-32-0432) at the end of the most severe inflammation period of EAM still significantly reduced the EAM induced expression of failure biomarkers. Furthermore, Ro-32-0432 reduced the ratio of Bax/Bcl-2 and suppressed the expression of cleaved caspase-3, both of which were increased in the heart of the EAM rats, suggesting an anti-apoptotic role of Ro-32-0432. Besides, Ro-32-0432 suppressed EAM-induced cardiac fibrosis and release of pro-inflammatory cytokines IL-1β and IL-17. These results suggest that inhibition of PKC may serve as a potential therapeutic strategy for the treatment of myocarditis.

Authors+Show Affiliations

Department of Basic Medical Sciences, Medical College of Xiamen University, Xiang'an Nan Lu, Xiamen, China.Department of Basic Medical Sciences, Medical College of Xiamen University, Xiang'an Nan Lu, Xiamen, China. Xiamen Cardiovascular Hospital, Medical College of Xiamen University, Xiamen, China.Department of Basic Medical Sciences, Medical College of Xiamen University, Xiang'an Nan Lu, Xiamen, China. Xiamen Cardiovascular Hospital, Medical College of Xiamen University, Xiamen, China.Department of Basic Medical Sciences, Medical College of Xiamen University, Xiang'an Nan Lu, Xiamen, China. Xiamen Cardiovascular Hospital, Medical College of Xiamen University, Xiamen, China.Department of Basic Medical Sciences, Medical College of Xiamen University, Xiang'an Nan Lu, Xiamen, China.Department of Basic Medical Sciences, Medical College of Xiamen University, Xiang'an Nan Lu, Xiamen, China.Department of Basic Medical Sciences, Medical College of Xiamen University, Xiang'an Nan Lu, Xiamen, China.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

28903333

Citation

Zhong, Chunlian, et al. "Effect of PKC Inhibitor On Experimental Autoimmune Myocarditis in Lewis Rats." Oncotarget, vol. 8, no. 33, 2017, pp. 54187-54198.
Zhong C, Wu Y, Chang H, et al. Effect of PKC inhibitor on experimental autoimmune myocarditis in Lewis rats. Oncotarget. 2017;8(33):54187-54198.
Zhong, C., Wu, Y., Chang, H., Liu, C., Zhou, L., Zou, J., & Qi, Z. (2017). Effect of PKC inhibitor on experimental autoimmune myocarditis in Lewis rats. Oncotarget, 8(33), 54187-54198. https://doi.org/10.18632/oncotarget.17018
Zhong C, et al. Effect of PKC Inhibitor On Experimental Autoimmune Myocarditis in Lewis Rats. Oncotarget. 2017 Aug 15;8(33):54187-54198. PubMed PMID: 28903333.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Effect of PKC inhibitor on experimental autoimmune myocarditis in Lewis rats. AU - Zhong,Chunlian, AU - Wu,Yang, AU - Chang,He, AU - Liu,Chunxiao, AU - Zhou,Li, AU - Zou,Jun, AU - Qi,Zhi, Y1 - 2017/04/10/ PY - 2017/01/02/received PY - 2017/03/31/accepted PY - 2017/9/15/entrez PY - 2017/9/15/pubmed PY - 2017/9/15/medline KW - PKC inhibitor KW - PKC signaling KW - apoptosis KW - inflammation KW - myocarditis SP - 54187 EP - 54198 JF - Oncotarget JO - Oncotarget VL - 8 IS - 33 N2 - Myocarditis is a major cause of sudden, unexpected death in young people. However, it is still one of the most challenging diseases to treat in cardiology. In the present study, we showed that both expression level and activity of PKC-α were up-regulated in the rat heart of experimental autoimmune myocarditis (EAM). Intraperitoneal administration of PKC inhibitor (Ro-32-0432) at the end of the most severe inflammation period of EAM still significantly reduced the EAM induced expression of failure biomarkers. Furthermore, Ro-32-0432 reduced the ratio of Bax/Bcl-2 and suppressed the expression of cleaved caspase-3, both of which were increased in the heart of the EAM rats, suggesting an anti-apoptotic role of Ro-32-0432. Besides, Ro-32-0432 suppressed EAM-induced cardiac fibrosis and release of pro-inflammatory cytokines IL-1β and IL-17. These results suggest that inhibition of PKC may serve as a potential therapeutic strategy for the treatment of myocarditis. SN - 1949-2553 UR - https://www.unboundmedicine.com/medline/citation/28903333/Effect_of_PKC_inhibitor_on_experimental_autoimmune_myocarditis_in_Lewis_rats_ L2 - http://www.impactjournals.com/oncotarget/misc/linkedout.php?pii=17018 DB - PRIME DP - Unbound Medicine ER -
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