Differential Activation of Ras/Raf/MAPK Pathway between Heart and Cerebral Artery in Isoproterenol-induced Cardiac Hypertrophy.
- Author:
Hyunju KIM
1
;
Nari KIM
;
Hyun JOO
;
Jae Boum YOUM
;
Won Sun PARK
;
Mohamed WARDA
;
Sunghyun KANG
;
Vu Thi THU
;
Tran Minh KHOA
;
Jin HAN
Author Information
1. Mitochondrial Signaling Laboratory, Department of Physiology and Biophysics, College of Medicine, Cardiovascular and Metabolic Disease Center, Biohealth Products Research Center, Inje University, Busan 614-735, Korea. phyhanj@ijnc.inje.ac.kr
- Publication Type:Original Article
- Keywords:
Cardiac hypertrophy;
Cerebrovascular events;
Ras/Raf/MAPK pathway
- MeSH:
Cardiomegaly*;
Cerebral Arteries*;
Heart*;
Isoproterenol;
Rabbits;
RNA, Messenger
- From:The Korean Journal of Physiology and Pharmacology
2005;9(5):299-304
- CountryRepublic of Korea
- Language:English
-
Abstract:
Cardiac hypertrophy contributes an increased risk to major cerebrovascular events. However, the molecular mechanisms underlying cerebrovascular dysfunction during cardiac hypertrophy have not yet been characterized. In the present study, we examined the molecular mechanism of isoproterenol (ISO) -evoked activation of Ras/Raf/MAPK pathways as well as PKA activity in cerebral artery of rabbits, and we also studied whether the activations of these signaling pathways were altered in cerebral artery, during ISO-induced cardiac hypertrophy compared to heart itself. The results show that the mRNA level of c-fos (not c-jun and c-myc) in heart and these genes in cerebral artery were considerably increased during cardiac hypertrophy. These results that the PKA activity and activations of Ras/Raf/ERK cascade as well as c-fos expression in rabbit heart during cardiac hypertrophy were consistent with previous reports. Interestingly, however, we also showed a novel finding that the decreased PKA activity might have differential effects on Ras and Raf expression in cerebral artery during cardiac hypertrophy. In conclusion, there are differences in molecular mechanisms between heart and cerebral artery during cardiac hypertrophy when stimulated with beta2 adrenoreceptor (AR), suggesting a possible mechanism underlying cerebrovascular dysfunction during cardiac hypertrophy.
