OBJECTIVE: Vascular remodeling via apoptotic mechanisms is an important factor in vascular diseases. c-Jun amino-terminal kinase (JNK) is a member of the mitogen-activated protein kinase family and initiates apoptosis mainly via phosphorylation of the c-Jun transcription factor. We performed this study to clarify the roles of the JNK/c-Jun pathway and apoptosis in the pathogenesis of cerebral aneurysms. METHODS: Cerebral aneurysms from 12 patients and control vessels from 5 patients were studied. We analyzed the expression of phosphorylated JNK and phosphorylated c-Jun in cerebral aneurysms by using immunohistochemical methods. RESULTS: Immunoreactivity for phosphorylated JNK and phosphorylated c-Jun was increased in the vascular walls of the cerebral aneurysms studied. Immunoreactivity for single-stranded deoxyribonucleic acid (a marker of deoxyribonucleic acid damage) was also increased in aneurysmal tissue, compared with control vessels, and was colocalized with that for phosphorylated JNK and phosphorylated c-Jun in smooth muscle cells. CONCLUSION: These observations may lead to better understanding of the role of the JNK/c-Jun pathway in the development of cerebral aneurysms and to new strategies for treatment.
OBJECTIVE: Vascular remodeling via apoptotic mechanisms is an important factor in vascular diseases. c-Jun amino-terminal kinase (JNK) is a member of the mitogen-activated protein kinase family and initiates apoptosis mainly via phosphorylation of the c-Jun transcription factor. We performed this study to clarify the roles of the JNK/c-Jun pathway and apoptosis in the pathogenesis of cerebral aneurysms. METHODS:Cerebral aneurysms from 12 patients and control vessels from 5 patients were studied. We analyzed the expression of phosphorylated JNK and phosphorylated c-Jun in cerebral aneurysms by using immunohistochemical methods. RESULTS: Immunoreactivity for phosphorylated JNK and phosphorylated c-Jun was increased in the vascular walls of the cerebral aneurysms studied. Immunoreactivity for single-stranded deoxyribonucleic acid (a marker of deoxyribonucleic acid damage) was also increased in aneurysmal tissue, compared with control vessels, and was colocalized with that for phosphorylated JNK and phosphorylated c-Jun in smooth muscle cells. CONCLUSION: These observations may lead to better understanding of the role of the JNK/c-Jun pathway in the development of cerebral aneurysms and to new strategies for treatment.
Authors: T Aoki; M Nishimura; T Matsuoka; K Yamamoto; T Furuyashiki; H Kataoka; S Kitaoka; R Ishibashi; A Ishibazawa; S Miyamoto; R Morishita; J Ando; N Hashimoto; K Nozaki; S Narumiya Journal: Br J Pharmacol Date: 2011-07 Impact factor: 8.739
Authors: Nohra Chalouhi; Muhammad S Ali; Pascal M Jabbour; Stavropoula I Tjoumakaris; L Fernando Gonzalez; Robert H Rosenwasser; Walter J Koch; Aaron S Dumont Journal: J Cereb Blood Flow Metab Date: 2012-07-11 Impact factor: 6.200
Authors: W I Mangrum; F Farassati; R Kadirvel; C P Kolbert; S Raghavakaimal; D Dai; Y H Ding; D Grill; V G Khurana; D F Kallmes Journal: AJNR Am J Neuroradiol Date: 2007-05 Impact factor: 3.825
Authors: Nohra Chalouhi; Muhammad S Ali; Robert M Starke; Pascal M Jabbour; Stavropoula I Tjoumakaris; L Fernando Gonzalez; Robert H Rosenwasser; Walter J Koch; Aaron S Dumont Journal: Mediators Inflamm Date: 2012-12-13 Impact factor: 4.711