Involvement of Mitogen-Activated Protein Kinase Signaling in Growth and Rupture of Human Intracranial Aneurysms

• DOI: 10.1161/strokeaha.107.497875
• Publication Date: 2008-02-01T02:49:25Z
• Authors: Elisa Laaksamo; Riikka Tulamo; Marc Baumann; Reza Dashti; Juha Hernesniemi; Seppo Juvela; Mika Niemelä; Aki Laakso
• Keywords: Adult; Aged, 80 and over; Male; Neurosciences; Surgery, anesthesiology, intensive care, radiology; JNK Mitogen-Activated Protein Kinases; Intracranial Aneurysm; Aneurysm, Ruptured; Middle Aged; p38 Mitogen-Activated Protein Kinases; Neurology and psychiatry; 03 medical and health sciences; 0302 clinical medicine; Matrix Metalloproteinase 9; Humans; Female; Mitogen-Activated Protein Kinases; Phosphorylation; Extracellular Signal-Regulated MAP Kinases; Aged; Signal Transduction

Mitogen-activated protein kinases (MAPKs) are involved in vascular wall remodeling, but their role the pathogenesis of intracranial aneurysms (IAs) is poorly known. We investigated expression and phosphorylation 3 major mitogen-activated kinases, c-Jun N-terminal kinase (JNK), p38, extracellular signal-regulated kinase, unruptured ruptured human IAs.Tissue samples (n=24, 12 IAs) were obtained during microneurosurgical clipping. The localization proteins was studied by immunofluorescent staining, levels state Western blotting.The p54 JNK increased 1.5-fold IAs phospho-p54 level its directly correlated with IA size. phosphorylated total p38 associated size as well. Extracellular did not associate or rupture status. Expression transcription factor c-Jun, a downstream target JNK, state. Furthermore, matrix metalloproteinase 9, known to have vessel degeneration, 4.3-fold IAs.Our results suggest that activity growth possibly growth. Thus, pharmacological therapy affecting stress-activated may enhance repair future.