Isolation, culture, and characterization of smooth muscle cells from human intracranial aneurysms

被引:10
作者
Bygglin, Henrik [2 ]
Laaksamo, Elisa [2 ]
Myllarniemi, Marjukka [3 ]
Tulamo, Riikka [2 ]
Hernesniemi, Juha [1 ]
Niemela, Mika [1 ,2 ]
Laakso, Aki [1 ,2 ]
机构
[1] Univ Helsinki, Cent Hosp, Dept Neurosurg, Hus Helsinki 00029, Finland
[2] Univ Helsinki, Cent Hosp, Biomedicum Helsinki, Neurosurg Res Grp, Hus Helsinki 00029, Finland
[3] Univ Helsinki, Cent Hosp, Div Pulm, Hus Helsinki 00029, Finland
关键词
alpha-smooth muscle cell actin; Calponin; Cell culture; Intracranial aneurysm; Prolyl-4-hydroxylase; Vascular smooth muscle cells; SUBARACHNOID HEMORRHAGE; RUPTURE; ARTERY; DIFFERENTIATION; DISEASE; GROWTH; WALLS; EXPRESSION; DIVERSITY; PATHWAYS;
D O I
10.1007/s00701-010-0836-x
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Smooth muscle cells (SMCs) play a critical role in the vascular wall and also participate in vascular repair mechanisms. Dysfunction of SMCs may also contribute to the formation of intracranial aneurysms (IAs) causing subarachnoid hemorrhage. Our aim was to investigate the possibility of using cultured SMCs as an in vitro model for the study of aneurysmal SMCs. IA tissue was obtained during microsurgical ligation of IAs. By using the explant method, cell cultures were established from the aneurysmal tissue. The phenotype of cultured cells from passage to passage was studied using immunoperoxidase staining and Western blotting. Eight cell lines could be established from 29 IA samples. Four lines showing most rigorous growth were investigated more thoroughly. Abundant expression of SMC markers, alpha-smooth muscle cell actin and calponin, as well as of prolyl-4-hydroxylases, a key enzyme family in the synthesis of collagens, was observed in all of them. Aneurysmal SMCs in culture maintained their phenotype and SMC characteristics through the early passages of growth. This is the first documented successful culture of SMCs from human IAs. An access to living human cells of aneurysmal origin gives us a new tool in our research of the formation, growth, and rupture of IAs.
引用
收藏
页码:311 / 318
页数:8
相关论文
共 26 条
[1]   Beyond mere markers - Functions for CD34 family of sialomucins in hematopoiesis [J].
Barton Furness, Sebastian George ;
McNagny, Kelly .
IMMUNOLOGIC RESEARCH, 2006, 34 (01) :13-32
[2]  
Boscolo E, 2006, INT J MOL MED, V18, P813
[3]   Calponin [J].
ElMezgueldi, M .
INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY, 1996, 28 (11) :1185-1189
[4]   Risk factors for subarachnoid hemorrhage - An updated systematic review of epidemiological studies [J].
Feigin, VL ;
Rinkel, GJE ;
Lawes, CMM ;
Algra, A ;
Bennett, DA ;
van Gijn, J ;
Anderson, CS .
STROKE, 2005, 36 (12) :2773-2780
[5]   Growth factor receptor expression and remodeling of saccular cerebral artery aneurysm walls:: Implications for biological therapy preventing rupture [J].
Frösen, J ;
Piippo, A ;
Paetau, A ;
Kangasniemi, M ;
Niemelä, M ;
Hernesniemi, J ;
Jääskeläinen, J .
NEUROSURGERY, 2006, 58 (03) :534-541
[6]   Remodeling of saccular cerebral artery aneurysm wall is associated with rupture -: Histological analysis of 24 unruptured and 42 ruptured cases [J].
Frösen, J ;
Piippo, A ;
Paetau, A ;
Kangasniemi, M ;
Niemelä, M ;
Hernesniemi, J ;
Jääskeläinen, J .
STROKE, 2004, 35 (10) :2287-2293
[7]   Arterial smooth muscle cell heterogeneity - Implications for atherosclerosis and restenosis development [J].
Hao, HY ;
Gabbiani, G ;
Bochaton-Piallat, ML .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 2003, 23 (09) :1510-1520
[8]  
Juvela S, 2002, ACTA NEUROCHIR SUPPL, V82, P27
[9]   Smooth muscle signalling pathways in health and disease [J].
Kim, H. R. ;
Appel, S. ;
Vetterkind, S. ;
Gangopadhyay, S. S. ;
Morgan, K. G. .
JOURNAL OF CELLULAR AND MOLECULAR MEDICINE, 2008, 12 (6A) :2165-2180
[10]   Involvement of mitogen-activated protein kinase signaling in growth and rupture of human intracranial aneurysms [J].
Laaksamo, Elisa ;
Tulamo, Riikka ;
Baumann, Marc ;
Dashti, Reza ;
Hernesniemi, Juha ;
Juvela, Seppo ;
Niemela, Mika ;
Laakso, Aki .
STROKE, 2008, 39 (03) :886-892