Expression profiles of nestin in vascular smooth muscle cells in vivo and in vitro

被引:34
|
作者
Oikawa, Hiroki [1 ,3 ]
Hayashi, Ken'ichiro [1 ]
Maesawa, Chihaya [3 ]
Masuda, Tomoyuki [3 ]
Sobue, Kenji [1 ,2 ]
机构
[1] Osaka Univ, Dept Neurosci D13, Grad Sch Med, Suita, Osaka 5650871, Japan
[2] Osaka Univ, Res Ctr Child Mental Dev, Grad Sch Med, Suita, Osaka 5650871, Japan
[3] Iwate Med Univ, Dept Pathol, Morioka, Iwate 0208505, Japan
关键词
Nestin; VSMCs; ERK; PKB(Akt); Growth factors and vascular remodeling; STEM-CELLS; GROWTH; SP1; TRANSACTIVATION; SUBPOPULATION; ASSOCIATION; ACTIVATION; PHENOTYPE; AKT;
D O I
10.1016/j.yexcr.2009.10.025
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Nestin is an intermediate filament protein expressed in neural and mesenchymal stem cells. Here, we investigated the expression of nestin in vascular smooth muscle cells (VSMCs) in vivo and in vitro. In the developing arteries, medial VSMCs were found to express nestin; its expression was prominent in embryos but was down-regulated after birth (3-6 weeks) in a region-dependent manner; its expression was abolished in the adult. Thus, the expression of nestin is specific to developing VSMCs. In primary VMSC cultures, nestin expression was induced by serum, but was independent of cell-cycle progression. Signaling analyses revealed that the serum-induced nestin expression depended on the extracellular signal-regulated kinase (ERK) and protein kinase B (PKB)(Akt) pathways, via the platelet derived growth factor (PDGF) and epidermal growth factor (EGF) receptors. Nestin expression was closely related to the up-regulation and activation of Sp1 and Sp3. Among major serum growth factors and cytokines, PDGF-BB was the most potent inducer of nestin expression. Nestin was also up-regulated in arteries undergoing vascular remodeling following balloon injury. Its expression was particularly strong in the cells lining the lumen of the neointima, suggesting a possible correlation between nestin expression and the progression of vascular remodeling. (C) 2009 Elsevier Inc. All rights reserved.
引用
收藏
页码:940 / 950
页数:11
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