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Stem Cells:血管细胞控制脂肪细胞发育

来源:ebiotrade 2008-09-25 12:56

来自印第安纳大学医学院的研究者近期研究发现血管细胞新功能。血管壁细胞是维持血管形态和功能的重要成分,新发现表明血管壁细胞还是控制脂肪细胞发育的重要因子。研究成果发表在近期Stem Cells上面。

研究者发现,祖细胞或者说干细胞接触血管内皮细胞后发育成为脂肪细胞的趋势显著降低。

据文章作者,印第安纳大学医学院血管生物和医学研究中心研究员Keith L.March介绍,研究者在观察脂肪组织的基质细胞时发现一旦接触毛细血管或是微血管内皮细胞时,基质细胞分化成脂肪细胞的几率就显著下降。

印第安纳大学医学院生理学和生物工程学教授March博士介绍道,首先研究者只是观察到基质细胞与内皮细胞接触后发生变化的现象,没有人知道究竟是什么样的机制让这一切发生。因此,研究者希望通过实验了解个中的机制。

科学家从脂肪组织提取脂肪干细胞,把脂肪干细胞与血管内皮细胞混合在一起,结果发现脂肪干细胞分化成为成熟脂肪细胞的几率大大下降。他们发现,血管内皮细胞会释放一种蛋白,Wnt,这一因子在脂肪细胞的发育过程中起关键的作用。Wnt在多种组织里存在,对组织细胞的发育和分化起调控作用,并且在老化过程中也起作用。

研究者推测,修复受损的血管内皮细胞可能对阻断脂肪细胞的发育具有积极意义。现在已经清楚血管内皮细胞是通过Wnt来调节脂肪细胞的发育,但是对于脂肪细胞对血管内皮细胞的反作用暂时不清楚。研究者希望通过深入的研究可以揭开这一谜团。

研究者推测,功能异常的血管内皮细胞会促进脂肪细胞发育,并伴随新血管生成。研究者希望打破这一循环。新的研究成果可能对心血管疾病和肥胖症治疗具有指导意义。(生物谷Bioon.com)

生物谷推荐原始出处:

Stem Cells First published online July 31, 2008

IFATS Series: Adipose Stromal Cell Differentiation is Reduced by Endothelial Cell Contact and Paracrine Communication: Role of Canonical Wnt-Signaling

Gangaraju Rajashekhar, Dmitry O. Traktuev, Christopher William Roell, Brian H. Johnstone, Stephanie Merfeld-Clauss, Bruce Van Natta, Elliot D. Rosen, Keith L March, Matthias Clauss

Adipose stromal cells (ASC) are multipotential mesenchymal progenitor cells which are readily induced to undergo adipogenic differentiation, and we have recently demonstrated to have functional and phenotypic overlap with pericytes lining microvessels in adipose tissues. In this study we addressed the hypothesis that modulation of ASC fate within this perivascular niche can occur via interaction with endothelial cells (EC) which serve to modulate the adipogenic potential of ASC. To this end, we investigated contact as well as paracrine effects of EC on ASC adipogenesis in 2D-co-culture and via conditioned media, and analyzed mutual gene expression changes by real time RT-PCR. A significant decrease in adipogenic differentiation was observed in ASC when co-cultured with EC but not control fibroblasts. This endothelial cell-specific effect was accompanied by increased expression of factors involved in Wnt signaling; most prominently Wnt1, Wnt4 and Wnt10a, well known inhibitors of adipogenesis. Suppression of Wnt1, but not Wnt 10a or scrambled control siRNA in co-cultures partially reversed the endothelial cell effect, thus increasing adipogenic differentiation, suggesting a plausible role of Wnt1 ligand in modulation of adipogenesis by the vasculature. Furthermore, addition of recombinant Wnt ligand or the Wnt signaling agonist inhibited adipogenic differentiation of ASC in the absence of EC. In conclusion, these data define the relationship in adipose tissue between ASC and EC in the perivascular niche, in which the latter act to repress adipogenesis, thereby stabilizing vasculature. It is tempting to speculate that abnormal endothelial function may be associated with pathologic de-repression of adipogenesis.

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