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首页> 外文期刊>Journal of Cellular Physiology >Clusterin (Apo J) regulates vascular smooth muscle cell differentiation in vitro.
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Clusterin (Apo J) regulates vascular smooth muscle cell differentiation in vitro.

机译：Clusterin (Apo J)调节血管平滑肌体外细胞分化。

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摘要

Previously we reported a significant and substantial increase in the synthesis and secretion of clusterin in cultured porcine vascular smooth muscle cells (VSMC) during the time when the VSMC culture modulates from a proliferating monolayer morphology to a nodular cell culture morphology. That in vitro process appears to recapitulate some aspects of in vivo vascular remodeling in response to injury and is facilitated by the presence of a well-developed extracellular matrix. To directly test the hypothesis that clusterin regulates VSMC phenotypic modulation, cultured VSMC were stably transfected with an expression plasmid containing the full-length murine clusterin sequence in antisense orientation. Twenty-four clones were selected on the basis of neomycin resistance and characterized for clusterin expression and culture morphology. In contrast to clone SM-CLU18AS, which expresses a high level of clusterin and forms multicellular nodules, clone SM-CLU13AS expresses a low level of clusterin and does not form nodules even in the presence of a preformed collagen gel. Importantly, clusterin-negative SM-CLU13AS retains the ability to form nodules in an environment containing exogenous clusterin. SM-CLU13AS forms nodules when cultured in Matrigel (which contains clusterin) and in the presence of clusterin-containing conditioned media prepared from nodular SMC cultures or SM-CLU18AS cultures. These results demonstrate that clusterin is required for VSMC nodule formation and suggest that it may play a role in smooth muscle cell reorganization in the vascular wall.
机译：之前我们报道一个重要在合成和大幅增加分泌clusterin培养的猪血管平滑肌细胞(VSMC)当VSMC文化调节的结节性增殖单层形态细胞培养形态。似乎反映出体内的某些方面血管重建损伤和促进发达的存在细胞外基质。假设clusterin调节VSMC表型调制,VSMC培养是稳定的转染表达质粒含有完整的小鼠clusterin序列反义方向。选择新霉素抗性和的基础上clusterin表达式和特征文化形态。SM-CLU18AS,表达高水平的clusterin并形成多细胞结节,克隆SM-CLU13AS clusterin和低水平的表达不形成结节甚至在的存在预成型的胶原蛋白凝胶。clusterin-negative SM-CLU13AS保留的能力在一个环境包含形成结节外生clusterin。在基底膜基质培养(包含clusterin)的存在clusterin-containing条件媒体准备结节性SMC文化或SM-CLU18AS文化。这些结果说明clusterin所需VSMC结节形成和建议它可能在平滑肌细胞中发挥作用血管壁的重组。

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