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游离脂肪酸与透析血清对成纤维细胞填充胶原格子收缩的影响

Free fatty acids and dialyzed serum alterations of fibroblast populated collagen lattice contraction.

作者信息

Rittenberg T, Ehrlich H P

机构信息

Department of Pathology and Surgery, Shriners Burns Institute, Massachusetts General Hospital, Boston 02114.

出版信息

Tissue Cell. 1992;24(2):243-51. doi: 10.1016/0040-8166(92)90097-q.

DOI:10.1016/0040-8166(92)90097-q
PMID:1589872
Abstract

Fibroblast populated collagen lattices (FPCL) have facilitated the in vitro study of wound contraction and scar contracture. Mixing fibroblasts, serum containing culture medium and soluble collagen, together and then incubating the mixture at 37 degrees C produces a FPCL. The fibroblasts elongate and spread within the collagen matrix, and by forces associated with cell locomotion they reorganize the collagen fibers. The reorganization of the collagen produces a reduction in size of the FPCL, called lattice contraction. It was also found that dialyzed fetal bovine serum did not support lattice contraction. Supplementing dialyzed serum with fatty acids accelerated lattice contraction. The fatty acid composition of the fibroblast plasma membrane influences that membrane fluidity. These studies demonstrated that lattice contraction was enhanced by the additions of saturated fatty acids in the order of laurate (C-12), palmitic (C-16), and stearate (C-18). With unsaturated fatty acids additions, the order of enhanced lattice contraction was arachidonate (4 C = C), linoleate (2 C = C) and oleate (1 C = C). The addition of dialyzed serum with or without fatty acids neither altered ATP-induced cell contraction activity nor cell proliferation. It was concluded that free fatty acid additions do not modulate FPCL contraction by enhancing microfilaments contraction or increasing cell numbers. The mechanism of action was proposed to be by altering cell membrane fluidity. This finding further supports the theory that the mechanism for lattice contraction is cell locomotion, rather than cell contraction.

摘要

成纤维细胞填充的胶原晶格(FPCL)促进了伤口收缩和瘢痕挛缩的体外研究。将成纤维细胞、含血清的培养基和可溶性胶原混合,然后在37℃孵育该混合物,即可产生FPCL。成纤维细胞在胶原基质中伸长并铺展,通过与细胞运动相关的力重新组织胶原纤维。胶原的重新组织导致FPCL尺寸减小,称为晶格收缩。还发现透析后的胎牛血清不支持晶格收缩。用脂肪酸补充透析后的血清可加速晶格收缩。成纤维细胞质膜的脂肪酸组成影响该膜的流动性。这些研究表明,添加饱和脂肪酸可增强晶格收缩,其顺序为月桂酸(C-12)、棕榈酸(C-16)和硬脂酸(C-18)。添加不饱和脂肪酸时,增强晶格收缩的顺序为花生四烯酸(4个碳碳双键)、亚油酸(2个碳碳双键)和油酸(1个碳碳双键)。添加含或不含脂肪酸的透析血清既不改变ATP诱导的细胞收缩活性,也不改变细胞增殖。得出的结论是,添加游离脂肪酸不会通过增强微丝收缩或增加细胞数量来调节FPCL收缩。其作用机制被认为是通过改变细胞膜流动性。这一发现进一步支持了晶格收缩机制是细胞运动而非细胞收缩的理论。

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