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VI型胶原蛋白可提高细胞存活率并防止抗β1整合素介导的细胞凋亡。

Type VI collagen increases cell survival and prevents anti-beta 1 integrin-mediated apoptosis.

作者信息

Howell S J, Doane K J

机构信息

Department of Anatomy, Northeastern Ohio Universities College of Medicine, Rootstown 44272-0095, USA.

出版信息

Exp Cell Res. 1998 May 25;241(1):230-41. doi: 10.1006/excr.1998.4051.

DOI:10.1006/excr.1998.4051
PMID:9633532
Abstract

Cell-matrix interactions are important in the development of the avian cornea. Type VI collagen is present within the periocular mesenchyme prior to the migration of cells into the corneal stroma and is abundant in the mature stroma. Whether the interaction of cells with type VI collagen is essential for cellular survival in the cornea is not known. In the present study, we examined the interaction of corneal cells with type VI collagen in vitro to determine if it can increase cell proliferation and decrease apoptosis. In vivo analysis demonstrated that apoptosis occurs in the periocular region during early stages of avian corneal development, but in fully mature corneas apoptosis only occurs in the corneal epithelium and not in the stroma. In vitro analysis examined the importance of beta 1 integrin interactions with type VI collagen in mature corneal fibroblasts and the precursor cells. Using an anti-beta 1 integrin blocking antibody, CSAT, integrin/matrix interactions were disrupted. Results indicated that viability of both corneal fibroblasts and periocular mesenchyme cells was greater on type VI collagen than on type I collagen or BSA-blocked glass. In addition, less apoptosis was observed for both cell types on type VI collagen when beta 1 integrin--matrix interactions were disrupted. These data indicated that these cells require intact beta 1 interactions with type I collagen and with BSA-coated glass controls to remain viable. Thus, type VI collagen may play a role in the rescue of corneal cells from anti-beta 1 integrin-induced apoptosis by increasing cell survival, probably via a non-beta 1 integrin-dependent mechanism.

摘要

细胞与基质的相互作用在鸟类角膜发育中很重要。VI型胶原在细胞迁移到角膜基质之前就存在于眼周间充质中,并且在成熟基质中含量丰富。细胞与VI型胶原的相互作用对于角膜中的细胞存活是否至关重要尚不清楚。在本研究中,我们在体外检测了角膜细胞与VI型胶原的相互作用,以确定其是否能增加细胞增殖并减少细胞凋亡。体内分析表明,在鸟类角膜发育早期,细胞凋亡发生在眼周区域,但在完全成熟的角膜中,细胞凋亡仅发生在角膜上皮,而不在基质中。体外分析检测了成熟角膜成纤维细胞和前体细胞中β1整合素与VI型胶原相互作用的重要性。使用抗β1整合素阻断抗体CSAT破坏整合素/基质相互作用。结果表明,VI型胶原上的角膜成纤维细胞和眼周间充质细胞的活力均高于I型胶原或牛血清白蛋白封闭的玻璃上的细胞。此外,当β1整合素-基质相互作用被破坏时,VI型胶原上两种细胞类型的凋亡均较少。这些数据表明,这些细胞需要与I型胶原和牛血清白蛋白包被的玻璃对照有完整的β1相互作用才能保持活力。因此,VI型胶原可能通过增加细胞存活,可能通过非β1整合素依赖性机制,在将角膜细胞从抗β1整合素诱导的凋亡中拯救出来发挥作用。

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