Type VI collagen increases cell survival and prevents anti-β1 integrin-mediated apoptosis
Type VI collagen increases cell survival and prevents anti-β1 integrin-mediated apoptosis
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DOI：
10.1006/excr.1998.4051
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发表时间：
1998-05-25
影响因子：
3.7
通讯作者：
Doane, KJ
中科院分区：
文献类型：
--
作者：
Howell, SJ;Doane, KJ
细胞-基质相互作用在鸟类角膜的发育中是重要的。VI型胶原在细胞迁移到角膜基质中之前存在于眼周间充质内，并且在成熟基质中丰富。是否与VI型细胞相互作用。胶原蛋白对于角膜中的细胞存活是必需的还不清楚。在本研究中，我们研究了角膜细胞与VI型胶原在体外的相互作用，以确定它是否可以增加细胞增殖和减少凋亡。体内分析表明，细胞凋亡发生在眼周区域在早期阶段的鸟类角膜发育，但在完全成熟的角膜细胞凋亡只发生在角膜上皮，而不是在基质。体外分析检测了β（1）整合素与成熟角膜成纤维细胞和前体细胞中VI型胶原相互作用的重要性。使用抗β（1）整联蛋白阻断抗体CSAT，破坏整联蛋白/基质相互作用。结果表明，角膜成纤维细胞和眼周间充质细胞的活力是更大的VI型胶原比I型胶原或BSA阻断玻璃。此外，当β（1）整合素-基质相互作用被破坏时，在VI型胶原上观察到两种细胞类型的凋亡较少。这些数据表明，这些细胞需要完整的β（1），与I型胶原和BSA涂层玻璃对照的相互作用，以保持活力。因此，VI型胶原可能通过增加细胞存活率（可能是通过非β 1整合素依赖性机制），在拯救角膜细胞免于抗β 1整合素诱导的凋亡中发挥作用。(C)北京：科学出版社.
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. (C) 1998 Academic Press.