TGFβ2 in corneal morphogenesis during mouse embryonic development
TGFβ2 in corneal morphogenesis during mouse embryonic development
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DOI：
10.1006/dbio.2001.0480
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发表时间：
2001-12-15
影响因子：
2.7
通讯作者：
Kao, WWY
中科院分区：
文献类型：
--
作者：
Saika, S;Saika, S;Kao, WWY
为了检查TGF β同种型对角膜形态发生的作用，在不同发育阶段分析缺乏TGF β的小鼠的眼睛的细胞增殖、迁移和凋亡，以及角蛋白12、光蛋白聚糖、角膜蛋白聚糖和胶原蛋白I的表达模式。在三只Tgfb（-/-）小鼠中，仅Tgfb 2（-/-）小鼠具有异常的眼形态发生，其特征在于薄的角膜基质、角膜内皮缺失、角膜与透镜融合（Peters样异常表型）以及玻璃体中透明细胞的积聚。在Tgfb 2（-/-）小鼠中，在ECM积累减少的基质中发现较少的角膜细胞;例如，Lumican、keratocan和胶原蛋白I大大减少。TGF β 2的缺乏不损害细胞增殖，也不增强细胞凋亡。由ECM合成减少导致的较薄的基质可能是Tgfb 2缺失小鼠基质中细胞数量减少的原因。角蛋白12的表达在Tgfb 2（-/-）小鼠中没有改变，暗示正常的角膜型上皮分化。在Tgfb 2（-/-）小鼠中观察到眼组织中巨噬细胞的延迟出现。功能障碍的巨噬细胞可能是Tgfb 2基因敲除小鼠玻璃体中细胞团积聚的原因。(C)2001年，爱思唯尔科学。
To examine the roles of TGFbeta isoforms on corneal morphogenesis, the eyes of mice that lack TGFbetas were analyzed at different developmental stages for cell proliferation, migration and apoptosis, and for expression patterns of keratin 12, lumican, keratocan and collagen I. Among the three Tgfb(-/-) mice, only Tgfb2(-/-) mice have abnormal ocular morphogenesis characterized by thin corneal stroma, absence of corneal endothelium, fusion of cornea to lens (a Peters'-like anomaly phenotype), and accumulation of hyaline cells in vitreous. In Tgfb2(-/-) mice, fewer keratocytes were found in stroma that has a decreased accumulation of ECM; for example, lumican, keratocan and collagen I were greatly diminished. The absence of TGFbeta2 did not compromise cell proliferation, nor enhance apoptosis. The thinner stroma resulting from decreased ECM synthesis may account for the decreased cell number in the stroma of Tgfb2 null mice. Keratin 12 expression was not altered in Tgfb2(-/-) mice, implicating normal corneal type epithelial differentiation. Delayed appearance of macrophages in ocular tissues was observed in Tgfb2(-/-) mice. Malfunctioning macrophages may account for accumulation of cell mass in vitreous of Tgfb2 null mice. (C) 2001 Elsevier Science.