Squamous metaplasia in organ cultures of vitamin A-deficient hamster trachea: cytokinetic and ultrastructural alterations.

Squamous metaplasia in organ cultures of vitamin A-deficient hamster trachea: cytokinetic and ultrastructural alterations.
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缺乏维生素 A 的仓鼠气管器官培养中的鳞状化生:细胞因子和超微结构的改变。

DOI:
10.1093/jnci/69.4.895
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发表时间:
1982
期刊:
Journal of the National Cancer Institute
影响因子:
--
通讯作者:
D. Chopra
D. Chopra
中科院分区:
--
文献类型:
--
作者:
D. Chopra

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细胞动力学和形态学研究阐明了维生素a缺乏的叙利亚金仓鼠气管器官培养中表皮样化生的起源。在外植体移植后2天,观察到鳞状化生的局灶性区域,在第10天,大约89%的外植体出现广泛的表皮样化生和角化。在前2天,基底细胞和黏液细胞增殖活跃。到第3天,总黏液细胞[3H]胸苷标记指数(LI)下降,并在剩余的培养期间保持在非常低的水平。培养后第3 ~ 9天,基底细胞LI也较较高水平有所下降,但仍保持在较粘液细胞较高的水平。在病变中,标记细胞一般局限于基底层,LI约为基底细胞总LI的30倍。随着病变的进展,由于潜在的活跃增殖的基底细胞和随后的子细胞的表皮样分化的群体压力,含有黏液和纤毛细胞的表层脱落。这些数据支持了维生素A缺乏引起的气管支气管上皮表皮样化生起源于生殖细胞或基底细胞的假设。
Cytokinetic and morphologic studies were performed to elucidate the origin of epidermoid metaplasia in organ cultures of tracheas derived from vitamin A-deficient Syrian golden hamsters. Focal areas of squamous metaplasia were observed 2 days after explantation, and extensive epidermoid metaplasia and cornification were present in approximately 89% of the explants at day 10. During the first 2 days, both basal and mucous cells proliferated actively. By day 3, the total mucous cell [3H]thymidine labeling index (LI) had declined and remained at very low levels during the remaining culture period. The basal cell LI also declined from its higher level, but it remained at relatively higher levels than those of the mucous cells between days 3 and 9 after culture. In the lesions, labeled cells were generally confined to the basal layer, and the LI was about thirtyfold greater than the total basal cell LI. As the lesions progressed, the surface layer containing the mucous and ciliated cells was exfoliated as a result of population pressure from the underlying actively proliferating basal cells and subsequent epidermoid differentiation of the daughter cells. These data support the hypothesis that epidermoid metaplasia of tracheobronchial epithelium caused by vitamin A deficiency originates from the generative or basal cells.