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凋亡:正常胃泌酸黏膜及肉眼愈合的胃溃疡黏膜中由基因编程的生理性细胞丢失。

Apoptosis: genetically programmed physiologic cell loss in normal gastric oxyntic mucosa and in mucosa of grossly healed gastric ulcer.

作者信息

Stachura J, Tarnawski A, Dabroś W

机构信息

Department of Pathomorphology, N. Copernicus University Medical School of Kraków, Poland.

出版信息

J Clin Gastroenterol. 1993;17 Suppl 1:S70-7.

PMID:8283018
Abstract

Maintenance of gastric mucosal structure depends on a dynamic balance between cell loss and cell renewal. The surface epithelial cells exfoliate at a rapid rate (usually in response to luminal contents) and are entirely replaced within 3-5 days. The loss of parietal, chief, and endocrine cells is much slower, but there is little information concerning the morphologic aspects of this process. Because in other tissues cells are physiologically eliminated through a process of apoptosis--genetically programmed cell self-destruction and loss--we studied whether this process occurs in normal gastric mucosa and in the mucosa of recently healed gastric ulcers in the rat. Degeneration and loss of the surface epithelial cells into the gastric lumen occurs in normal oxyntic mucosa, and more extensive desquamation of poorly differentiated mucous cells in the dilated gastric glands takes place within mucosal scars of grossly healed gastric ulcers. Apoptosis of parietal, chief, and endocrine cells in normal oxyntic mucosa and apoptosis of poorly differentiated cells lining dilated glands in mucosal scar were assessed and characterized by electron microscopy. Apoptosis affects single glandular cells and involves a rapid initial condensation of both nucleus and cytoplasm, with subsequent fragmentation. Finally, the cell is converted into a cluster of membrane-bound apoptotic bodies, which usually are engulfed by adjacent cells or disposed into a glandular lumen. Desquamation of surface epithelium and apoptotic self-destruction of glandular epithelium stimulate a constant cell renewal and thus contribute to the maintenance of the ulcer healing process. Rapid and "excessive" proliferation of regenerating gastric epithelium enables re-epithelialization of ulcer crater.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

胃黏膜结构的维持依赖于细胞丢失与细胞更新之间的动态平衡。表面上皮细胞以快速的速率脱落(通常是对管腔内容物的反应),并在3 - 5天内被完全替换。壁细胞、主细胞和内分泌细胞的丢失则要慢得多,但关于这一过程的形态学方面的信息很少。因为在其他组织中,细胞是通过凋亡过程——基因编程的细胞自我毁灭和丢失——进行生理性清除的,所以我们研究了这一过程是否发生在正常胃黏膜以及大鼠近期愈合的胃溃疡黏膜中。正常泌酸黏膜中表面上皮细胞会发生退变并脱落至胃腔,在大体愈合的胃溃疡黏膜瘢痕内,扩张的胃腺中分化差的黏液细胞会出现更广泛的脱屑。通过电子显微镜评估并描述了正常泌酸黏膜中壁细胞、主细胞和内分泌细胞的凋亡以及黏膜瘢痕中扩张腺体内衬的分化差细胞的凋亡。凋亡影响单个腺细胞,涉及细胞核和细胞质迅速开始凝聚,随后碎片化。最后,细胞转化为一群膜结合的凋亡小体,这些凋亡小体通常被相邻细胞吞噬或排入腺腔。表面上皮的脱屑和腺上皮的凋亡性自我毁灭刺激了持续的细胞更新,从而有助于维持溃疡愈合过程。再生胃上皮的快速且“过度”增殖使得溃疡 crater得以重新上皮化。(摘要截选至250词)

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