终末鳃体降钙素诱导的LLC-PK1细胞生长抑制及形态变化

Growth inhibition and morphological changes of LLC-PK1 induced by ultimobranchial calcitonins.

作者信息

Inoue A, Komatsu Y, Ochiai J, Itagaki S, Nishide H, Shikano M, Hemmi H, Numao N

机构信息

Sagami Chemical Research Center, Kanagawa, Japan.

出版信息

Cell Biol Int Rep. 1990 Oct;14(10):887-96. doi: 10.1016/0309-1651(90)91158-z.

DOI:10.1016/0309-1651(90)91158-z

PMID:2176131

Abstract

Ultimobranchial calcitonins (CTs), known to stimulate cAMP production, inhibited the growth of a porcine kidney cell line LLC-PK1. This inhibition was accompanied by degenerative changes including vacuole formation and cell detachment. The electron microscopic study revealed marked swelling of rough endoplasmic reticulum (RER). Other cAMP-increasing agents such as human CT, arginine, vasopressin, and forskolin showed less growth inhibitory activities and no induction of the degenerative changes. These results indicate that the growth inhibition of LLC-PK1 by ultimobranchial CTs is mainly due to cellular death caused by the swelling of RER via a signalling pathway other than the cAMP-dependent event(s).

摘要

已知能刺激环磷酸腺苷（cAMP）产生的终末鳃体降钙素（CTs）可抑制猪肾细胞系LLC-PK1的生长。这种抑制伴随着包括空泡形成和细胞脱离在内的退行性变化。电子显微镜研究显示粗面内质网（RER）明显肿胀。其他增加cAMP的物质，如人CT、精氨酸、血管加压素和福斯高林，显示出较小的生长抑制活性，且未诱导退行性变化。这些结果表明，终末鳃体CTs对LLC-PK1的生长抑制主要是由于RER肿胀通过cAMP依赖性事件以外的信号通路导致细胞死亡。