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人类和小鼠胚胎细胞在暴露于热休克或致畸剂后产生的热休克蛋白

Heat shock proteins in human and mouse embryonic cells after exposure to heat shock or teratogenic agents.

作者信息

Honda K, Hatayama T, Takahashi K, Yukioka M

机构信息

Department of Biochemistry, Osaka City University Medical School, Japan.

出版信息

Teratog Carcinog Mutagen. 1991;11(5):235-44. doi: 10.1002/tcm.1770110503.

DOI:10.1002/tcm.1770110503
PMID:1687901
Abstract

In human chorionic villus tissue at the 10-17th week of a normal pregnancy, heat shock proteins (hsp70, hsp73, hsp85, and hsp105) were induced in vitro by a heat shock or by exposure to sodium arsenite or cadmium chloride. In dispersed cells of the whole mouse embryo on the 11th day of development, heat shock proteins (hsp73 and hsp105) were induced by a heat shock or by exposure to sodium arsenite, but not by exposure to cadmium chloride. After a maternal hyperthermia or an intraperitoneal injection of sodium arsenite or cadmium chloride into a pregnant mouse, heat shock proteins accumulated in the embryo on the 9th day of development, especially in the neuroepithelial tissue. The significance of heat shock proteins in the embryo is discussed.

摘要

在正常妊娠10 - 17周的人绒毛膜绒毛组织中,热休克蛋白(hsp70、hsp73、hsp85和hsp105)可通过热休克或暴露于亚砷酸钠或氯化镉在体外诱导产生。在发育第11天的全小鼠胚胎分散细胞中,热休克蛋白(hsp73和hsp105)可通过热休克或暴露于亚砷酸钠诱导产生,但不能通过暴露于氯化镉诱导产生。在给怀孕小鼠进行母体高温处理或腹腔注射亚砷酸钠或氯化镉后,热休克蛋白在发育第9天的胚胎中积累,尤其是在神经上皮组织中。文中讨论了热休克蛋白在胚胎中的意义。

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引用本文的文献

1
Cellular stress mechanisms of prenatal maternal stress: Heat shock factors and oxidative stress.产前母体应激的细胞应激机制:热休克因子和氧化应激。
Neurosci Lett. 2019 Sep 14;709:134368. doi: 10.1016/j.neulet.2019.134368. Epub 2019 Jul 9.
2
Mitochondrial dysmorphology in the neuroepithelium of rat embryos following a single dose of maternal hyperthermia during gestation.孕期单次母体高温暴露后大鼠胚胎神经上皮中的线粒体形态异常
Exp Brain Res. 2006 Aug;173(2):298-308. doi: 10.1007/s00221-006-0489-4. Epub 2006 Jul 18.
3
Stress proteins in reproductive toxicology.
生殖毒理学中的应激蛋白。
Environ Health Perspect. 1997 Apr;105(4):436-8. doi: 10.1289/ehp.97105436.