Humanin improves impaired metabolic activity and prolongs survival of serum-deprived human lymphocytes

被引：42

作者：

Kariya, S ^{[1
]}

Takahashi, N ^{[1
]}

Hirano, M ^{[1
]}

Ueno, S ^{[1
]}

机构：

[1] Nara Med Univ, Dept Neurol, Nara 6348522, Japan

来源：

MOLECULAR AND CELLULAR BIOCHEMISTRY | 2003年 / 254卷 / 1-2期

关键词：

humanin; Alzheimer's disease; serum deprivation; human lymphocyte; metabolic activity;

D O I：

10.1023/A:1027372519726

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Humanin (HN) has been reported to be an endogenous peptide that exerts highly selective neuroprotection against cell death induced by various types of Alzheimer's disease-related insults. We previously proposed the much broader cytoprotective potential of HN from the result that HN suppressed serum-deprivation-induced death of rat pheochromocytoma cells. In this study, we showed that HN also suppressed death of human lymphocytes cultured under serum-deprived condition. Further, we revealed, by assaying metabolic activity and survival rate, that HN was a potent factor capable of increasing the metabolic activity of individual serum-deprived lymphocytes. To our knowledge, there is no report described about a rescue factor that increases the metabolic activity of individual serum-deprived cells and prolongs their survival. This novel feature of HN may enable us to apply this peptide for the management of diseases involving poor metabolic activity, such as mitochondria-related disorders and brain ischemia.

引用

页码：83 / 89

页数：7

共 26 条

[1] ELEVATED GAMMA-AMINOBUTYRIC-ACID LEVELS ATTENUATE THE METABOLIC RESPONSE TO BILATERAL ISCHEMIA [J].