Open AccessOmi/HtrA2 Participates in Age-Related Autophagic Deficiency in Rat Liver
Author(s) -
Jiahui Xu,
Kun Jiang,
Xin Liu,
Qi Sun,
Ke Wang,
Haibo Xu,
Shangyue Zhang,
Ye Wu,
Linguo Wu,
Dan Liu,
Wen Wang,
Huirong Liu
Publication year - 2018
Publication title -
aging and disease
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.808
H-Index - 54
ISSN - 2152-5250
DOI - 10.14336/ad.2018.0221
Subject(s) - autophagy , apoptosis , medicine , homeostasis , mechanism (biology) , liver injury , microbiology and biotechnology , cancer research , biology , biochemistry , philosophy , epistemology
Liver is a vital organ with many important functions, and the maintenance of normal hepatic function is necessary for health. As an essential mechanism for maintaining cellular homeostasis, autophagy plays an important role in ensuring normal organ function. Studies have indicated that the degeneration of hepatic function is associated with autophagic deficiency in aging liver. However, the underlying mechanisms still remain unclear. The serine protease Omi/HtrA2 belongs to the HtrA family and promotes apoptosis through either the caspase-dependent or caspase-independent pathway. Mice lacking Omi/HtrA2 exhibited progeria symptoms (premature aging), which were similar to the characteristics of autophagic insufficiency. In this study, we demonstrated that both the protein level of Omi/HtrA2 in liver and hepatic function were reduced as rats aged, and there was a positive correlation between them. Furthermore, several autophagy-related proteins (LC3II/I, Beclin-1 and LAMP2) in rat liver were decreased significantly with the increasing of age. Finally, inhibition of Omi/HtrA2 resulted in reduced autophagy and hepatic dysfunction. In conclusion, these results suggest that Omi/HtrA2 participates in age-related autophagic deficiency in rat liver. This study may offer a novel insight into the mechanism involved in liver aging.