Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0038454 (
stroke
)
147,016
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Cerebral ischemia/reperfusion-induced injury plays a significant role in the development of multi-subcellular organelles injury after ischemic
stroke
.
UBIAD1
was discovered originally as a potential tumor suppressor protein. Recently, analysis of
UBIAD1
has indicated it is a prenyltransferase enzyme for both non-mitochondrial CoQ10 and vitamin K2 production. Further,
UBIAD1
has been localized to multiple subcellular organelles. Particularly,
UBIAD1
plays an important role in the regulation of oxidative stress, apoptosis and cell proliferation, cholesterol and lipid metabolism, which was closely associated with the cerebral ischemic/reperfusion mechanism. However, the mechanism underlying effects of
UBIAD1
on cerebral ischemia/reperfusion-induced injury remains largely unknown. We aimed to investigate the effects of
UBIAD1
on ischemia/reperfusion-induced multiple subcellular organelles injury in vitro, mouse N2A cells were subjected to a classical oxygen-glucose deprivation and reperfusion (OGD/R) insult. The expression of
UBIAD1
was reduced in mouse N2A cells after OGD/R.
UBIAD1
exhibits multi-subcellular organelles co-localization in N2a cells, including in the mitochondria, endoplasmic reticulum, and Golgi apparatus. The over-expression of
UBIAD1
significantly protects against OGD/R-induced cell death.
UBIAD1
over-expression also attenuated OGD/R-induced mitochondrial fragmentation and dysfunction and mediated the level of apoptosis-associated protein. Moreover, we observed that the over-expression of
UBIAD1
ameliorated OGD/R-induced fragmentation and reduced the level of oxidative stress-related protein expression in both the endoplasmic reticulum and Golgi apparatus. Besides, the neuroprotective effect of
UBIAD1
was correlated with the PI3K/AKT pathway, which was demonstrated using the PI3K inhibitor LY294002 and perifosion. Collectively, these findings identified that
UBIAD1
protects against OGD/R-induced multiple subcellular organelles injury through PI3K/AKT Pathway.
...
PMID:UBIAD1 protects against oxygen-glucose deprivation/reperfusion-induced multiple subcellular organelles injury through PI3K/AKT pathway in N2A cells. 2966 77