Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 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.
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PMID:UBIAD1 protects against oxygen-glucose deprivation/reperfusion-induced multiple subcellular organelles injury through PI3K/AKT pathway in N2A cells. 2966 77

The study examined the effect of endogenous lipid-soluble antioxidant coenzyme Q10 on the expression of UbiA gene of prenyltransferase domain-containing protein 1 (UbiAd1) involved in synthesis of vitamin K2 (and probably of coenzyme Q10) on a rat model of ischemic stroke provoked by ligation of the middle cerebral artery in the left hemisphere. Ischemia enhanced expression of mRNA of UbiAd1 gene in both cerebral hemispheres, but the effect was significant only in the contralateral one. The study revealed no effect of intraperitoneal injection of coenzyme Q10 (30 mg/kg) on ischemia-produced elevation of mRNA of UbiAd1 gene. Further studies are needed to assess possible neuroprotective effects of antioxidant coenzyme Q10.
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PMID:Effect of Coenzyme Q10 on Expression of UbiAd1 Gene in Rat Model of Local Cerebral Ischemia. 2979 20