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Title

Cyclooxygenase-2 over-expression inhibits liver apoptosis induced by hyperglycemia

AuthorsFrancés, Daniel E.; Ingaramo, Paola I.; Mayoral, Rafael ; Través, Paqui G.; Casado, Marta ; Valverde, Ángela M.; Martín-Sanz, Paloma ; Carnovale, Cristina E.
Issue Date2013
PublisherWiley-Blackwell
CitationJournal of Cellular Biochemistry 114(3): 669-680 (2013)
AbstractIncreased expression of COX-2 has been linked to inflammation and carcinogenesis. Constitutive expression of COX-2 protects hepatocytes from several pro-apoptotic stimuli. Increased hepatic apoptosis has been observed in experimental models of diabetes. Our present aim was to analyze the role of COX-2 as a regulator of apoptosis in diabetic mouse liver. Mice of C57BL/6 strain wild type (Wt) and transgenic in COX-2 (hCOX-2 Tg) were separated into Control (vehicle) and SID (streptozotocin induced diabetes, 200 mg/kg body weight, i.p.). Seven days post-injection, Wt diabetic animals showed a decrease in PI3K activity and P-Akt levels, an increase of P-JNK, P-p38, pro-apoptotic Bad and Bax, release of cytochrome c and activities of caspases-3 and -9, leading to an increased apoptotic index. This situation was improved in diabetic COX-2 Tg. In addition, SID COX-2 Tg showed increased expression of anti-apoptotic Mcl-1 and XIAP. Pro-apoptotic state in the liver of diabetic animals was improved by over-expression of COX-2. We also analyzed the roles of high glucose-induced apoptosis and hCOX-2 in vitro. Non-transfected and hCOX-2-transfected cells were cultured at 5 and 25 mM of glucose by 72 h. At 25 mM there was an increase in apoptosis in non-transfected cells versus those exposed to 5 mM. This increase was partly prevented in transfected cells at 25 mM. Moreover, the protective effect observed in hCOX-2-transfected cells was suppressed by addition of DFU (COX-2 selective inhibitor), and mimicked by addition of PGE2 in non-transfected cells. Taken together, these results demonstrate that hyperglycemia-induced hepatic apoptosis is protected by hCOX-2 expression. J. Cell. Biochem. 114: 669-680, 2013. © 2012 Wiley Periodicals, Inc.
Publisher version (URL)https://doi.org/10.1002/jcb.24409
URIhttp://hdl.handle.net/10261/76658
Identifiersdoi: 10.1002/jcb.24409
issn: 0730-2312
e-issn: 1097-4644
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