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The liver injury following ischemia and reperfusion is worse in experimental knockout heterozygote mouse model for expression of connexin 431 1 Research performed at Medical Investigation Laboratory (LIM 37), Universidade de São Paulo (USP), Brazil. Part of PhD degree thesis, Postgraduate Program in Medicine Science in Gastroenterology. Tutor: Prof. Wellington Andraus.

Abstract

Purpose:

To evaluate that Connexin (Cx43) plays a role in lesions after hepatic ischemia/reperfusion (IR) injury.

Methods:

We use Cx43 deficient model (heterozygotes mice) and compared to a wild group. The groups underwent 1 hour ischemia and 24 hours reperfusion. The heterozygote genotype was confirmed by PCR. We analyzed the hepatic enzymes (AST, ALT, GGT) and histology.

Results:

The mice with Cx43 deficiency showed an ALT mean value of 4166 vs. 307 in the control group (p<0.001); AST mean value of 7231 vs. 471 in the control group (p<0.001); GGT mean value of 9.4 vs. 1.7 in the control group (p=0.001); histology showed necrosis and inflammation in the knockout group.

Conclusions:

This research demonstrated that the deficiency of Cx43 worses the prognosis for liver injury. The topic is a promising target for therapeutics advancements in liver diseases and procedures.

Key words:
GAP junctions; Connexin 43; Ischemia; Reperfusion; Liver; Cell communication; Mice

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