Abstract

Goldfish is one of the most potent hypoxic-tolerant freshwater fish and exhibit gill remodeling when exposed to hypoxia or warm water. In this study we reported that hypoxia decreased the expression of the pro-apoptotic protein BimEL through activation of ERK1/2 and/or miR-24 in gill of goldfish. Pretreatment with either SCH772984 (an ERK1/2 inhibitor) or bortezomib (a proteasome inhibitor) was able to block the hypoxia-induced down-regulation of BimEL and the reduction of interlamellar cell mass (ILCM). Additionally, high temperature inhibited the binding of 70-kilodalton heat shock cognate protein (HSC70), a Bim mRNA stabilizer, with 3’-UTR of Bim mRNA. Our results demonstrate that water oxygen level and temperature regulate ILCM size via BimEL in gill remodeling of goldfish, suggesting that BimEL may promote cell survival in ILCM cells.

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