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Ketone bodies upregulate endothelial connexin 43 (Cx43) gap junctions

By Chia-Fang Ho, Kun-Wei Chan, Hung-I Yeh, James Kuo, Hung-Jen Liu and Chi-Young Wang

Abstract

Ketosis occurs as a metabolic consequence of negative energy balance in post-calving lactating dairycows. Metabolism of free fatty acids, released from adipose tissue, generates excessive amounts of acetoacetate(AcAc), b-hydroxybutyrate (BHB), and acetone (Ac) in the liver, which are released into theblood. The effects of ketone bodies on endothelial cells include increased rates of portal vein and liverblood flow and decreased cytokine secretion in response to both bacterial and viral infections. The aimof the current study was to understand the effects of AcAc, BHB and Ac, on expression of connexin 43(Cx43) and gap junctional intercellular coupling (GJIC) in bovine aortic endothelial cells (BAECs).Confocal microscopy, Western blotting, and real-time quantitative RT-PCR indicated that Cx43 mRNAand protein expression increased after endothelial cell exposure to ketone bodies and that this wasaccompanied by upregulation of GJIC and cell migration. These effects were most obvious when BAECswere treated with a combination of the three ketones. Ketone bodies were shown to activate ERK andp38 MAPK as early as 3 h after treatment and an ERK inhibitor (PD98059) or p38 MAPK inhibitor(SB203580) were found to antagonise the ketone-induced increase in Cx43 protein expression. Thus,ketone bodies up-regulate Cx43 expression and GJIC in BAECs via activation of ERK and p38 MAPK

Topics: Cell migration, Endothelial cells, Gap junction, Ketone body, Ketosis
Year: 2014
DOI identifier: 10.1016/j.tvjl.2013.09.069
OAI identifier: oai:ir.lib.nchu.edu.tw:11455/85302
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