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This galley proof is being listed electronically before publishing the final manuscript (It's not final version).

 
Activation of pannexin-1 mediates triglyceride-induced macrophage cell death
Byung Chul Jung 1,2 (Research worker), Sung Hoon Kim 2,3 (Professor), Jaewon Lim 2,4 (Professor), Yoon Suk Kim 2,* (Professor)
1Department of Nutritional Sciences and Toxicology, University of California, Berkeley, State of California 94720, United States,
2Department of Biomedical Laboratory Science, College of Health Sciences, Yonsei University, Wonju, Gangwon-do 26493, Republic of Korea,
3Department of Biomedical Laboratory Science, Korea Nazarene University, Cheonan, Chungcheongnam-do 31172, Republic of Korea,
4Department of Biomedical Laboratory Science, College of Medical Sciences, Daegu Haany University, Gyeongsan, Gyeongsangbuk-do 38610, Republic of Korea
Abstract
The accumulation of triglycerides (TGs) in macrophages induces cell death, a risk factor in the pathogenesis of atherosclerosis. We had previously reported that TG-induced macrophage death is triggered by caspase-1 and -2, therefore we investigated the mechanism underlying this phenomenon. We found that potassium efflux is increased in TG-treated THP-1 macrophages and that the inhibition of potassium efflux blocks TG-induced cell death as well as caspase-1 and -2 activation. Furthermore, reducing ATP concentration (known to induce potassium efflux), restored cell viability and caspase-1 and -2 activity. The activation of pannexin-1 (a channel that releases ATP), was increased after TG treatment in THP-1 macrophages. Inhibition of pannexin-1 activity using its inhibitor, probenecid, recovered cell viability and blocked the activation of caspase-1 and -2 in TG-treated macrophages. These results suggest that TG-induced THP-1 macrophage cell death is induced via pannexin-1 activation, which increases extracellular ATP, leading to an increase in potassium efflux.
Abstract, Accepted Manuscript(in press) [Submitted on August 27, 2020, Accepted on September 28, 2020]
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