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Expression of ABC transporter and scavenger receptor mRNAs in PBMCs in 100‐km ultramarathon runners
Author(s) -
Juan ChiChang,
Li LiHua,
Hou SenKuang,
Liu PingShiou,
Kao WeiFong,
Chiu YuHui,
How ChorngKuang
Publication year - 2021
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1111/eci.13365
Subject(s) - scavenger receptor , abca1 , abcg1 , cd36 , medicine , endocrinology , peripheral blood mononuclear cell , cholesterol , biology , lipoprotein , chemistry , receptor , transporter , in vitro , biochemistry , gene
Abstract Background Cholesterol metabolism is tightly regulated at the cellular level. This study was to measure the expression levels of ATP‐binding cassette transporter A1 (ABCA1) and G1 (ABCG1), scavenger receptor class B type I (SR‐BI) and class A (SRA), and CD36 mRNAs in peripheral blood mononuclear cells (PBMCs) in response to 100‐km ultramarathon event and determine any correlation between these ABC transporters/scavenger receptor expression levels and plasma cholesterol homeostasis. Materials and Methods Twenty‐six participants were enrolled. Blood was drawn from each individual 1 week prior, immediately after, and 24 hours after the race. The expression levels of ABCA1, ABCG1, SR‐BI, SRA and CD36 in PBMCs were measured by using real‐time quantitative reverse transcription polymerase chain reaction. Results Plasma triglyceride levels were significantly increased immediately after the race and dropped at 24‐hour post‐race compared with pre‐race values. The 100‐km ultramarathon boosted high‐density lipoprotein cholesterol (HDL‐C) levels and decreased low‐density lipoprotein cholesterol (LDL‐C) levels 24‐hour post‐race. The expression levels of ABCA1, ABCG1 and SR‐BI were markedly decreased, whereas that of CD36 was slightly but significantly upregulated in runners’ PBMCs immediately after the race. Ultramarathon resulted in immediate large‐scale stimulation of inflammatory cytokines with increased plasma interleukin‐6 and tumour necrosis factor‐alpha levels. Moreover, by using in vitro models with human monocytic cell lines, incubation of runners’ plasma immediately after the race significantly downregulated ABCA1 and ABCG1, and upregulated CD36 expression in these cells. Conclusions ABCA1, ABCG1 and CD36 gene expressions in PBMCS might be associated with endurance exercise‐induced plasma cholesterol homeostasis and systemic inflammatory response.