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Article

Interleukin-32 promotes lipid accumulation through inhibition of cholesterol efflux

  • Authors:
    • Zonglei Xu
    • Aizhi Dong
    • Zerui Feng
    • Jing Li
  • View Affiliations / Copyright

    Affiliations: Department of Internal Medicine Cardiovascular Medicine, Liaocheng Development Hospital, Liaocheng, Shandong 252000, P.R. China, VIP Ward, Shandong Liaocheng No. 2 People's Hospital, Liaocheng, Shandong 252600, P.R. China, Department of Internal Medicine Cardiovascular Medicine, Shandong Liaocheng No. 2 People's Hospital, Liaocheng, Shandong 252600, P.R. China, Department of Internal Medicine Cardiovascular Medicine, Ankang City Central Hospital, Ankang, Shanxi 725000, P.R. China
  • Pages: 947-952
    |
    Published online on: June 13, 2017
       https://doi.org/10.3892/etm.2017.4596
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Abstract

Interleukin-32 (IL-32) is a pro‑inflammatory cytokine and its effects in various inflammatory diseases have been investigated. However, the role of IL‑32 on atherosclerosis, an inflammatory disease, remains unknown. The present study examined the use of IL‑32α, the most abundant transcript of IL‑32, in the treatment of oxidized low‑density lipoprotein (ox‑LDL)‑stimulated THP‑1 macrophages for 24 h, which simulates a foam cell formation model. The effect of IL‑32α (20, 50 and 100 ng/ml) on lipid deposition in the macrophages was analyzed using Oil Red O staining, while the cholesterol efflux on apolipoprotein A‑I was also measured. The mRNA and protein expression levels of peroxisome proliferator-activated receptor γ (PPARγ), liver X receptor α (LXRα), ATP‑binding cassette transporter A1 (ABCA1) and ABCG1 were quantified by reverse transcription‑quantitative polymerase chain reaction and western blot analysis, respectively. The results indicated that IL‑32α exposure enhanced the lipid deposition and attenuated the cholesterol efflux from ox‑LDL‑stimulated THP‑1 macrophages in a dose‑dependent manner. Furthermore, the expression levels of ABCA1, LXRα and PPARγ were dose‑dependently decreased by IL‑32α at the mRNA and protein levels. Addition of the PPARγ agonist 15d‑PGJ2 or overexpression of PPARγ in THP‑1 macrophages abrogated the IL‑32α‑mediated inhibition of cholesterol efflux and reversed the IL‑32α‑mediated downregulation of ABCA1 and LXRα. In conclusion, IL‑32α enhances lipid accumulation and inhibits cholesterol efflux from ox‑LDL‑exposed THP‑1 macrophages by regulating the PPARγ-LXRα-ABCA1 pathway.
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Copy and paste a formatted citation
Spandidos Publications style
Xu Z, Dong A, Feng Z and Li J: Interleukin-32 promotes lipid accumulation through inhibition of cholesterol efflux. Exp Ther Med 14: 947-952, 2017.
APA
Xu, Z., Dong, A., Feng, Z., & Li, J. (2017). Interleukin-32 promotes lipid accumulation through inhibition of cholesterol efflux. Experimental and Therapeutic Medicine, 14, 947-952. https://doi.org/10.3892/etm.2017.4596
MLA
Xu, Z., Dong, A., Feng, Z., Li, J."Interleukin-32 promotes lipid accumulation through inhibition of cholesterol efflux". Experimental and Therapeutic Medicine 14.2 (2017): 947-952.
Chicago
Xu, Z., Dong, A., Feng, Z., Li, J."Interleukin-32 promotes lipid accumulation through inhibition of cholesterol efflux". Experimental and Therapeutic Medicine 14, no. 2 (2017): 947-952. https://doi.org/10.3892/etm.2017.4596
Copy and paste a formatted citation
x
Spandidos Publications style
Xu Z, Dong A, Feng Z and Li J: Interleukin-32 promotes lipid accumulation through inhibition of cholesterol efflux. Exp Ther Med 14: 947-952, 2017.
APA
Xu, Z., Dong, A., Feng, Z., & Li, J. (2017). Interleukin-32 promotes lipid accumulation through inhibition of cholesterol efflux. Experimental and Therapeutic Medicine, 14, 947-952. https://doi.org/10.3892/etm.2017.4596
MLA
Xu, Z., Dong, A., Feng, Z., Li, J."Interleukin-32 promotes lipid accumulation through inhibition of cholesterol efflux". Experimental and Therapeutic Medicine 14.2 (2017): 947-952.
Chicago
Xu, Z., Dong, A., Feng, Z., Li, J."Interleukin-32 promotes lipid accumulation through inhibition of cholesterol efflux". Experimental and Therapeutic Medicine 14, no. 2 (2017): 947-952. https://doi.org/10.3892/etm.2017.4596
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