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Article

MicroRNA let-7g inhibits angiotensin II-induced endothelial senescence via the LOX-1-independent mechanism

  • Authors:
    • Po‑Yuan Hsu
    • Wen‑Yi Lin
    • Ruey‑Tay Lin
    • Suh‑Hang H. Juo
  • View Affiliations / Copyright

    Affiliations: Department of Medical Research, China Medical University Hospital, Taichung 40402, Taiwan R.O.C., Department of Occupational Medicine, Kaohsiung Municipal Hsiaokang Hospital, Kaohsiung 80708, Taiwan R.O.C., Department of Neurology, Kaohsiung Medical University Hospital, Kaohsiung 80708, Taiwan R.O.C.
  • Pages: 2243-2251
    |
    Published online on: January 23, 2018
       https://doi.org/10.3892/ijmm.2018.3416
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Abstract

Endothelial senescence leads to cell dysfunction, which in turn eventually results in cardiovascular disease. Identifying factors that regulate endothelial senescence may provide insight into the pathogenesis of aging. Insulin-like growth factor (IGF) signaling has a significant role in the physiology of endothelial cells (ECs). Overactivation of IGF signaling has been implicated in promoting the aging process. Lectin‑like oxidized low‑density lipoprotein (oxLDL) receptor‑1 (LOX‑1) is a scavenger receptor that mediates the internalization of oxLDL into cells. Previous studies by our group have indicated that microRNA let‑7g exerts an anti‑aging effect on ECs and also suppresses LOX-1 expression. Since LOX‑1 also induces the aging process, the present study we explored whether let‑7g still exerts an anti‑aging effect on ECs when LOX‑1 is suppressed. Angiotensin II (Ang II) was used to induce senescence in ECs. It was revealed that Ang II significantly increased the expression of aging markers, including β‑galactosidase, LOX‑1, IGF1 and its receptor IGF1R. On the contrary, Ang II decreased the expression of the anti‑aging gene sirtuin 1 (SIRT1). When LOX‑1 was knocked down by small interfering RNA, let‑7g still dose‑dependently decreased the expression of β‑galactosidase (β‑gal), LOX‑1, IGF1 and IGF1R, and SIRT1 was still upregulated. Using senescence‑associated β‑gal staining, it was confirmed that let‑7g exerts a LOX‑1‑independent anti‑aging effect on ECs. In conclusion, the present study demonstrated that let‑7g has an anti‑aging effect regardless of the presence or absence of LOX-1.
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Copy and paste a formatted citation
Spandidos Publications style
Hsu PY, Lin WY, Lin RT and Juo SHH: MicroRNA let-7g inhibits angiotensin II-induced endothelial senescence via the LOX-1-independent mechanism. Int J Mol Med 41: 2243-2251, 2018.
APA
Hsu, P., Lin, W., Lin, R., & Juo, S.H. (2018). MicroRNA let-7g inhibits angiotensin II-induced endothelial senescence via the LOX-1-independent mechanism. International Journal of Molecular Medicine, 41, 2243-2251. https://doi.org/10.3892/ijmm.2018.3416
MLA
Hsu, P., Lin, W., Lin, R., Juo, S. H."MicroRNA let-7g inhibits angiotensin II-induced endothelial senescence via the LOX-1-independent mechanism". International Journal of Molecular Medicine 41.4 (2018): 2243-2251.
Chicago
Hsu, P., Lin, W., Lin, R., Juo, S. H."MicroRNA let-7g inhibits angiotensin II-induced endothelial senescence via the LOX-1-independent mechanism". International Journal of Molecular Medicine 41, no. 4 (2018): 2243-2251. https://doi.org/10.3892/ijmm.2018.3416
Copy and paste a formatted citation
x
Spandidos Publications style
Hsu PY, Lin WY, Lin RT and Juo SHH: MicroRNA let-7g inhibits angiotensin II-induced endothelial senescence via the LOX-1-independent mechanism. Int J Mol Med 41: 2243-2251, 2018.
APA
Hsu, P., Lin, W., Lin, R., & Juo, S.H. (2018). MicroRNA let-7g inhibits angiotensin II-induced endothelial senescence via the LOX-1-independent mechanism. International Journal of Molecular Medicine, 41, 2243-2251. https://doi.org/10.3892/ijmm.2018.3416
MLA
Hsu, P., Lin, W., Lin, R., Juo, S. H."MicroRNA let-7g inhibits angiotensin II-induced endothelial senescence via the LOX-1-independent mechanism". International Journal of Molecular Medicine 41.4 (2018): 2243-2251.
Chicago
Hsu, P., Lin, W., Lin, R., Juo, S. H."MicroRNA let-7g inhibits angiotensin II-induced endothelial senescence via the LOX-1-independent mechanism". International Journal of Molecular Medicine 41, no. 4 (2018): 2243-2251. https://doi.org/10.3892/ijmm.2018.3416
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