Journal of Internal Medicine Concepts & Practice ›› 2021, Vol. 16 ›› Issue (03): 172-177.doi: 10.16138/j.1673-6087.2021.03.007

• Original article • Previous Articles     Next Articles

Follistatin like protein 1 mitigates oxidized low-density lipoprotein-stimulated phenotypic transformation of mouse vascular smooth muscle cell

XIAO Fan, ZHA Qing, LIU Ya, YANG Ling, YE Jiawen, LIU Yan()   

  1. Department of Cardiology, Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200011, China
  • Received:2021-01-06 Online:2021-06-25 Published:2022-07-26
  • Contact: LIU Yan E-mail:liuyan_ivy@126.com

Abstract:

Objective To investigate the effect of follistatin like protein 1(FSTL1) on oxidized low-density lipoprotein (Ox-LDL)-stimulated the phenotypic transformation of mouse vascular smooth muscle cell (VSMC). Methods Firstly, under Ox-LDL-stimulating, the expression of FSTL1 in VSMC was detected. Secondly, Western blotting was used to detect the signature proteins, α-smooth muscle actin(α-SMA) and osteopontin(OPN). Finally, the proliferation of VSMC was verified by proliferation experiments under the influence of Ox-LDL and FSTL1. Results Comparing to the normal group, the expression of FSTL1 was lower in the abnormal vessel regions, which was filled with Ox-LDL(0.223±0.010 vs. 0.097±0.019, P<0.01). VSMC was stimulated by Ox-LDL at 0, 12.5, 25 and 50 mg/L for 24 h respectively and the expression level of FSTL1 detected by Western blotting was 1.330±0.055, 0.905±0.027, 0.753±0.037 and 0.243±0.016 accordingly. It showed that the lowest expression level of FSTL1 was observed when Ox-LDL concentration increased to 50 mg/L (F=260.600, P<0.000 1). The expression of FSTL1 was 1.383±0.033, 0.782±0.047, 0.381±0.022 and 0.230±0.017 after 50 mg/L Ox-LDL stimulating VSMC for 0, 6, 12 and 24 h respectively, in which the expression of FSTL1 was the lowest when Ox-LDL induced 24 h(F=151.000, P<0.000 1). In addition, Ox-LDL stimulation reduced the expression of α-SMA(1.303±0.030 vs. 0.493±0.069, P<0.01) and SIRT1(0.993±0.044 vs. 0.613±0.030, P<0.01), while increasing the expression of OPN(1.001±0.031 vs. 2.698±0.001, P<0.01). However, the expression of OPN, α-SMA and SIRT1 showed opposite trend when VSMC was stimulated with both FSTL1 and Ox-LDL(OPN 2.698±0.002 vs. 1.590±0.001, P<0.05; α-SMA 0.493±0.062 vs. 0.653±0.015, P<0.05; SIRT1 0.613±0.030 vs. 1.231±0.011, P<0.05). Compared with Ox-LDL+FSTL1+DMSO group, VSMC in Ox-LDL+FSTL1+SIRT1 inhibitor group showed reduced α-SMA(0.530±0.033 vs. 0.283±0.032, P<0.01) and SIRT1(1.056±0.020 vs. 0.207±0.021, P<0.01), and increased OPN(1.643±0.047 vs. 3.533±0.100, P<0.01). The proliferation of VSMC was enhanced by Ox-LDL stimulation(0.870±0.010 vs. 1.890±0.020, P<0.01), while FSTL1 reduced this proliferation(1.890±0.021 vs. 1.200±0.023, P<0.05) via SIRT1(1.280±0.033 vs. 2.030±0.092, P<0.01). Conclusions Ox-LDL reduced the expression of FSTL1. FSTL1 could mitigate Ox-LDL-stimulated proliferation via SIRT1 effectively.

Key words: Follistatin like protein 1, Oxidized low-density lipoprotein, Proliferation, Phenotypic transformation, α-Smooth muscle actin, Silencing information regulatory protein 1, Osteopontin

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