The role of SPARCL1 in atherosclerotic plaque formation
10.19405/j.cnki.issn1000-1492.2024.03.016
- VernacularTitle:SPARCL1在动脉粥样硬化斑块形成中的作用研究
- Author:
Xu CHENG
1
;
Xinyan CHEN
;
Tingting CHEN
;
Xiaowen CHENG
;
Huaqing ZHU
;
Shenglin GE
Author Information
1. 安徽医科大学第一附属医院 心脏外科,合肥 230022
- Keywords:
SPARCL1;
atherosclerosis;
macrophages;
SPARCL1 recombinant adenovirus;
cell scratching assay
- From:
Acta Universitatis Medicinalis Anhui
2024;59(3):473-478
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of cysteine-rich acidic secretory protein-like protein 1(SPARCL1)on atherosclerosis(AS)plaque formation.Methods A case-control study design was used,394 patients with con-firmed AS were selected as the case group,and 394 healthy medical examiners matched for age and gender were se-lected as the control group.The expression level of serum SPARCL1 was determined by enzyme-linked immunosor-bent assay;immunohistochemistry was used to assess the expression level and localization of SPARCL1 protein in the AS plaque region,and the expression of SPARCL1 protein was also detected in the neutrophils and monocytes of peripheral blood of AS patients and normal controls;SPARCL1 overexpressing and the recombinant adenoviral vec-tors were constructed to inhibit SPARCL1 overexpression and expression,and the effects of SPARCL1 on cell mi-gration were observed in the cell scratch assay using mouse macrophage cells(J774A.1)as target cells.Results Serum SPARCL1 levels in the AS patient group were lower than those in the healthy group(P<0.05);high SPARCL1 expression was detected in AS plaques and was mainly expressed in the cytoplasm of foamy cells;SPARCL1 expression levels in peripheral blood neutrophils and monocytes were lower than those in normal controls in AS patients(P<0.05);recombinant SPARCL1 overexpression and inhibition of expression of adenovirus was successfully constructed;the cell migration rate was decreased in J774A.1 cells that inhibited SPARCL1 expression and increased in J774A.1 cells that overexpressed SPARCL1(P<0.05).Conclusion SPARCL1 is highly ex-pressed in foam cells at the site of AS lesions,which may result from compensatory recruitment of peripheral blood monocytes and neutrophils,and SPARCL1 may be involved as a protective factors for blood vessels in inhibiting the development of AS plaques.
