Found programs:
Authors:Cheng Xu; Chen Xinyan; Chen Tingting; Cheng Xiaowen; Zhu huaqing; Ge Shenglin
Keywords:SPARCL1;atherosclerosis;macrophages;SPARCL1 recombinant adenovirus;cell scratching assay
DOI:10.19405/j.cnki.issn1000-1492.2024.03.016
〔Abstract〕 Objective To investigate the effect of cysteine-rich acidic secretory protein-like protein 1(SPARC L1)on atherosclerosis(AS) plaque formation.Methods A case-control study design was used,394 patients with confirmed AS were selected as the case group,and 394 healthy medical examiners matched for age and gender were selected as the control group.The expression level of serum SPARC L1 was determined by enzyme-linked immunosorbent assay;immunohistochemistry was used to assess the expression level and localization of SPARC L1 protein in the AS plaque region,and the expression of SPARC L1 protein was also detected in the neutrophils and monocytes of peripheral blood of AS patients and normal controls;SPARCL1 overexpressing and the recombinant adenoviral vectors were constructed to inhibit SPARC L1 overexpression and expression,and the effects of SPARC L1 on cell migration were observed in the cell scratch assay using mouse macrophage cells(J774A.1) as target cells.Results Serum SPARC L1 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;SPARC L1 expression levels in peripheral blood neutrophils and monocytes were lower than those in normal controls in AS patients(P<0.05);recombinant SPARC L1 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 SPARC L1(P<0.05).Conclusion SPARC L1 is highly expressed in foam cells at the site of AS lesions,which may result from compensatory recruitment of peripheral blood monocytes and neutrophils,and SPARC L1 may be involved as a protective factors for blood vessels in inhibiting the development of AS plaques.