Levels of acylation stimulating protein and the complement component 3 precursor are associated with the occurrence and development of coronary heart disease

Abstract

The aim of the present study was to investigate whether acylation stimulating protein (ASP) and complement component 3 (C3) are associated with the occurrence and development of coronary heart disease (CHD). The participants of the study were divided into three groups, including the healthy control (n=42), metabolic syndrome (MS, n=56) and CHD (n=62) groups. An enzyme-linked immunosorbent assay was used to measure the ASP concentrations, while an immunoturbidimetric assay was employed to determine the C3 concentrations. In addition, coronary angiography was performed to determine the severity of coronary artery disease in the CHD group. The CHD group was divided into three subgroups, according to the final Gensini score of coronary artery stenosis for each patient (mild, ≤20 points; moderate, 21–40 points; severe, >40 points). Western blotting and quantitative reverse transcription-polymerase chain reaction (RT-PCR) were performed to analyze the protein and mRNA expression levels of C3 in the CHD subgroups and the healthy control group. The concentrations of ASP and C3 in the CHD group were found to be significantly higher compared with the control and MS groups. In addition, the levels of ASP and C3 in the mild and moderate CHD subgroups were significantly higher compared with the healthy controls or mild CHD patients. Furthermore, the protein expression levels of C3 in the moderate and severe CHD patients were found to be significantly higher compared with the healthy individuals and the mild CHD patients. The quantitative RT-PCR results revealed that the mRNA expression levels of C3 in the moderate and severe CHD patients were significantly higher compared with the healthy control group and the mild CHD patients. Furthermore, the mean levels of C3 transcripts in the severe CHD patients were found to be higher compared with the moderate CHD subgroup (P<0.05). Therefore, ASP and C3 were found to be associated with the occurrence and development of CHD; thus, may be used as novel indexes for CHD.

Complement C3 gene polymorphisms are associated with lipid levels, but not the risk of coronary artery disease: a case-control study

“…Bratti et al revealed that the C3 level was positively correlated with body mass index and significantly decreased with weight loss after bariatric surgery. Jiang et al found that in CAD patients, serum C3 was significantly higher than in controls, and was positively associated with the severity of CAD [9, 10].…”

Acylation-stimulating protein is a surrogate biomarker for acute myocardial infarction: Role of statins

“…[30] Furthermore, ASP levels were positively correlated with cTnI in patients with acute MI regardless of statins therapy, since ASP levels are positively correlated with severity of CAD and cTnI indicating that ASP is implicated in pathogenesis of CAD due to metabolic alterations in lipid profile. [31] There are numerous limitations of the current study, relative small sample size, determination of ASP receptors in coronary vessels, and HMG-CoA activity in response to the ASP levels are the main points that limit the present study. On the other hand, this study may be to our knowledge, the first novel study regarding the effect of statins on ASP levels in CAD.…”

Spermine and spermidine reversed age-related cardiac deterioration in rats

“…The protein and mRNA expression levels of complement C3 were found to be associated with the occurrence and development of coronary heart disease [ 36 ], higher C3 was significantly associated with presence and greater extent of arterial calcification, and C3 could be a potential non-invasive biomarker of early diagnosis of atherosclerosis [ 37 ]. Activation of the immune response by elevating hydroperoxides levels, further activating NF-kB signaling, may be a key aging feature in the mouse heart [ 38 ]. In addition, Lian et al reported that astroglial NF-kB/C3 activation led to impaired synaptic density and dendritic morphology in brain tissue of Alzheimer’s disease (AD) patients [ 39 ], and the expressions of C3, C4 and C5 mRNA increased with age in C57BL/6 mice brain [ 37 - 39 ].…”