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LL-37-ApoB-100 Complex Serves as a Biomarker of Coronary Artery Disease
Yaqun Fang1, Zhiye Zhang1,2, Qiqi Cao1
1Engineering Laboratory of Peptides of Chinese Academy of Sciences, Key Laboratory of Bioactive Peptides of Yunnan Province, KIZ-CUHK Joint Laboratory of Bioresources and Molecular Research in Common Diseases, National Resource Center for Non-Human Primates, National Research Facility for Phenotypic & Genetic Analysis of Model Animals (Primate Facility), State Key Laboratory of Genetic Evolution & Animal Models, Sino-African Joint Research Center, and New Cornerstone Science Laboratory, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, Yunnan, P.R. China (Y.F., Z.Z., Q.C., Z.D., G.W., J.G., M.L., Z.S.M., Z.W., R.C., Q.L., R.L.).
Insights
The LL-37-ApoB-100 complex is elevated in patients with coronary artery disease (CAD). This complex serves as a valuable and independent biomarker for diagnosing obstructive CAD and assessing its severity.
Area of Science:
- Cardiovascular Research
- Biomarker Discovery
- Atherosclerosis Research
Background:
- Apolipoprotein B (ApoB)-containing lipoproteins are established risk factors for atherosclerotic coronary artery disease (CAD).
- Human cathelicidin LL-37 has been shown to bind to ApoB-100 in the context of atherosclerosis.
Purpose of the Study:
- To investigate the potential of the circulating LL-37-ApoB-100 complex as a diagnostic biomarker for CAD.
- To determine the association between LL-37-ApoB-100 levels and the severity of obstructive CAD.
Main Methods:
- Surface plasmon resonance and protein-protein docking were used to confirm the LL-37-ApoB-100 interaction.
- A specific polyclonal antibody was developed to quantify complex levels in human plasma and atherosclerotic plaques, and in Apoe-/- mice.
- An observational case-control study involving 1103 patients undergoing coronary angiography assessed the biomarker's association with obstructive CAD.
Main Results:
- LL-37 was found to interact with multiple binding sites on ApoB-100.
- Plasma levels of the LL-37-ApoB-100 complex were significantly elevated in patients with atherosclerosis and correlated positively with plaque area in mice.
- In the human cohort, elevated complex levels were associated with obstructive CAD and disease severity (Gensini score; r=0.60, P<0.001), demonstrating diagnostic value (AUC=0.82).
- LL-37-ApoB-100 remained an independent predictor of obstructive CAD after adjusting for clinical and lipid measures (aOR=6.51).
Conclusions:
- Circulating LL-37-ApoB-100 levels are strongly associated with angiographically confirmed CAD.
- The LL-37-ApoB-100 complex is a promising, independent biomarker for the diagnosis and assessment of obstructive CAD severity.
Background:
ApoB (apolipoprotein B)-containing lipoproteins are causal risk factors for atherosclerotic coronary artery disease (CAD). Since LL-37 (human cathelicidin peptide) binds to ApoB-100 in this pathological context, we investigated whether the circulating LL-37-ApoB-100 complex could serve as a biomarker for CAD.
Methods:
We performed surface plasmon resonance and protein-protein docking to demonstrate the direct LL-37-ApoB-100 interaction. We developed a specific polyclonal antibody against the complex and measured its levels in human atherosclerotic plaques and plasma, as well as in Apoe-/- mice. An observational case-control study of 1103 patients undergoing coronary angiography from 2 independent centers assessed the association between LL-37-ApoB-100 and obstructive CAD.
Results:
We identified that LL-37 directly interacted with multiple distinct binding sites on ApoB-100. Plasma levels of LL-37-ApoB-100 complex were significantly elevated in human patients with atherosclerosis. Consistently, levels of this complex were positively correlated with atherosclerotic plaque area in Apoe-/- mice. In the observational cohort from center 1, plasma LL-37-ApoB-100 levels were also significantly elevated in patients with obstructive CAD and strongly correlated with disease severity (Gensini score; r=0.60, P<0.001). Receiver operating characteristic curve analysis further demonstrated that LL-37-ApoB-100 was a valuable biomarker for the diagnosis of obstructive CAD, with an area under the curve of 0.82 (95% CIs, 0.81-0.85, P<0.001). After adjustment for lipid and clinical measures, elevated LL-37-ApoB-100 levels remained an independent predictor of obstructive CAD, with an adjusted odds ratio of 6.51 (95% CI, 4.34-9.77, P<0.001) for the upper quartiles. Observational analyses in center 2 showed consistent results.
Conclusions:
Circulating LL-37-ApoB-100 levels are strongly associated with angiographically documented CAD, highlighting LL-37-ApoB-100 as an independent predictor for CAD.
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