Related Experiment Video
Updated: Aug 5, 2026

Coronary Progenitor Cells and Soluble Biomarkers in Cardiovascular Prognosis after Coronary Angioplasty
Published on: January 28, 2020
The significance of CD105, TGFbeta and CD105/TGFbeta complexes in coronary artery disease
C G Li1, H Bethell, P B Wilson
1Department of Pathological Sciences, Medical School, The University, M13 9PT, Manchester, UK.
Insights
Levels of CD105 and transforming growth factor beta (TGFbeta) were altered in patients with triple vessel disease (TVD). Higher CD105/TGFbeta complexes in TVD patients suggest a role in atherosclerosis, warranting further investigation.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Biomarker Discovery
Background:
- Atherosclerosis involves complex molecular interactions.
- CD105 and transforming growth factor beta (TGFbeta) are implicated in vascular health.
- Understanding their roles in coronary artery disease is crucial.
Purpose of the Study:
- To quantify serum levels of CD105, TGFbeta, and their complexes in patients with coronary artery disease.
- To investigate the association of these molecules with triple vessel disease (TVD) and non-obstructive coronary artery disease (NCA).
Main Methods:
- Sera from healthy individuals (n=31), TVD patients (n=36), and NCA patients (n=30) were analyzed.
- Levels of CD105, active TGFbeta1, (a+l)TGFbeta1, TGFbeta3, and receptor-ligand complexes were measured.
- Statistical analysis was performed to compare groups and identify correlations.
Main Results:
- Active TGFbeta1 and (a+l)TGFbeta1 were significantly lower in TVD patients.
- CD105 levels were diminished in TVD patients but elevated in NCA patients.
- Higher CD105/TGFbeta1 complexes were found in TVD patients, correlating with lower receptor and ligand levels.
- Elevated CD105/TGFbeta3 levels were observed in NCA patients compared to TVD and healthy individuals.
- CD105 showed significant correlations with TGFbeta1 and TGFbeta3 and their complexes.
Conclusions:
- Altered levels of CD105, TGFbeta1, and their complexes in serum suggest a role in the pathobiology of atherosclerosis.
- These molecules may serve as potential biomarkers for coronary artery disease.
- Further research with larger cohorts and sequential sampling is needed to establish causality.
Abstract:
We have quantified levels of CD105, its ligand TGFbeta and receptor-ligand complexes in sera from healthy individuals (n=31), patients with triple vessel disease documented by coronary angiography (TVD; n=36) and patients with chest pain and a positive exercise electrocardiogram but with normal coronary angiogram (NCA; n=30). Both active TGFbeta1 and active plus acid-activatable TGFbeta1 [(a+l)TGFbeta1] were significantly depressed in patients with TVD compared with the other two groups (P=0.04). CD105 levels in TVD patients were also diminished but elevated in NCA patients. In contrast, patients with TVD had more CD105/TGFbeta1 complex in their sera than the other two groups, suggesting that this may be the reason why TVD patients had low levels of receptor and ligand. TGFbeta3 levels were similar in the three groups, but elevated CD105/TGFbeta3 levels were noted in patients with NCA compared with those with TVD and healthy individuals (P< or =0.02). CD105 was correlated with both active TGFbeta1 and (a+l)TGFbeta1 (P=0.02). CD105 also strongly correlated with TGFbeta3 and CD105/TGFbeta3 complexes (P=0.001 in both cases). The changes in levels of CD105, TGFbeta1 and the receptor-ligand complexes in sera of patients with atherosclerosis suggest that these molecules may be important in the pathobiology of the atherosclerotic disease. Further studies on sequential samples from a larger cohort of patients are needed to define a causal relationship between these molecules and the disease progression.
More Related Videos
Related Concept Videos
TGF - β Signaling Pathway
Intracellular Signaling Affects Focal Adhesions
Some...
T Cell Activation and Clonal Selection
Naive T cells that have not yet encountered an antigen express two primary CD...
Coronary Artery Disease I: Introduction
Coronary Artery Disease II: Pathophysiology

