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Quantitative Analysis and Characterization of Atherosclerotic Lesions in the Murine Aortic Sinus
Published on: December 7, 2013
Integrative Analysis of VSMC, Macrophage, and Fibroblast Responses to LDLs in Aortic Pathologies
Ulyana Khovantseva1,2, Diana Kiseleva1,3, Vadim Cherednichenko1
1Petrovsky National Research Center of Surgery, 119435 Moscow, Russia.
Insights
Vascular cells like smooth muscle cells and fibroblasts become inflammatory when exposed to low-density lipoproteins (LDLs), contributing to cardiovascular disease (CVD) progression. Macrophages also show increased inflammatory markers and lipid uptake.
Area of Science:
- Molecular Biology
- Cardiovascular Research
- Cellular Immunology
Background:
- Cardiovascular diseases (CVDs) are a leading cause of death globally.
- Aortic pathologies like atherosclerosis and aneurysm are significant CVD risks.
- Understanding cellular responses in the aortic wall is crucial for CVD mechanisms.
Purpose of the Study:
- To investigate molecular mechanisms of CVDs by examining aortic wall cells.
- To analyze the response of vascular smooth muscle cells (VSMCs), fibroblasts, and macrophages to low-density lipoproteins (LDLs).
- To assess phenotypic changes, LDL uptake, and pro-inflammatory mediator release.
Main Methods:
- Utilized in vitro models with primary VSMCs, fibroblasts (977hTERT), and THP-1 macrophages.
- Assessed LDL internalization via fluorescence staining (BDP 630/650).
- Measured cytokine secretion (IL-6, IL-8, IL-1β, CCL2) and gene expression using ELISA and RT-qPCR.
Main Results:
- All tested cell types internalized LDLs; macrophages showed the highest lipid accumulation.
- VSMCs and fibroblasts acquired pro-inflammatory characteristics, increasing secretion of IL-6, IL-8, and CCL2.
- LDL exposure enhanced scavenger receptor CD36 expression and pro-inflammatory cytokine production (especially IL-1β) in macrophages.
Conclusions:
- VSMCs and fibroblasts can adopt pro-inflammatory roles in pathological conditions.
- Macrophages play a significant role in lipid accumulation and inflammation in response to LDLs.
- These cellular responses provide insight into the molecular pathogenesis of aortic diseases and CVDs.
Abstract:
Cardiovascular diseases (CVDs) remain the leading cause of global mortality, with aortic pathologies such as atherosclerosis and thoracic aortic aneurysm posing significant risks due to their asymptomatic nature and potential fatal complications. This study investigates molecular mechanisms underlying CVDs by examining key cellular components of the aortic wall-vascular smooth muscle cells (VSMCs), fibroblasts, and macrophages-and their responses to low-density lipoproteins (LDLs). Using in vitro models, we analyzed phenotypic characteristics, LDL internalization capacity, and secretion/expression of pro-inflammatory mediators (IL-6, IL-8, IL-1β, CCL2) in primary VSMCs (from tunica intima and media), fibroblasts (977hTERT), and THP-1 macrophages. Fluorescence staining with BDP 630/650 revealed that all cell types internalize LDLs, with macrophages showing the highest lipid accumulation. ELISA and RT-qPCR demonstrated cell-specific patterns of cytokine secretion and gene expression, both in control conditions and after LDL exposure. The results indicate that VSMCs and fibroblasts, normally involved in vascular tone maintenance and extracellular matrix (ECM) synthesis, acquire pro-inflammatory features under pathological conditions, including increased secretion of IL-6, IL-8, and CCL2. Macrophages exhibited enhanced expression of the scavenger receptor CD36 and pro-inflammatory cytokines (especially IL-1β) after LDL treatment.
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