AI Article Synopsis
- The study investigates the role of C-reactive protein (CRP) from perivascular adipose tissue (PVAT) in obesity and how it influences cardiovascular disorders following vascular injury.
- A high-fat diet (HFD) led to increased CRP levels in PVAT, and experiments showed that PVAT from transgenic mice with elevated CRP led to more vascular damage compared to normal PVAT.
- The findings indicate that CRP promotes inflammatory processes and hyperplasia in blood vessels, suggesting a potential link between obesity-related inflammation and cardiovascular diseases.
Article Abstract
Aim: Inflammation within the perivascular adipose tissue (PVAT) in obesity plays an important role in cardiovascular disorders. C-reactive protein (CRP) level in obesity patients is significantly increased and associated with the occurrence and progression of cardiovascular disease. We tested the hypothesis CRP derived from PVAT in obesity contributes to vascular remodeling after injury.
Methods: A high-fat diet (HFD) significantly increased CRP expression in PVAT. We transplanted thoracic aortic PVAT from wild-type (WT) or transgenic CRP-expressing (CRPTG) mice to the injured femoral artery in WT mice.
Results: At 4 weeks after femoral artery injury, the neointimal/media ratio was increased significantly in WT mice that received PVAT from CRPTG mice compared with that in WT mice that received WT PVAT. Transplanted CRPTG PVAT also significantly accelerated adventitial macrophage infiltration and vasa vasorum proliferation. It was revealed greater macrophage infiltration in CRPTG adipose tissue than in WT adipose tissue and CRP significantly increased the adhesion rate of monocytes through receptor Fcγ RI. Proteome profiling showed CRP over-expression promoted the expression of chemokine (C-X-C motif) ligand 7 (CXCL7) in adipose tissue, transwell assay showed CRP increased monocyte migration indirectly via the induction of CXCL7 expression in adipocytes.
Conclusion: CRP derived from PVAT was significantly increased in HFD mice and promoted neointimal hyperplasia after vascular injury.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7011279 | PMC |
| http://dx.doi.org/10.1186/s12967-020-02226-x | DOI Listing |
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