ArticleExperimental and therapeutic medicine2016
Study of the functional mechanisms of osteopontin and chemokine-like factor 1 in the development and progression of abdominal aortic aneurysms in rats.
Article in Experimental and therapeutic medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 12 citations in OpenAlex.
- CKLF1 interference alleviates IL‑1β‑induced inflammation, apoptosis and degradation of the extracellular matrix in chondrocytes via CCR5.Experimental and therapeutic medicine · 2023Article
- Role of chemokine-like factor 1 as an inflammatory marker in diseases.Frontiers in immunology · 2023Review
- Article
- Chemokine-like factor 1: A promising therapeutic target in human diseases.Experimental biology and medicine (Maywood, N.J.) · 2020Review
- Chemokine-Like Factor-Like MARVEL Transmembrane Domain-Containing Family in Hepatocellular Carcinoma: Latest Advances.Frontiers in oncology · 2020Review
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of the study was to investigate the functional mechanisms of osteopontin (Opn) and chemokine-like factor 1 (Cklf1) during the development and progression of abdominal aortic aneurysms (AAA) in rats. Healthy adult Sprague-Dawley rats (n=30) were randomly divided into the AAA, control and sham groups (10 rats/group) and experimental rat models of AAA were generated by enzyme perfusion in abdominal aorta for 30 min. The AAA formation was assessed by measuring the aortal diameter and hematoxylin and eosin staining as well as specific staining to detect the structural changes of the aorta and inflammatory cell infiltration. Immunohistochemistry, western blot analysis and statistical analysis were also performed to examine the expression levels of Opn, Cklf1 and matrix metalloproteinase (MMP)-2 in the arterial tissue. Rat models of AAA were successfully established by protease perfusion. After perfusion, the diameter expansion rate of abdominal aorta was significantly higher (P<0.01) compared to controls, elastin present at the middle layer was significantly reduced and inflammatory cell infiltration was significantly higher in AAA rats. The expression of Opn, Cklf1 and MMP-2 in the AAA group was significantly increased compared to the control group (P<0.05) as revealed by immunohistochemical staining. The western blot analysis revealed that, the expression levels of Opn, Cklf1 and MMP-2 in the AAA group were significantly higher than the sham and control groups (P<0.01). We also found that the expression of Opn and MMP-2 was positively correlated. In conclusion, in rat models of AAA, Opn and Cklf1 function synergistically to upregulate the expression of MMP-2, causing accelerated degradation of extracellular matrix and eventually leading to the development and progression of AAA.
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