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Upregulation of ADAMTS-7 and downregulation of COMP are associated with aortic aneurysm

Aortic aneurysm (AA) remains a fatal condition with high rates of morbidity and mortality, and the associated underlying mechanism influencing its pathology remains to be elucidated. A disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS)-7 has previously been demonstrated to be invo...

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Detalles Bibliográficos
Autores principales: Qin, Wei, Cao, Yide, Li, Liangpeng, Chen, Wen, Chen, Xin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5647091/
https://www.ncbi.nlm.nih.gov/pubmed/28849199
http://dx.doi.org/10.3892/mmr.2017.7293
Descripción
Sumario:Aortic aneurysm (AA) remains a fatal condition with high rates of morbidity and mortality, and the associated underlying mechanism influencing its pathology remains to be elucidated. A disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS)-7 has previously been demonstrated to be involved in the pathogenesis of vascular atherosclerosis via degradation of cartilage oligomeric matrix protein (COMP). The ADAMTS-7/COMP pathway may therefore act as a potential therapeutic target for vascular disorders. To the best of the author's knowledge, the present study aimed to investigate for the first time, the expression of ADAMTS-7 and COMP in human AA. Human aortic aneurysm samples were collected from patients with AA (n=24), and ascending aorta control samples were harvested from dilated cardiomyopathy patients who underwent heart transplantation (n=18). Expression levels of ADAMTS-7 and matrix metalloproteinase-9 were significantly increased in the AA group, as detected by immunohistochemistry (P<0.05). The COMP protein level was markedly decreased in the AA group when compared with the control group, as demonstrated via immunohistochemistry and western blot analysis (P<0.05). The findings suggest that upregulation of ADAMTS-7 and downregulation of COMP are associated with induction of human AA. ADAMTS-7/COMP pathway may provide therefore act as a potential therapeutic target in human AA for efficient, optimal treatment interventions in the future.