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    A brief reconnoitre about effects of MMP9 on aortic dissection
    (DergiPark, 2021) Salman Yaylaz, Burcu; Sarıman, Melda; Ekmekçi, Ahmet; Ergül, Emel; Uluganyan, Mahmut; Çosan, Fulya; Totuk Gedar, Özgün Melike; Abacı, Neslihan
    Objective: Matrix metalloproteinases (MMPs) are the extracellular ma-trix regulators that frequently investigate cardiovascular diseases and cancer metastasis. Our study aimed to examine specific polymorphisms in the MMP9 gene in our patients with aortic dissection and compare the effect of MMP9 on aortic dissection with expression datasets. Materials and Methods: Q279R and P574R polymorphisms were analyzed in 44 aortic dissection patients and 40 healthy donors via polymerase chain reaction-restriction fragment length polymorphism. (PCR-RFLP) methods. Q279R and P574R prevalence was statistically compared with the medical data of the patients. Additionally, we col-lected datasets of aortic dissection from NCBI GEO to reanalyze GEO2R and RStudio to see metalloproteinase activity on samples. Later, enrich-ment analysis was processed on widely used databases. Results: Genotypic distribution of alleles was similar in the two study groups. In addition to this, female CG carriers had a higher risk of de-veloping aortic dissection than those of males. As the results of the protein-protein interaction analysis of MMP9 and patients’ clinical data, hypertension was found to be the significant outcome of P574R varia-tion in the patients. In array analysis, MMP9 expression did not change critically, but TIMPs had been downregulated in many samples. Also, MMP9 targeted miRNA expression levels were detected as low in aortic tissue and blood. Conclusion: Q279R and P574R are two polymorphisms that do not di-rectly affect MMP9 protein structure. Consequently, studied polymor-phisms and performed meta-analysis show that MMP9 does not spark off the phenotype but sets the stage for aortic dissection development as seen in the statistical results. Furthermore, enrichment analysis on datasets shows MMP9 was not a primary reason for vascular remodeling.