AI Article Synopsis

  • The study investigates mRNA expression in human thoracic aortic dissection (TAD) using mRNA microarray analysis and real-time PCR to identify critical genes involved in its pathogenesis.
  • The top hub genes found include CDK1, CDC20, and others linked to cell cycle regulation and specific signaling pathways, indicating their potential involvement in TAD progression.
  • CDK1, in particular, shows promise as both a diagnostic biomarker and a therapeutic target for TAD due to its increased expression in affected tissues.

Article Abstract

Background: To assess the mRNA expression profile and explore the hub mRNAs and potential molecular mechanisms in the pathogenesis of human thoracic aortic dissection (TAD).

Methodology: mRNA microarray expression signatures of TAD tissues (n = 6) and non-TAD tissues (NT; n = 6) were analyzed by an Arraystar human mRNA microarray. Real-time PCR (qRT-PCR) was used to validate the results of the mRNA microarray. Bioinformatic tools, including Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway analysis, were utilized. Protein-protein interaction (PPI) networks were constructed based on data from the STRING database. Molecular Complex Detection (MCODE) and cytoHubba analyses were used to predict the strongest hub gene and pathway.

Results: The top 10 hub genes were CDK1, CDC20, CCNB2, CCNB1, MAD2L1, AURKA, C3AR1, NCAPG, CXCL12 and ASPM, which were identified from the PPI network. Module analysis revealed that TAD was associated with the cell cycle, oocyte meiosis, the p53 signaling pathway, and progesterone-mediated oocyte maturation. The qRT-PCR results showed that the expression of all hub genes was significantly increased in TAD samples (p < 0.05). Immunostaining of Ki-67 and CDK1 showed a high proliferation state and high expression in TAD, respectively.

Conclusions: CDK1 could be used as a potential diagnostic biomarker and therapeutic target of TAD.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6872142PMC
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0224922PLOS

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