Yankai Xia
The etiology and pathogenesis of Hirschsprung’s disease (HSCR) remain largely unknown. Here we employed a multiple ‘omics’-analysis to explore the important pathway related to the development of HSCR. We examined colon tissues from three independent populations with a combined analysis of metabolomics, transcriptomics and proteomics to understand HSCR. Mouse model was used for examining PGE2 induced clinical presentation of HSCR. SH-SY5Y and SK-NBE(2) cell lines were used for examining PGE2 inhibited cell migration through EP2.
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