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Войти в исследования Epigenomics · 2026
Exosome-transmitted microRNA-323a-3p participated in the occurrence of Hirschsprung's disease.
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Shen Haoran, Wang Chenglong, Lv Xiurui, Gao Zichuan, Qiu Yuanxiang, Zhi Zhengke, Tang Jie, Du Chunxia, Zhang Ruyi, Li Hongxing, Tang Weibing
Аннотация
BACKGROUND: Hirschsprung's disease (HSCR) is caused by defective enteric neural crest cell (ENCC) migration. Exosome-transmitted microRNAs are implicated in HSCR pathogenesis, but mechanisms remain unclear.
METHODS: Plasma exosomes and colon tissues were collected from HSCR patients and controls. We assessed the effects of exosomal miR-323a-3p on the proliferation and migration of immortalized ENCC-derived neural cell line (iENC) in vitro using CCK-8, EdU and Transwell assays, and its impact on ENCC migration in vivo using a zebrafish model.
RESULTS: Exosomal miR-323a-3p was significantly upregulated in the plasma of HSCR and exhibited prospective diagnostic relevance (AUC = 0.7269, p = 0.0043). Exosomal miR-323a-3p was taken up by iENCs and suppressed their proliferation and migration. TET2 was identified as a potential miR-323a-3p target. TET2 was downregulated in HSCR aganglionic tissues, and its knockdown inhibited iENC proliferation and migration. In the zebrafish model, exosomal miR-323a-3p impaired distal ENCC colonization.
CONCLUSION: Exosomal miR-323a-3p is upregulated in HSCR and associated with impaired ENCC-derived cell function, potentially via TET2. These findings suggest exosome-transmitted microRNA-323a-3p participated in the occurrence of Hirschsprung's disease and exhibit promising potential as a prospective diagnostic biomarker.
METHODS: Plasma exosomes and colon tissues were collected from HSCR patients and controls. We assessed the effects of exosomal miR-323a-3p on the proliferation and migration of immortalized ENCC-derived neural cell line (iENC) in vitro using CCK-8, EdU and Transwell assays, and its impact on ENCC migration in vivo using a zebrafish model.
RESULTS: Exosomal miR-323a-3p was significantly upregulated in the plasma of HSCR and exhibited prospective diagnostic relevance (AUC = 0.7269, p = 0.0043). Exosomal miR-323a-3p was taken up by iENCs and suppressed their proliferation and migration. TET2 was identified as a potential miR-323a-3p target. TET2 was downregulated in HSCR aganglionic tissues, and its knockdown inhibited iENC proliferation and migration. In the zebrafish model, exosomal miR-323a-3p impaired distal ENCC colonization.
CONCLUSION: Exosomal miR-323a-3p is upregulated in HSCR and associated with impaired ENCC-derived cell function, potentially via TET2. These findings suggest exosome-transmitted microRNA-323a-3p participated in the occurrence of Hirschsprung's disease and exhibit promising potential as a prospective diagnostic biomarker.