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首页> 外文期刊>Genomics >Genomic phenotype of non-cultured pulmonary fibroblasts in idiopathic pulmonary fibrosis.
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Genomic phenotype of non-cultured pulmonary fibroblasts in idiopathic pulmonary fibrosis.

机译：非培养性肺成纤维细胞在特发性肺纤维化中的基因表型。

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摘要

Activated fibroblasts are the central effector cells of the progressive fibrotic process in idiopathic pulmonary fibrosis (IPF). Characterizing the genomic phenotype of isolated fibroblasts is essential to understanding IPF pathogenesis. Comparing the genomic phenotype of non-cultured pulmonary fibroblasts from advanced IPF patients' and normal lungs revealed novel genes, biological processes and concomitant pathways previously unreported in IPF fibroblasts. We demonstrate altered expression in proteasomal constituents, ubiquitination-mediators, Wnt, apoptosis and vitamin metabolic pathways and cell cycle regulators, suggestive of loss of cellular homeostasis. Specifically, FBXO32, CXCL14, BDKRB1 and NMNAT1 were up-regulated, while RARA and CDKN2D were down-regulated. Paradoxically, pro-apoptotic inducers TNFSF10, BAX and CASP6 were also found to be increased. This comprehensive description of altered gene expression in isolated IPF fibroblasts underscores the complex biological processes characteristic of IPF and may provide a foundation for future research into this devastating disease.
机译：活化的成纤维细胞是特发性肺纤维化（IPF）中进行性纤维化过程的中心效应细胞。表征分离的成纤维细胞的基因组表型对于理解IPF发病机理至关重要。比较来自晚期IPF患者和正常肺的未培养肺成纤维细胞的基因组表型，发现了IPF成纤维细胞以前未报道的新基因，生物学过程和伴随途径。我们证明了蛋白酶体成分，泛素介导剂，Wnt，细胞凋亡和维生素代谢途径以及细胞周期调节剂中表达的改变，提示细胞稳态的丧失。具体来说，上调FBXO32，CXCL14，BDKRB1和NMNAT1，而下调RARA和CDKN2D。矛盾的是，还发现促凋亡诱导剂TNFSF10，BAX和CASP6升高。对分离的IPF成纤维细胞中基因表达改变的这种全面描述强调了IPF的复杂生物学过程，并且可能为对该破坏性疾病的未来研究提供基础。

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