ENA-78 is an important angiogenic factor in idiopathic pulmonary fibrosis
ENA-78 is an important angiogenic factor in idiopathic pulmonary fibrosis
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DOI：
10.1164/ajrccm.164.12.2104106
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发表时间：
2001-12-15
影响因子：
24.7
通讯作者：
Strieter, RM
中科院分区：
文献类型：
--
作者：
Keane, MP;Belperio, JA;Strieter, RM
特发性肺纤维化（IPF）是一种慢性且经常致命的疾病。纤维增生和细胞外基质沉积部分依赖于血管生成和血管重塑。我们从除间质性肺疾病（对照组）以外的原因接受胸外科手术的患者（n = 78）和IPF患者（n = 91）中进行开放式肺活检。我们发现，与对照组相比，IPF患者组织标本中上皮中性粒细胞激活肽78 （ENA-78）的水平更高。当从IPF组织标本中去除ENA-78时，组织源性血管生成活性明显降低。对ENA-78的免疫定位表明，增生性11型肺细胞和巨噬细胞是ENA-78的主要细胞来源。这些发现支持了ENA-78可能是调节IPF血管生成活性的重要附加因子的观点。
Idiopathic pulmonary fibrosis (IPF) is a chronic and often fatal disorder. Fibroplasia and deposition of extracellular matrix are dependent, in part, on angiogenesis and vascular remodeling. We obtained open lung biopsies from patients undergoing thoracic surgery for reasons other than interstitial lung disease (control) (n = 78) and from patients with IPF (n = 91). We found that levels of epithelial neutrophil-activating peptide 78 (ENA-78) were greater from tissue specimens of IPF patients, as compared with control subjects. When ENA-78 was depleted from IPF tissue specimens, tissue-derived angiogenic activity was markedly reduced. Immunolocalization of ENA-78 demonstrated that hyperplastic Type 11 pneumocytes and macrophages were the predominant cellular sources of ENA-78. These findings support the notion that ENA-78 may be an important additional factor that regulates angiogenic activity in IPF.