ROLE OF MESENCHYMAL CELL-DEATH IN LUNG REMODELING AFTER INJURY
ROLE OF MESENCHYMAL CELL-DEATH IN LUNG REMODELING AFTER INJURY
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DOI：
10.1172/jci116578
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发表时间：
1993-07-01
影响因子：
15.9
通讯作者：
BITTERMAN, PB
中科院分区：
文献类型：
--
作者：
POLUNOVSKY, VA;CHEN, B;BITTERMAN, PB
急性肺损伤后的修复需要从肺泡气隙中清除肉芽组织。我们假设在肺修复过程中，能够诱导肉芽组织的两种主要细胞成分成纤维细胞和内皮细胞死亡的信号将存在于空气-肺界面。在肺修复过程中从患者获得的支气管肺泡灌洗液诱导成纤维细胞和内皮细胞死亡，而在损伤时或从患者对照组获得的液体则不会。内皮细胞的死亡方式为凋亡。成纤维细胞死亡，虽然形态上不同于坏死，也不同于典型的凋亡。灌洗液中的生物活性物质对增殖期细胞敏感，对胰蛋白酶敏感，不溶于脂。对肺损伤后患者的肺组织进行组织学检查，发现在气腔肉芽组织内存在凋亡细胞的证据。我们的研究结果表明，由存在于空气-肺界面的肽诱导的细胞死亡可能参与了伴随损伤后组织修复的重塑过程。
Repair after acute lung injury requires elimination of granulation tissue from the alveolar airspace. We hypothesized that during lung repair, signals capable of inducing the death of the two principal cellular elements of granulation tissue, fibroblasts and endothelial cells, would be present at the air-lung interface. Bronchoalveolar lavage fluid obtained from patients during lung repair induced both fibroblast and endothelial cell death, while fluid obtained at the time of injury or from patient controls did not. The mode of cell death for endothelial cells was apoptosis. Fibroblast death, while morphologically distinct from necrosis, also differed from typical apoptosis. Only proliferating cells were susceptible to the bioactivities in lavage fluid, which were trypsin sensitive and lipid insoluble. Histological examination of lung tissue from patients after lung injury revealed evidence of apoptotic cells within airspace granulation tissue. Our results suggest that cell death induced by peptide(s) present at the air-lung interface may participate in the remodeling process that accompanies tissue repair after injury.