The pleural mesothelium in development and disease.
The pleural mesothelium in development and disease.
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DOI：
10.3389/fphys.2014.00284
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发表时间：
2014
影响因子：
4
通讯作者：
Antony VB
中科院分区：
文献类型：
--
作者：
Batra H;Antony VB
胸膜间皮来源于胚胎中胚层，由一层代谢活跃的单层细胞组成，这些细胞分别覆盖在壁面和内脏表面的胸壁和肺。胸膜和肺的形成是中胚层和内胚层在发育过程中复杂关系的结果。间充质信号通路如Wnt/B-catenin、Bmp4和Sonic Hedgehog似乎是肺发育的典型信号通路。已知胸膜间皮细胞(PMC)表达Wilms Tumor-1(Wt1)基因，在发育胚胎的谱系标记研究中，PMC被发现跟踪进入肺实质，并经历间皮-间充质转化，形成间充质和血管系统的α-平滑肌肌动蛋白(α-SMA)阳性细胞。有确凿的证据表明间皮细胞可以分化，这似乎在胸膜和实质病理中起着重要作用。间皮细胞可以分化为脂肪细胞、软骨细胞和成骨细胞；并在小鼠模型中被证明克隆生成成纤维细胞和平滑肌细胞。这支持了这样一种可能性，即它们也可能通过重新激活成人的发育程序来调节肺损伤修复，这些程序反映了一种改变的发育重演，对肺的再生生物学有影响。在采用谱系追踪研究的小鼠肺纤维化模型中，PMCs失去了它们的极性和细胞-细胞连接复合体，迁移到肺实质，并在促纤维化介质转化生长因子-β1(转化生长因子-β1)的反应下发生表型转变为肌成纤维细胞。然而，胸膜腔内注射血红素加氧酶-1(HO-1)抑制了气管内纤维化损伤后PMC的迁移。胸膜内荧光素异硫氰酸酯标记的纳米颗粒表面修饰着间皮细胞的表面抗体，迁移到肺实质中，PMCs支持基于胸膜的治疗调节胸膜间皮激活和实质疾病进展的潜在作用。
The pleural mesothelium, derived from the embryonic mesoderm, is formed by a metabolically active monolayer of cells that blanket the chest wall and lungs on the parietal and visceral surfaces, respectively. The pleura and lungs are formed as a result of an intricate relationship between the mesoderm and the endoderm during development. Mesenchymal signaling pathways such as Wnt/B-catenin, Bmp4, and sonic hedgehog appear to be quintessential for lung development. Pleural Mesothelial Cells (PMCs) are known to express Wilms tumor-1 (Wt1) gene and in lineage labeling studies of the developing embryo, PMCs were found to track into the lung parenchyma and undergo mesothelial-mesenchymal transition (MMT) to form α-smooth muscle actin (α-SMA)-positive cells of the mesenchyme and vasculature. There is definite evidence that mesothelial cells can differentiate and this seems to play an important role in pleural and parenchymal pathologies. Mesothelial cells can differentiate into adipocytes, chondrocytes, and osteoblasts; and have been shown to clonally generate fibroblasts and smooth muscle cells in murine models. This supports the possibility that they may also modulate lung injury-repair by re-activation of developmental programs in the adult reflecting an altered recapitulation of development, with implications for regenerative biology of the lung. In a mouse model of lung fibrosis using lineage-tracing studies, PMCs lost their polarity and cell-cell junctional complexes, migrated into lung parenchyma, and underwent phenotypic transition into myofibroblasts in response to the pro-fibrotic mediator, transforming growth factor-β1 (TGF-β1). However, intra-pleural heme-oxygenase-1 (HO-1) induction inhibited PMC migration after intra-tracheal fibrogenic injury. Intra-pleural fluorescein isothiocyanate labeled nanoparticles decorated with a surface antibody to mesothelin, a surface marker of mesothelial cells, migrate into the lung parenchyma with PMCs supporting a potential role for pleural based therapies to modulate pleural mesothelial activation and parenchymal disease progression.
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影响因子：
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作者：
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通讯作者：
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DOI：
10.1164/ajrccm.162.1.9903129
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