Hepatocyte growth factor stimulates DNA synthesis in alveolar epithelial type II cells in vitro.

Shiratori, Masanori; Michalopoulos, George K.; Shinozuka, Hisashi; Singh, Gurmukh; Ogasawara, Hayato; Katyal, Sikandar L.

doi:10.1165/ajrcmb.12.2.7532419

Cited by 63 publications

(41 citation statements)

References 38 publications

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“…Evidence is accumulating that HGF stimulates proliferation of bronchial and alveolar type II epithelial cells through DNA synthesis in vivo as well in vitro (16,17,33,34). Moreover, Yamada et al (25) demonstrated that the neutralization of HGF strongly inhibited DNA synthesis of alveolar epithelial cells in the ischemic-reperfused lung injury.…”

Section: Discussionmentioning

confidence: 99%

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Essential Contribution of Monocyte Chemoattractant Protein-1/C-C Chemokine Ligand-2 to Resolution and Repair Processes in Acute Bacterial Pneumonia

Amano

Morimoto

Senba³

et al. 2004

The Journal of Immunology

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Neutrophil infiltration is the first step in eradication of bacterial infection, but neutrophils rapidly die after killing bacteria. Subsequent accumulation of macrophage lineage cells, such as alveolar macrophages (AMs), is essential to remove dying neutrophils, which are a source of injurious substances. Macrophage lineage cells can promote tissue repair, by producing potential growth factors including hepatocyte growth factor (HGF). However, it remains elusive which factor activates macrophage in these processes. Intratracheal instillation of Pseudomonas aeruginosa caused neutrophil infiltration in the airspace; subsequently, the numbers of total AMs and neutrophil ingested AMs were increased. Bronchoalveolar lavage (BAL) fluid levels of monocyte chemoattractant protein (MCP)-1/CC chemokine ligand-2 (CCL2), a potent macrophage-activating factor, were increased before the increases in the number of AM ingesting neutrophils and HGF levels in BAL fluid. Immunoreactive MCP-1 proteins were detected in alveolar type II epithelial cells and AMs only after P. aeruginosa infection. The administration of anti-MCP-1/CCL2 Abs reduced the increases in the number of AM-ingesting neutrophils and HGF levels in BAL fluid, and eventually aggravated lung tissue injury. In contrast, the administration of MCP-1/CCL2 enhanced the increases in the number of AM ingesting neutrophils and HGF levels in BAL fluid, and eventually attenuated lung tissue injury. Furthermore, MCP-1/CCL2 enhanced the ingestion of apoptotic neutrophils and HGF production by a mouse macrophage cell line, RAW 267.4, in a dose-dependent manner. Collectively, MCP-1/CCL2 has a crucial role in the resolution and repair processes of acute bacterial pneumonia by enhancing the removal of dying neutrophils and HGF production by AMs

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Section: Discussionmentioning

confidence: 99%

“…Intratracheal and i.v. administration of recombinant HGF stimulates DNA synthesis of alveolar type II cells in the rat lung after acute lung injury (16,17). Moreover, exogenously administered HGF attenuated bleomycininduced lung fibrosis in mice (18).…”

mentioning

confidence: 99%

Essential Contribution of Monocyte Chemoattractant Protein-1/C-C Chemokine Ligand-2 to Resolution and Repair Processes in Acute Bacterial Pneumonia

Amano

Morimoto

Senba³

et al. 2004

The Journal of Immunology

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“…37,38 It stimulates DNA synthesis 39,40 and proliferation of alveolar type II epithelial cells, 41 thus contributing to regeneration of alveolar structures following injury. Previous studies have also shown that administration of exogenous HGF via systemic 20 or intratracheal route 19 into bleomycin-injured mice resulted in the reduction of pulmonary fibrosis.…”

Section: Discussionmentioning

confidence: 99%

The Plasminogen Activation System Reduces Fibrosis in the Lung by a Hepatocyte Growth Factor-Dependent Mechanism

Hattori

Mizuno

Yoshida

et al. 2004

The American Journal of Pathology

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Mice deficient in the plasminogen activator inhibitor-1 gene (PAI-1؊/؊ mice) are relatively protected from developing pulmonary fibrosis from bleomycin administration. We hypothesized that one of the protective mechanisms may be the ability of the plasminogen system to enhance hepatocyte growth factor (HGF) effects, which have been reported to be antifibrotic in the lung. HGF is known to be sequestered in tissues by binding to extracellular matrix components. Following bleomycin administration, we found that HGF protein levels were higher in bronchoalveolar lavage fluid from PAI-1 ؊/؊ mice com- Abnormal accumulation of fibrin occurs within the interstitium and alveolar spaces of the lung in a variety of pulmonary diseases in which the integrity of the capillary alveolar barrier is damaged.

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“…Macrophage lineage cells promote tissue repair by producing potential growth factors such as hepatocyte growth factor or HGF (25,26). HGF is a mitogen for various types of epithelia, including bronchial and alveolar epithelial cells (27,28). Recombinant HGF augments DNA synthesis of alveolar type II cells in acute lung injury, and also reduces pulmonary fibrosis during bleomycin-mediated lung injury (29).…”

Section: Clinical Relevancementioning

confidence: 99%

MCP-1 Antibody Treatment Enhances Damage and Impedes Repair of the Alveolar Epithelium in Influenza Pneumonitis

Narasaraju¹,

Ng²,

Phoon³

et al. 2010

Am J Respir Cell Mol Biol

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Recent studies have demonstrated an essential role of alveolar macrophages during influenza virus infection. Enhanced mortalities were observed in macrophage-depleted mice and pigs after influenza virus infection, but the basis for the enhanced pathogenesis is unclear. This study revealed that blocking macrophage recruitment into the lungs in a mouse model of influenza pneumonitis resulted in enhanced alveolar epithelial damage and apoptosis, as evaluated by histopathology, immunohistochemistry, Western blot, RT-PCR, and TUNEL assays. Abrogation of macrophage recruitment was achieved by treatment with monoclonal antibody against monocyte chemoattractant protein-1 (MCP-1) after sub-lethal challenge with mouse-adapted human influenza A/Aichi/2/68 virus. Interestingly, elevated levels of hepatocyte growth factor (HGF), a mitogen for alveolar epithelium, were detected in bronchoalveolar lavage samples and in lung homogenates of control untreated and nonimmune immunoglobulin (Ig)G-treated mice after infection compared with anti-MCP-1-treated infected mice. The lungs of control animals also displayed strongly positive HGF staining in alveolar macrophages as well as alveolar epithelial cell hyperplasia. Co-culture of influenza virus-infected alveolar epithelial cells with freshly isolated alveolar macrophages induced HGF production and phagocytic activity of macrophages. Recombinant HGF added to mouse lung explants after influenza virus infection resulted in enhanced BrdU labeling of alveolar type II epithelial cells, indicating their proliferation, in contrast with anti-HGF treatment showing significantly reduced epithelial regeneration. Our data indicate that inhibition of macrophage recruitment augmented alveolar epithelial damage and apoptosis during influenza pneumonitis, and that HGF produced by macrophages in response to influenza participates in the resolution of alveolar epithelium.

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Hepatocyte growth factor stimulates DNA synthesis in alveolar epithelial type II cells in vitro.

Cited by 63 publications

References 38 publications

Essential Contribution of Monocyte Chemoattractant Protein-1/C-C Chemokine Ligand-2 to Resolution and Repair Processes in Acute Bacterial Pneumonia

Essential Contribution of Monocyte Chemoattractant Protein-1/C-C Chemokine Ligand-2 to Resolution and Repair Processes in Acute Bacterial Pneumonia

The Plasminogen Activation System Reduces Fibrosis in the Lung by a Hepatocyte Growth Factor-Dependent Mechanism

MCP-1 Antibody Treatment Enhances Damage and Impedes Repair of the Alveolar Epithelium in Influenza Pneumonitis

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