ArticleRespiratory research2014
Rac2 is involved in bleomycin-induced lung inflammation leading to pulmonary fibrosis.
Article in Respiratory research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 37 citations in OpenAlex.
- Article
- Monocytes and macrophages: emerging mechanisms and novel therapeutic targets in pulmonary fibrosis.American journal of physiology. Cell physiology · 2023Review
- Review
- Classical monocyte-derived macrophages as therapeutic targets of umbilical cord mesenchymal stem cells: comparison of intratracheal and intravenous administration in a mouse model of pulmonary fibrosis.Respiratory research · 2023Article
- Novel Clotrimazole andSaudi journal of biological sciences · 2022Article
- Immune dysregulation as a driver of idiopathic pulmonary fibrosis.The Journal of clinical investigation · 2021Review
- Article
- Prediction of repurposed drugs for treating lung injury in COVID-19.F1000Research · 2020Article
- Distal airway stem cells ameliorate bleomycin-induced pulmonary fibrosis in mice.Stem cell research & therapy · 2019Article
- Overexpression of Ras-Related C3 Botulinum Toxin Substrate 2 Radiosensitizes Melanoma CellsOxidative medicine and cellular longevity · 2019Article
- Glycogen depletion can increase the specificity of mucin detection in airway tissues.BMC research notes · 2018Article
- Emodin Attenuates Bleomycin-Induced Pulmonary Fibrosis via Anti-Inflammatory and Anti-Oxidative Activities in Rats.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- Pulmonary Emphysema Cross-Linking with Pulmonary Fibrosis and Vice Versa: a Non-usual Experimental Intervention with Elastase and Bleomycin.Inflammation · 2017Article
- Deficiency of α7 nicotinic acetylcholine receptor attenuates bleomycin-induced lung fibrosis in mice.Molecular medicine (Cambridge, Mass.) · 2017Article
- Rac2 is required for alternative macrophage activation and bleomycin induced pulmonary fibrosis; a macrophage autonomous phenotype.PloS one · 2017Article
- Tissue turnover of collagen type I, III and elastin is elevated in the PCLS model of IPF and can be restored back to vehicle levels using a phosphodiesterase inhibitor.Respiratory research · 2016Article
- Salidroside protects against bleomycin-induced pulmonary fibrosis: activation of Nrf2-antioxidant signaling, and inhibition of NF-κB and TGF-β1/Smad-2/-3 pathways.Cell stress & chaperones · 2016Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPulmonary fibrotic diseases induce significant morbidity and mortality, for which there are limited therapeutic options available. Rac2, a ras-related guanosine triphosphatase expressed mainly in hematopoietic cells, is a crucial molecule regulating a diversity of mast cell, macrophage, and neutrophil functions. All these cell types have been implicated in the development of pulmonary fibrosis in a variety of animal models. For the studies described here we hypothesized that Rac2 deficiency protects mice from bleomycin-induced pulmonary fibrosis.
methodsTo determine the role of Rac2 in pulmonary fibrosis we used a bleomycin-induced mouse model. Anesthetized C57BL/6 wild type and rac2-/- mice were instilled intratracheally with bleomycin sulphate (1.25 U/Kg) or saline as control. Bronchoalveolar lavage (BAL) samples were collected at days 3 and 7 of treatment and analyzed for matrix metalloproteinases (MMPs). On day 21 after bleomycin treatment, we measured airway resistance and elastance in tracheotomized animals. Lung sections were stained for histological analysis, while homogenates were analyzed for hydroxyproline and total collagen content.
resultsBLM-treated rac2-/- mice had reduced MMP-9 levels in the BAL on day 3 and reduced neutrophilia and TNF and CCL3/MIP-1α levels in the BAL on day 7 compared to BLM-treated WT mice. We also showed that rac2-/- mice had significantly lower mortality (30%) than WT mice (70%) at day 21 of bleomycin treatment. Lung function was diminished in bleomycin-treated WT mice, while it was unaffected in bleomycin-treated rac2-/- mice. Histological analysis of inflammation and fibrosis as well as collagen and hydroxyproline content in the lungs did not show significant differences between BLM-treated rac2-/- and WT and mice that survived to day 21.
conclusionRac2 plays an important role in bleomycin-induced lung injury. It is an important signaling molecule leading to BLM-induced mortality and it also mediates the physiological changes seen in the airways after BLM-induced injury.
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