Suppr超能文献

二氧化硅在体外促进大鼠循环纤维细胞的转分化。

Silica promotes the transdifferentiation of rat circulating fibrocytes in vitro.

作者信息

Yao Wu, Liu Suna, Li Ju, Hao Changfu

机构信息

Department of Public Health, Zhengzhou University, Zhengzhou, Henan 450001, P.R. China.

出版信息

Mol Med Rep. 2015 Oct;12(4):5828-36. doi: 10.3892/mmr.2015.4212. Epub 2015 Aug 11.

Abstract

To investigate the effects of silica on circulating fibrocytes (cFbs), the present study established a primary culture model of rat alveolar macrophages and cFbs in vitro. Macrophages were treated with free silica, and their supernatant was used to stimulate cFbs. The mRNA expression levels of collagen I, collagen III and α‑smooth muscle actin (SMA) in cFbs were analyzed by reverse transcription‑quantitative polymerase chain reaction. The intracellular and extracellular protein expression levels of collagen I, collagen III and α‑SMA were detected by ELISA and immunofluorescence staining. The results indicated that in the cell model, the free silica effectively increased the protein and mRNA expression levels of collagen‑I, collagen‑III and α‑SMA. The free silica significantly promoted the transdifferentiation of cFbs into myofibroblasts in a dose‑and time-dependent manner.

摘要

为研究二氧化硅对循环纤维细胞(cFbs)的影响,本研究建立了大鼠肺泡巨噬细胞和cFbs的体外原代培养模型。用游离二氧化硅处理巨噬细胞,并用其培养上清液刺激cFbs。通过逆转录-定量聚合酶链反应分析cFbs中I型胶原、III型胶原和α-平滑肌肌动蛋白(SMA)的mRNA表达水平。通过酶联免疫吸附测定法和免疫荧光染色检测I型胶原、III型胶原和α-SMA的细胞内和细胞外蛋白表达水平。结果表明,在该细胞模型中,游离二氧化硅有效提高了I型胶原、III型胶原和α-SMA的蛋白和mRNA表达水平。游离二氧化硅以剂量和时间依赖性方式显著促进cFbs向肌成纤维细胞的转分化。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/86be/4581811/1c0ccb7c50d1/MMR-12-04-5828-g00.jpg

相似文献

1
Silica promotes the transdifferentiation of rat circulating fibrocytes in vitro.
Mol Med Rep. 2015 Oct;12(4):5828-36. doi: 10.3892/mmr.2015.4212. Epub 2015 Aug 11.
2
Regulation of silicosis formation by lysophosphatidic acid and its receptors.
Exp Lung Res. 2014 Sep;40(7):317-26. doi: 10.3109/01902148.2014.920438. Epub 2014 Jun 13.
6
The biological basis for poly-L-lactic acid-induced augmentation.
J Dermatol Sci. 2015 Apr;78(1):26-33. doi: 10.1016/j.jdermsci.2015.01.012. Epub 2015 Feb 7.
7
Plasminogen activator inhibitor-1 promotes the proliferation and inhibits the apoptosis of pulmonary fibroblasts by Ca(2+) signaling.
Thromb Res. 2013 Jan;131(1):64-71. doi: 10.1016/j.thromres.2012.09.003. Epub 2012 Sep 25.
8
Anti‑fibrotic effects and the mechanism of action of miR‑29c in silicosis.
Mol Med Rep. 2021 Apr;23(4). doi: 10.3892/mmr.2021.11932. Epub 2021 Mar 2.

引用本文的文献

1
Macrophage polarization in tissue fibrosis.
PeerJ. 2023 Oct 13;11:e16092. doi: 10.7717/peerj.16092. eCollection 2023.

本文引用的文献

1
Fibrocytes in the fibrotic lung: altered phenotype detected by flow cytometry.
Front Pharmacol. 2014 Jun 16;5:141. doi: 10.3389/fphar.2014.00141. eCollection 2014.
2
Protective effects of methyl palmitate against silica-induced pulmonary fibrosis in rats.
Int Immunopharmacol. 2013 Jun;16(2):191-8. doi: 10.1016/j.intimp.2013.04.007. Epub 2013 Apr 18.
4
Incidence of silicosis in flourmill workers.
Indian J Occup Environ Med. 2011 Sep;15(3):104-8. doi: 10.4103/0019-5278.93199.
6
Fibrocytes: emerging effector cells in chronic inflammation.
Nat Rev Immunol. 2011 Jun;11(6):427-35. doi: 10.1038/nri2990. Epub 2011 May 20.
7
Human circulating fibrocytes have the capacity to differentiate osteoblasts and chondrocytes.
Int J Biochem Cell Biol. 2010 May;42(5):662-71. doi: 10.1016/j.biocel.2009.12.011. Epub 2009 Dec 23.
9
Circulating fibrocytes are an indicator of poor prognosis in idiopathic pulmonary fibrosis.
Am J Respir Crit Care Med. 2009 Apr 1;179(7):588-94. doi: 10.1164/rccm.200810-1534OC. Epub 2009 Jan 16.
10
Critical role of MARCO in crystalline silica-induced pulmonary inflammation.
Toxicol Sci. 2009 Apr;108(2):462-71. doi: 10.1093/toxsci/kfp011. Epub 2009 Jan 16.

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验