Role of human pulmonary fibroblast-derived MCP-1 in cell activation and migration in experimental silicosis

Liu, Xueting; Fang, Shencun; Liu, Haijun; Wang, Xingang; Dai, Xiang; Yin, Qian; Yun, Tianwei; Wang, Wei; Zhang, Ying‐Ming; Liao, Hong; Zhang, Wei; Yao, Honghong; Chao, Jie

doi:10.1016/j.taap.2015.07.002

Cited by 39 publications

(39 citation statements)

References 38 publications

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“…Briefly, the medium was replaced with DMEM containing 10 μg/ml puromycin and 10 % FBS, and the cells were cultured at 37 °C in 5 % CO 2 for 24 h. Then, the cells were washed twice with fresh medium. Purified transduced HPF-a cell cultures were expanded and/or stored in liquid nitrogen as described previously [41]. …”

Section: Methodsmentioning

confidence: 99%

Macrophage-derived MCPIP1 mediates silica-induced pulmonary fibrosis via autophagy

et al. 2016

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BackgroundSilicosis is characterized by accumulation of fibroblasts and excessive deposition of extracellular matrix. Monocyte chemotactic protein-1-induced protein 1 (MCPIP1) plays a critical role in fibrosis induced by SiO2. However, the details of the downstream events of MCPIP1 activity in pulmonary fibrosis remain unclear. To elucidate the role of MCPIP1-induced autophagy in SiO2-induced fibrosis, both the upstream molecular mechanisms and the functional effects of SiO2 on cell apoptosis, proliferation and migration were investigated.ResultsExperiments using primary cultures of alveolar macrophages from healthy donors and silicosis patients as well as differentiated U937 macrophages demonstrated the following results: 1) SiO2 induced macrophage autophagy in association with enhanced expression of MCPIP1; 2) autophagy promoted apoptosis and activation of macrophages exposed to SiO2, and these events induced the development of silicosis; 3) MCPIP1 facilitated macrophage apoptosis and activation via p53 signaling-mediated autophagy; and 4) SiO2-activated macrophages promoted the proliferation and migration of fibroblasts via the MCPIP1/p53-mediated autophagy pathway.ConclusionsOur results elucidated a link between SiO2-induced fibrosis and MCPIP1/p53 signaling-mediated autophagy. These findings provide novel insight into the potential targeting of MCPIP1 or autophagy in the development of potential therapeutic strategies for silicosis.Electronic supplementary materialThe online version of this article (doi:10.1186/s12989-016-0167-z) contains supplementary material, which is available to authorized users.

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Section: Methodsmentioning

confidence: 99%

Macrophage-derived MCPIP1 mediates silica-induced pulmonary fibrosis via autophagy

et al. 2016

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“…HUVECs were transduced with LV-GFP lentivirus (Hanbio, Inc., Shanghai, CN) as previously described [5,[38][39][40][41]. Briefly, HUVECs (P3-5) were cultured in a 24-well plate (1 × 10 4 cells/well) in 10% FBS in DMEM for 48 h. The medium was then replaced with 1 mL of fresh medium and 8 µg/mL polybrene.…”

Section: Lentiviral Transduction Of Huvecsmentioning

confidence: 99%

“…Cell viability was measured using the 3-(4,5-dmethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) method [38]. Briefly, cells were collected and seeded onto 96-well plates.…”

Section: Mtt Assaymentioning

confidence: 99%

iNOS Induces Vascular Endothelial Cell Migration and Apoptosis Via Autophagy in Ischemia/Reperfusion Injury

Zhu

Yao

Wang

et al. 2016

Cell Physiol Biochem

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Background/Aims: Inducible nitric oxide synthase (iNOS) plays a crucial role in ischemia/reperfusion (I/R). Autophagy is involved in irreversible cell injury and death under extreme conditions. However, whether iNOS mediates myocardial ischemia/reperfusion (I/R) injury in endothelial cells via autophagy remains ill-defined. In this study, we examined whether I/R-mediated up-regulation of iNOS is critical in the modulation of cell migration and apoptosis via autophagy in human umbilical vein endothelial cells (HUVECs). Methods: iNOS expression was detected in HUVECs using Western blotting analyses and immunocytochemistry. An in vitro scratch assay was performed to detect cell migration. The autophagy markers ATG5, LC3B and BECN were detected using Western blotting analysis and adenovirus-mRFP-GFP-LC3. The pharmacological inhibitor of autophagy 3-MA was also applied to confirm the role of autophagy in I/R. Results: I/R induced the expression of iNOS, which subsequently increased the migration and apoptosis of HUVECs and was associated with the up-regulation of autophagy. The iNOS specific inhibitor L-NAME abolished I/R-induced autophagy, while L-NAME and 3-MA both attenuated cell apoptosis and migration induced by I/R. Conclusion: These findings suggested that I/R-induced iNOS regulates migration and apoptosis in HUVECs via autophagy, which indicates a new therapeutic strategy for individuals with I/R injury.

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“…HUVECs were transduced with LV-RFP lentivirus (Hanbio, Inc., Shanghai, CN) as previously described [36,37]. Briefly, HUVECs were cultured in a 24-well plate (1 x 10 4 cells/well) in 10% FBS in DMEM for 48 h. The medium was then replaced with 1 mL fresh medium and 8 µg/mL polybrene.…”

Section: Lentiviral Transduction Of Huvecsmentioning

confidence: 99%

“…Cell viability was measured via the 3-(4,5-dmethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) method [36]. Briefly, cells were collected and seeded into 96-well plates.…”

Section: Mtt Assaymentioning

confidence: 99%

The Role of MCPIP1 in Ischemia/Reperfusion Injury-Induced HUVEC Migration and Apoptosis

Zhu

Yao

Hu³

et al. 2015

Cell Physiol Biochem

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Background/Aims: Monocyte chemotactic protein-induced protein 1 (MCPIP1) plays a crucial role in various cellular processes, including neurogenesis. However, the relationship between MCPIP1 and myocardial ischemia/reperfusion (I/R) injury remained illdefined. In this study, we explored whether the I/R-mediated up-regulation of MCPIP1 is critical in the modulation of both cell migration and apoptosis in human umbilical vein endothelial cells (HUVECs). Methods: Using Western blot analysis and quantitative real-time PCR, the protein expression and mRNA transcription, respectively, of MCPIP1 was detected in HUVECs. To investigate cell migration, an in vitro scratch assay and a nested matrix model were applied. Results: I/R increased the expression of MCPIP1 via the activation of the mitogen-activated protein kinase (MAPK) and PI3K/Akt pathways. I/R increased migration and apoptosis of HUVECs, which were significantly inhibited by MCPIP1 siRNA. Conclusion: These findings suggest that I/R-mediated up-regulation of MCPIP1 regulates migration and apoptosis in HUVECs. Understanding the regulation of MCPIP1 expression and function may aid in the development of an adjunct therapeutic strategy in the treatment of individuals with I/R injury.

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Role of human pulmonary fibroblast-derived MCP-1 in cell activation and migration in experimental silicosis

Cited by 39 publications

References 38 publications

Macrophage-derived MCPIP1 mediates silica-induced pulmonary fibrosis via autophagy

Macrophage-derived MCPIP1 mediates silica-induced pulmonary fibrosis via autophagy

iNOS Induces Vascular Endothelial Cell Migration and Apoptosis Via Autophagy in Ischemia/Reperfusion Injury

The Role of MCPIP1 in Ischemia/Reperfusion Injury-Induced HUVEC Migration and Apoptosis

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