Analyzing the Effect of Vitronectin on Cell Growth and Mesenchymal-Epithelial Transition of Pulmonary Fibroblast Cells

Lung ◽  
2021 ◽  
Ya Zeng ◽  
Jiahua Yu ◽  
Mina Liu ◽  
Qin Zhang ◽  
Xuwei Cai
1971 ◽  
Vol 8 (3) ◽  
pp. 701-708
G. J. BLAKER ◽  

The uptake of biotin, choline, folic acid, hypoxanthine, inositol, nicotinamide, pantothenic acid, pyridoxine, riboflavin, thiamine and vitamin B12 by mouse LS cells in suspension culture was determined by microbiological assay methods. Based on the extent of uptake during cell growth, vitamin growth yields (cells produced/unit mass of vitamin utilized) were estimated for all of the vitamins, except folic acid, thiamine and B12. The growth yields were lower during the early phases of culture. No uptakes of folic acid or B12 could be demonstrated. During the period of incubation about half of the thiamine was irretrievably lost through spontaneous decomposition.

2003 ◽  
Vol 284 (3) ◽  
pp. C640-C648 ◽  
Gele Liu ◽  
Mohammad H. Ghahremani ◽  
Behzad Banihashemi ◽  
Paul R. Albert

Diacylglycerol (DAG) and ceramide are important second messengers affecting cell growth, differentiation, and apoptosis. Balb/c-3T3 fibroblast cells expressing dopamine-D2S (short) receptors (Balb-D2S cells) provide a model of G protein-mediated cell growth and transformation. In Balb-D2S cells, apomorphine (EC50= 10 nM) stimulated DAG and ceramide formation by 5.6- and 4.3-fold, respectively, maximal at 1 h and persisting over 6 h. These actions were blocked by pretreatment with pertussis toxin (PTX), implicating Gi/Goproteins. To address which G proteins are involved, Balb-D2S clones expressing individual PTX-insensitive Gαiproteins were treated with PTX and tested for apomorphine-induced responses. Neither PTX-insensitive Gαi2nor Gαi3rescued D2S-induced DAG or ceramide formation. Both D2S-induced DAG and ceramide signals required Gβγ-subunits and were blocked by inhibitors of phospholipase C [1-(6-[([17β]-3-methoxyestra-1,2,3[10]-trien- 17yl)amino]hexyl)-1H-pyrrole-2,5-dione (U-73122) and partially by D609]. The similar G protein specificity of D2S-induced calcium mobilization, DAG, and ceramide formation indicates a common Gβγ-dependent phospholipase C-mediated pathway. Both D2 agonists and ceramide specifically induced mitogen-activated protein kinase (ERK1/2), suggesting that ceramide mediates a novel pathway of D2S-induced ERK1/2 activation, leading to cell growth.

2020 ◽  
Hammad Ghafoor ◽  
Han Chu ◽  
Jie Huang ◽  
Menglin Chen ◽  
Zhangyan Wang ◽  

Abstract Background Pulmonary fibrosis is the sequela of many pulmonary diseases, such as pneumoconiosis and idiopathic pulmonary fibrosis. The principal characteristics of pulmonary fibrosis comprise myofibroblast proliferation, alveolar damage and deposition of extracellular matrix components, which causes abnormal lung structure remodeling and an irreversible decline in lung function; however, the detailed mechanisms remain unclear. The current study focused on the role of ZC3H4, a new member of the zinc finger protein family, in SiO2-induced pulmonary fibrosis. Methods The expression of ZC3H4 and fibroblast activation markers (COL1A1, COL3A1 and ACTA1) was measured by western blotting and immunofluorescence staining after SiO2 exposure (50 µg/cm2). The functional change in fibroblasts was studied with a scratch assay and a 3D migration assay. The CRISPR/Cas9 system was used to explore the regulatory mechanisms of ZC3H4 in pulmonary fibroblast cells. Results The expression levels of ZC3H4 and sigmar1 (a key regulator of ER stress) were increased in pulmonary fibroblast cells and were associated with fibroblast activation, as indicated by the increase in COL1A1, COL3A1 and ACTA1, as well as the migration ability. The SiO2-enhanced fibroblast activation was attenuated by specific knockdown of ZC3H4 and inhibition of ER stress, demonstrating that ZC3H4 activated fibroblasts via the sigmar1/ER stress pathway. Interestingly, an ER stress blockade also inhibited ZC3H4 expression, indicating the positive feedback regulatory mechanism of ER stress on ZC3H4. Conclusions Our results demonstrate that ZC3H4 and sigmar1 might act as novel therapeutic targets for silicosis, providing a reference for further pulmonary fibrosis research.

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