THE ROLE OF FIBROBLAST TRANSDIFFERENTIATION IN LUNG EPITHELIAL CELL PROLIFERATION, DIFFERENTIATION, AND REPAIR IN VITRO

2003 ◽  
Vol 22 (3) ◽  
pp. 189-207 ◽  
Author(s):  
J. S. Torday ◽  
E. Torres ◽  
V. K. Rehan
Keyword(s):  
Cell Proliferation ◽  
Epithelial Cell ◽  
Lung Epithelial Cell ◽  
Epithelial Cell Proliferation ◽  
Lung Epithelial

Enteric glia inhibit intestinal epithelial cell proliferation partly through a TGF-β1-dependent pathway

2007 ◽  
Vol 292 (1) ◽  
pp. G231-G241 ◽  
Author(s):  
M. Neunlist ◽  
P. Aubert ◽  
S. Bonnaud ◽  
L. Van Landeghem ◽  
E. Coron ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Epithelial Cell ◽  
Cell Density ◽  
Intestinal Epithelial Cell ◽  
Intestinal Barrier ◽  
Intestinal Epithelial ◽  
Epithelial Cell Proliferation ◽  
Coculture Model

Although recent studies have shown that enteric neurons control intestinal barrier function, the role of enteric glial cells (EGCs) in this control remains unknown. Therefore, our goal was to characterize the role of EGCs in the control of intestinal epithelial cell proliferation using an in vivo transgenic and an in vitro coculture model. Assessment of intestinal epithelial cell proliferation after ablation of EGCs in transgenic mice demonstrated a significant increase in crypt cell hyperplasia. Furthermore, mucosal glial network (assessed by immunohistochemical detection of S-100β) is altered in colon adenocarcinoma compared with control tissue. In an in vitro coculture model of subconfluent Caco-2 cells seeded onto Transwell filters with EGCs, Caco-2 cell density and [3H]thymidine incorporation were significantly lower than in control (Caco-2 cultured alone). Flow cytometry analysis showed that EGCs had no effect on Caco-2 cell viability. EGCs induced a significant increase in Caco-2 cell surface area without any sign of cellular hypertrophy. These effects by EGCs were also seen in various transformed or nontransformed intestinal epithelial cell lines. Furthermore, TGF-β1 mRNA was expressed, and TGF-β1 was secreted by EGCs. Exogenously added TGF-β1 reproduced partly the EGC-mediated effects on cell density and surface area. In addition, EGC effects on Caco-2 cell density were significantly reduced by a neutralizing TGF-β antibody. In conclusion, EGCs have profound antiproliferative effects on intestinal epithelial cells. Functional alterations in EGCs may therefore modify intestinal barrier functions and be involved in pathologies such as cancer or inflammatory bowel diseases.

scholarly journals The LIM-domain only protein 4 contributes to lung epithelial cell proliferation but is not essential for tumor progression

2015 ◽  
Vol 16 (1) ◽  
Author(s):  
Aliaksei Z. Holik ◽  
Caitlin E. Filby ◽  
Julie Pasquet ◽  
Kati Viitaniemi ◽  
John Ciciulla ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Epithelial Cell ◽  
Tumor Progression ◽  
Lung Epithelial Cell ◽  
Epithelial Cell Proliferation ◽  
Lim Domain ◽  
Lung Epithelial

scholarly journals SARS-CoV-2 ORF8 Forms Intracellular Aggregates and Inhibits IFNγ-Induced Antiviral Gene Expression in Human Lung Epithelial Cells

2021 ◽  
Vol 12 ◽  
Author(s):  
Hua Geng ◽  
Saravanan Subramanian ◽  
Longtao Wu ◽  
Heng-Fu Bu ◽  
Xiao Wang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Epithelial Cell ◽  
Epithelial Cells ◽  
Viral Infection ◽  
Human Lung ◽  
Lung Epithelial Cells ◽  
Lung Epithelial Cell ◽  
Accessory Protein ◽  
Epithelial Cell Proliferation ◽  
Lung Epithelial

Infection with the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes COVID-19, a disease that involves significant lung tissue damage. How SARS-CoV-2 infection leads to lung injury remains elusive. The open reading frame 8 (ORF8) protein of SARS-CoV-2 (ORF8SARS-CoV-2) is a unique accessory protein, yet little is known about its cellular function. We examined the cellular distribution of ORF8SARS-CoV-2 and its role in the regulation of human lung epithelial cell proliferation and antiviral immunity. Using live imaging and immunofluorescent staining analyses, we found that ectopically expressed ORF8SARS-CoV-2 forms aggregates in the cytosol and nuclear compartments of lung epithelial cells. Using in silico bioinformatic analysis, we found that ORF8SARS-CoV-2 possesses an intrinsic aggregation characteristic at its N-terminal residues 1-18. Cell culture did not reveal any effects of ORF8SARS-CoV-2 expression on lung epithelial cell proliferation and cell cycle progression, suggesting that ORF8SARS-CoV-2 aggregates do not affect these cellular processes. Interestingly, ectopic expression of ORF8SARS-CoV-2 in lung epithelial cells suppressed basal expression of several antiviral molecules, including DHX58, ZBP1, MX1, and MX2. In addition, expression of ORF8SARS-CoV-2 attenuated the induction of antiviral molecules by IFNγ but not by IFNβ in lung epithelial cells. Taken together, ORF8SARS-CoV-2 is a unique viral accessory protein that forms aggregates when expressing in lung epithelial cells. It potently inhibits the expression of lung cellular anti-viral proteins at baseline and in response to IFNγ in lung epithelial cells, which may facilitate SARS-CoV-2 escape from the host antiviral innate immune response during early viral infection. In addition, it seems that formation of ORF8SARS-CoV-2 aggregate is independent from the viral infection. Thus, it would be interesting to examine whether any COVID-19 patients exhibit persistent ORF8 SARS-CoV-2 expression after recovering from SARS-CoV-2 infection. If so, the pathogenic effect of prolonged ORF8SARS-CoV-2 expression and its association with post-COVID symptoms warrant investigation in the future.

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