scholarly journals The TGF-β /NADPH Oxidases Axis in the Regulation of Liver Cell Biology in Health and Disease

Cells ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 2312
Author(s):  
Macarena Herranz-Itúrbide ◽  
Irene Peñuelas-Haro ◽  
Rut Espinosa-Sotelo ◽  
Esther Bertran ◽  
Isabel Fabregat
Keyword(s):  
Transforming Growth Factor Beta ◽  
Cell Biology ◽  
Transforming Growth Factor ◽  
Relevant Factor ◽  
Nadph Oxidases ◽  
The Family ◽  
Nox Inhibitors ◽  
Health And Disease ◽  
Growth Factor Beta ◽  
Therapeutic Tools

The Transforming Growth Factor-beta (TGF-β) pathway plays essential roles in liver development and homeostasis and become a relevant factor involved in different liver pathologies, particularly fibrosis and cancer. The family of NADPH oxidases (NOXs) has emerged in recent years as targets of the TGF-β pathway mediating many of its effects on hepatocytes, stellate cells and macrophages. This review focuses on how the axis TGF-β/NOXs may regulate the biology of different liver cells and how this influences physiological situations, such as liver regeneration, and pathological circumstances, such as liver fibrosis and cancer. Finally, we discuss whether NOX inhibitors may be considered as potential therapeutic tools in liver diseases.

scholarly journals TGF-βSignaling in Neuronal Stem Cells

2008 ◽  
Vol 24 (4-5) ◽  
pp. 251-255 ◽  
Author(s):  
Chohee Yun ◽  
Jonathan Mendelson ◽  
Tiffany Blake ◽  
Lopa Mishra ◽  
Bibhuti Mishra
Keyword(s):  
Transforming Growth Factor Beta ◽  
Cell Biology ◽  
Neuronal Development ◽  
Transforming Growth Factor ◽  
Es Cells ◽  
Lineage Specification ◽  
Neuronal Stem Cells ◽  
Biological Phenomena ◽  
Growth Factor Beta

Transforming growth factor beta (TGF-β) signaling has diverse and complex roles in various biological phenomena such as cell growth, differentiation, embryogenesis and morphogenesis. ES cells provide an essential model for understanding the role of TGF-βsignaling in lineage specification and differentiation. Recent studies have suggested significant role of TGF-βin stem/progenitor cell biology. Here in this review, we focus on the role of the TGF-βsuperfamily in neuronal development.

scholarly journals Comparison of normal and tumorigenic endothelial cells: differences in thrombospondin production and responses to transforming growth factor-beta

1994 ◽  
Vol 107 (1) ◽  
pp. 39-46
Author(s):  
A. RayChaudhury ◽  
W.A. Frazier ◽  
P.A. D'Amore
Keyword(s):  
Extracellular Matrix ◽  
Endothelial Cells ◽  
Endothelial Cell ◽  
Growth Factor ◽  
Cell Lines ◽  
Transforming Growth Factor Beta ◽  
Cell Biology ◽  
Transforming Growth Factor ◽  
Vascular Malformations ◽  
Growth Factor Beta

Cultured endothelial cells constitutively synthesize significant levels of thrombospondin, an extracellular matrix-associated protein with reported anti-anti-angiogenic properties. However, two murine endothelial cell lines, bEND.3 and Py-4-1, which have been immortalized with polyoma T oncogenes and which generate vascular malformations in vivo, produce little or no thrombospondin though bEND.3 (but not Py-4-1) growth is inhibited by the addition of exogenous thrombospondin. In addition, Py-4-1 cells are not growth-inhibited by transforming growth factor-beta, a potent endothelial inhibitor. These results indicate that these two cell lines may be useful tools in understanding the role and mechanism of action of thrombospondin and transforming growth factor-beta in endothelial cell biology. A role for thrombospondin in vascular development is further suggested by the observation of significant differences in the levels of thrombospondin mRNA and protein between capillary and aortic endothelial cells. Transforming growth factor-beta-1 treatment of normal endothelial cells increases steady-state levels of thrombospondin mRNA and protein and results in extensive deposition of thrombospondin into the extracellular matrix. In contrast, transforming growth factor-beta-1 has little effect on thrombospondin levels in the tumorigenic endothelial cell lines. In view of our earlier finding that contact between endothelial cells and mural cells generates activated transforming growth factor-beta-1, and the fact that thrombospondin is present in a fibrillar network around vascular structures in vitro, we speculate that modulation of thrombospondin production and distribution by transforming growth factor-beta may be a physiological process to enjoin stabilization of vessels and cessation of vessel growth.

scholarly journals Transforming Growth Factor-Beta and Matrix Metalloproteinases: Functional Interactions in Tumor Stroma-Infiltrating Myeloid Cells

2014 ◽  
Vol 2014 ◽  
pp. 1-14 ◽  
Author(s):  
Jelena Krstic ◽  
Juan F. Santibanez
Keyword(s):  
Growth Factor ◽  
Matrix Metalloproteinases ◽  
Cancer Cells ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Tumor Stroma ◽  
System Response ◽  
Health And Disease ◽  
Growth Factor Beta ◽  
Tumor Growth And Metastasis

Transforming growth factor-beta (TGF-β) is a pleiotropic factor with several different roles in health and disease. In tumorigenesis, it may act as a protumorigenic factor and have a profound impact on the regulation of the immune system response. Matrix metalloproteinases (MMPs) are a family that comprises more than 25 members, which have recently been proposed as important regulators acting in tumor stroma by regulating the response of noncellular and cellular microenvironment. Tumor stroma consists of several types of resident cells and infiltrating cells derived from bone marrow, which together play crucial roles in the promotion of tumor growth and metastasis. In cancer cells, TGF-βregulates MMPs expression, while MMPs, produced by either cancer cells or residents’ stroma cells, activate latent TGF-βin the extracellular matrix, together facilitating the enhancement of tumor progression. In this review we will focus on the compartment of myeloid stroma cells, such as tumor-associated macrophages, neutrophils, and dendritic and mast cells, which are potently regulated by TGF-βand produce large amounts of MMPs. Their interplay and mutual implications in the generation of pro-tumorigenic cancer microenvironment will be analyzed.

scholarly journals Heterogeneity of subsets in glioblastoma mediated by Smad3 palmitoylation

Oncogenesis ◽  
2021 ◽  
Vol 10 (10) ◽  
Author(s):  
Xiaoqing Fan ◽  
Junqi Fan ◽  
Haoran Yang ◽  
Chenggang Zhao ◽  
Wanxiang Niu ◽  
...  
Keyword(s):  
Growth Factor ◽  
Signaling Pathway ◽  
Transforming Growth Factor Beta ◽  
Cell Biology ◽  
Transforming Growth Factor ◽  
Hypoxia Inducible Factor ◽  
Stem Cell Biology ◽  
Isocitrate Dehydrogenase 1 ◽  
Hypoxia Inducible Factor 1 ◽  
Growth Factor Beta

AbstractGlioblastoma (GBM) is the most common and deadly of the primary intracranial tumors and is comprised of subsets that show plasticity and marked heterogeneity, contributing to the lack of success in genomic profiling to guide development of precision medicine for these tumors. In this study, a mutation in isocitrate dehydrogenase 1 was found to suppress the transforming growth factor-beta signaling pathway and E2F4 interacted with Smad3 to inhibit expression of mesenchymal markers. However, palmitoylation of Smad3 mediated by palmitoyltransferase ZDHHC19 promoted activation of the transforming growth factor-beta signaling pathway, and its interaction with EP300 promoted expression of mesenchymal markers in the mesenchymal subtype of GBM. Smad3 and hypoxia-inducible factor 1-alpha may be important molecular targets for treatment of glioma because they appear to coordinate the basic aspects of cancer stem cell biology.

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