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Cells
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Mechanisms of TGF-β Signaling in Disease Progression
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Mechanisms of TGF-β Signaling in Disease Progression

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell Signaling".

Deadline for manuscript submissions: closed (10 February 2023) | Viewed by 5606

Special Issue Editors

Dr. Hong-Jian Zhu

E-Mail Website
Guest Editor
Department of Surgery, The University of Melbourne, Parkville 3050, Australia
Interests: cytokine/growth factor signalling; cancer biology; exosomes; cancer immunology
Dr. Rodney Luwor

E-Mail Website
Guest Editor
Department of Surgery, University of Melbourne, Parkville 3050, Australia
Interests: brain tumor progression and signaling
Dr. Jingyi Sheng

E-Mail Website
Guest Editor
Biological and Medical Nanotechnology Group, Southeast University, Nanjing, China
Interests: cancer immunology-TGF-β; nanomedicine; magnetic nanomaterials
Dr. Lin Liu

E-Mail Website
Guest Editor
The Walter and Eliza Hall Institute of Medical Research, Parkville, VIC 3052, Australia
Interests: TGF-β signaling; exosome; TNF signaling; cell death; ADP ribosylation

Special Issue Information

Dear Colleagues,

The Transforming Growth Factor-beta (TGF-β) superfamily is made up a of large number of secreted pleiotropic growth factors that regulate many processes involved in development, homeostasis of tissue function and repair, immune response and regulation, vasculature formation and muscle growth and maintenance. Due to its diverse range of functions, not surprisingly, dysregulation of signaling of the TGF-β superfamily results in a multitude of diseases including cancer, fibrosis, osteoarthritis, autoimmunity, rheumatoid arthritis, diabetes mellitus, multiple sclerosis, atherosclerosis, asthma, inflammatory bowel disease, glomerulonephritis, vascular disease, motor neuron disease and muscle atrophy and cachexia. However, the critical spatiotemporal mechanisms utilized by TGF-β to drive this multitude of pathological conditions and, importantly, how these mechanisms can be reversed therapeutically are not completely understood.

This Special Issue welcomes original research papers or focused reviews elucidating key and novel mechanistic regulation of TGF-β signaling involved in disease progression. It will also include articles that discuss the possible improvement of current therapeutic strategies targeting TGF-β signaling that are currently under investigation. This Special Issue aims to discover critical knowledge of TGF-β biology, which will underpin novel and improved therapeutic interventions targeting TGF-β signaling and activity.

Dr. Hong-Jian Zhu
Dr. Rodney Luwor
Dr. Jingyi Sheng
Dr. Lin Liu
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • TGF-β
  • TGF-β signaling
  • mechanistic regulation
  • diseases
  • treatment

Published Papers (3 papers)

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Research

21 pages, 4859 KiB  
Article
Activin and BMP Signalling in Human Testicular Cancer Cell Lines, and a Role for the Nucleocytoplasmic Transport Protein Importin-5 in Their Crosstalk
by Karthika Radhakrishnan, Michael Luu, Josie Iaria, Jessie M. Sutherland, Eileen A. McLaughlin, Hong-Jian Zhu and Kate L. Loveland
Cells 2023, 12(7), 1000; https://doi.org/10.3390/cells12071000 - 24 Mar 2023
Viewed by 1642
Abstract
Testicular germ cell tumours (TGCTs) are the most common malignancy in young men. Originating from foetal testicular germ cells that fail to differentiate correctly, TGCTs appear after puberty as germ cell neoplasia in situ cells that transform through unknown mechanisms into distinct seminoma [...] Read more.
Testicular germ cell tumours (TGCTs) are the most common malignancy in young men. Originating from foetal testicular germ cells that fail to differentiate correctly, TGCTs appear after puberty as germ cell neoplasia in situ cells that transform through unknown mechanisms into distinct seminoma and non-seminoma tumour types. A balance between activin and BMP signalling may influence TGCT emergence and progression, and we investigated this using human cell line models of seminoma (TCam-2) and non-seminoma (NT2/D1). Activin A- and BMP4-regulated transcripts measured at 6 h post-treatment by RNA-sequencing revealed fewer altered transcripts in TCam-2 cells but a greater responsiveness to activin A, while BMP4 altered more transcripts in NT2/D1 cells. Activin significantly elevated transcripts linked to pluripotency, cancer, TGF-β, Notch, p53, and Hippo signalling in both lines, whereas BMP4 altered TGF-β, pluripotency, Hippo and Wnt signalling components. Dose-dependent antagonism of BMP4 signalling by activin A in TCam-2 cells demonstrated signalling crosstalk between these two TGF-β superfamily arms. Levels of the nuclear transport protein, IPO5, implicated in BMP4 and WNT signalling, are highly regulated in the foetal mouse germline. IPO5 knockdown in TCam-2 cells using siRNA blunted BMP4-induced transcript changes, indicating that IPO5 levels could determine TGF-β signalling pathway outcomes in TGCTs. Full article
(This article belongs to the Special Issue Mechanisms of TGF-β Signaling in Disease Progression)
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14 pages, 46944 KiB  
Article
NFATc1 Regulation of Dexamethasone-Induced TGFB2 Expression Is Cell Cycle Dependent in Trabecular Meshwork Cells
by Mark S. Filla, Jennifer A. Faralli, Caleigh R. Dunn, Haania Khan and Donna M. Peters
Cells 2023, 12(3), 504; https://doi.org/10.3390/cells12030504 - 03 Feb 2023
Cited by 1 | Viewed by 1593
Abstract
Although elevated TGFβ2 levels appear to be a causative factor in glaucoma pathogenesis, little is known about how TGFβ2 expression is regulated in the trabecular meshwork (TM). Here, we investigated if activation of the cytokine regulator NFATc1 controlled transcription of TGFβ2 in human [...] Read more.
Although elevated TGFβ2 levels appear to be a causative factor in glaucoma pathogenesis, little is known about how TGFβ2 expression is regulated in the trabecular meshwork (TM). Here, we investigated if activation of the cytokine regulator NFATc1 controlled transcription of TGFβ2 in human TM cells by using dexamethasone (DEX) to induce NFATc1 activity. The study used both proliferating and cell cycle arrested quiescent cells. Cell cycle arrest was achieved by either cell–cell contact inhibition or serum starvation. β-catenin staining and p21 and Ki-67 nuclear labeling were used to verify the formation of cell–cell contacts and activity of the cell cycle. NFATc1 inhibitors cyclosporine A (CsA) or 11R-VIVIT were used to determine the role of NFATc1. mRNA levels were determined by RT-qPCR. DEX increased TGFβ2 mRNA expression by 3.5-fold in proliferating cells but not in quiescent cells or serum-starved cells, and both CsA and 11R-VIVIT inhibited this increase. In contrast, the expression of other DEX/NFATc1-induced mRNAs (myocilin and β3 integrin) occurred regardless of the proliferative state of the cells. These studies show that NAFTc1 regulates TGFβ2 transcription in TM cells and reveals a previously unknown connection between the TM cell cycle and modulation of gene expression by NFATc1 and/or DEX in TM cells. Full article
(This article belongs to the Special Issue Mechanisms of TGF-β Signaling in Disease Progression)
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19 pages, 6222 KiB  
Article
Alpinetin Suppresses Effects of TGF-β1 on Stimulating the Production and Organization of Fibrotic Markers in Human Primary Dermal Fibroblasts
by Nitwara Wikan, Saranyapin Potikanond and Wutigri Nimlamool
Cells 2022, 11(17), 2731; https://doi.org/10.3390/cells11172731 - 01 Sep 2022
Cited by 3 | Viewed by 1486
Abstract
Overgrowths of dermal fibroblasts and myofibroblast phenoconversion in response to TGF-β stimulation are the hallmarks of skin fibrosis. Constitutive activation of dermal fibroblasts by TGF-β induces the excessive production of extracellular matrix as well as certain key intracellular proteins which form a complex [...] Read more.
Overgrowths of dermal fibroblasts and myofibroblast phenoconversion in response to TGF-β stimulation are the hallmarks of skin fibrosis. Constitutive activation of dermal fibroblasts by TGF-β induces the excessive production of extracellular matrix as well as certain key intracellular proteins which form a complex interaction network. Current therapies include monoclonal anti-bodies against TGF-β and surgery, but these treatments generally elicit a limited effect on certain kinds of skin fibrosis. In the current study, we investigated the effects of alpinetin (AP) on human primary dermal fibroblasts (HPDFs) stimulated with TGF-β1. Results demonstrated that AP exhibited strong inhibitory effects on TGF-β1-induced proliferation and migration of HPDFs. AP also inhibited TGF-β1-induced morphological changes of fibroblasts to myofibroblasts, and these were found to be from its effects on blocking actin stress fiber formation and organization. The expression of major fibrotic molecules including α-SMA and type I collagen upon TGF-β1 stimulation was also inhibited by AP. In addition, AP attenuated TGF-β1-induced production and organization of vimentin, β-catenin, and N-cadherin, important for the pathophysiology of skin fibrosis. In conclusion, we revealed that AP has an ability to reverse the fibrotic effects of TGF-β1 at the cellular level, and this discovery suggests the therapeutic potential of AP for skin fibrosis. Full article
(This article belongs to the Special Issue Mechanisms of TGF-β Signaling in Disease Progression)
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