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TGF-Beta Super Family Signaling 3.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (30 June 2021) | Viewed by 5119

Special Issue Editor

Special Issue Information

Dear Colleagues,

This Special Issue is the continuation of our 2017 Special Issue “TGF-Beta Super Family Signaling”, and 2018 Special Issue "TGF-Beta Super Family Signaling 2.0”.

Our knowledge of this superfamily is quickly expanding into previously uncharted areas of biology and human pathogenesis. TGF-β superfamily members play pivotal roles throughout development and later in adult homeostasis to orchestrate complex processes. Consistent with their diversity of function, aberrant signaling by members of the TGF-β superfamily is associated with a wide range of human pathologies, including immune system compromise, cardiovascular and fibrotic diseases, aging processes, and, critically, cancer.

The goal of this Special Issue is to broaden the molecular understanding of the key roles of TGF-β superfamily members, including TGF-βs, nodal, activins, BMPs, and GDFs in pathophysiological processes.  The mechanisms of aberrations in this signaling pathway, which lead to human disease pathologies, will be especially highlighted.

Topics will include (but are not limited to) cancer biology, stem cell biology, cellular plasticity, RNA metabolism, inflammation, immune surveillance escape, stress response, tissue fibrosis, vasculature and tissue transformation (EndMT/EMT), tissue microenvironment dynamics, and therapeutic frontiers of TGF-β signaling.

Up-to-date review articles and experimental papers are all welcome. We look forward to your contributions.

Prof. Dr. Jun-ichi Hanai
Guest Editor

Manuscript Submission Information

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Keywords

  • Signaling crosstalk
  • EMT
  • EndoMT
  • Immune and inflammatory response
  • Stress response
  • Tissue morphogenesis and cellular plasticity
  • Oncogenic stem cells (cancer initiating cells)
  • Tissue microenvironment dynamics
  • Wound healing and Tissue fibrosis
  • Epigenetic regulation
  • RNA metabolism
  • Senescence/aging
  • Therapeutic frontiers

Published Papers (2 papers)

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Research

17 pages, 3079 KiB  
Article
MMP9 Differentially Regulates Proteins Involved in Actin Polymerization and Cell Migration during TGF-β-Induced EMT in the Lens
by Zi Zhen (Ginny) Liu, Aftab Taiyab and Judith A. West-Mays
Int. J. Mol. Sci. 2021, 22(21), 11988; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms222111988 - 05 Nov 2021
Cited by 7 | Viewed by 2190
Abstract
Fibrotic cataracts have been attributed to transforming growth factor-beta (TGF-β)-induced epithelial-to-mesenchymal transition (EMT). Using mouse knockout (KO) models, our laboratory has identified MMP9 as a crucial protein in the TGF-β-induced EMT process. In this study, we further revealed an absence of alpha-smooth muscle [...] Read more.
Fibrotic cataracts have been attributed to transforming growth factor-beta (TGF-β)-induced epithelial-to-mesenchymal transition (EMT). Using mouse knockout (KO) models, our laboratory has identified MMP9 as a crucial protein in the TGF-β-induced EMT process. In this study, we further revealed an absence of alpha-smooth muscle actin (αSMA) and filamentous-actin (F-actin) stress fibers in MMP9KO mouse lens epithelial cell explants (LECs). Expression analysis using NanoString revealed no marked differences in αSMA (ACTA2) and beta-actin (β-actin) (ACTB) mRNA between the lenses of TGF-β-overexpressing (TGF-βtg) mice and TGF-βtg mice on a MMP9KO background. We subsequently conducted a protein array that revealed differential regulation of proteins known to be involved in actin polymerization and cell migration in TGF-β-treated MMP9KO mouse LECs when compared to untreated controls. Immunofluorescence analyses using rat LECs and the novel MMP9-specific inhibitor, JNJ0966, revealed similar differential regulation of cortactin, FAK, LIMK1 and MLC2 as observed in the array. Finally, a reduction in the nuclear localization of MRTF-A, a master regulator of cytoskeletal remodeling during EMT, was observed in rat LECs co-treated with JNJ0966 and TGF-β. In conclusion, MMP9 deficiency results in differential regulation of proteins involved in actin polymerization and cell migration, and this in turn prevents TGF-β-induced EMT in the lens. Full article
(This article belongs to the Special Issue TGF-Beta Super Family Signaling 3.0)
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13 pages, 2398 KiB  
Article
SMA-10 Is a Non-Canonical Member of the TGF-β Sma/Mab Pathway and Immunity Regulator via the DAF-2 Insulin Receptor in Caenorhabditis elegans
by María Pilar de Lucas, Marta Jiménez, Paloma Sánchez-Pavón, Alberto G. Sáez and Encarnación Lozano
Int. J. Mol. Sci. 2021, 22(2), 638; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22020638 - 11 Jan 2021
Cited by 2 | Viewed by 2118
Abstract
Transforming growth factor β (TGF-β) signalling pathways are highly conserved across metazoa and play essential roles not only during development but also in adult tissue maintenance. Alterations of these pathways usually result in a plethora of pathologies. In the nematode Caenorhabditis elegans, [...] Read more.
Transforming growth factor β (TGF-β) signalling pathways are highly conserved across metazoa and play essential roles not only during development but also in adult tissue maintenance. Alterations of these pathways usually result in a plethora of pathologies. In the nematode Caenorhabditis elegans, the TGF-β Sma/Mab (small/male abnormal) pathway regulates various worm phenotypes such as body size, immune response, ageing, matricide and reproductive span. SMA-10 has been described as a positive modulator of worm body size through the TGF-β Sma/Mab pathway. To better understand if SMA-10 is a core component of the pathway, we use gene epistatic analysis to assess the contribution of SMA-10 to various phenotypes regulated by TGF-β Sma/Mab. We confirm that SMA-10 controls body size and find that it also affects the matricide and reproductive span of the nematodes. However, neither male tail formation (previously reported) nor ageing appeared altered. Lastly, although null sma-10 worms are more susceptible to Pseudomonas aeruginosa infections than wild-types, this response does not depend on TGF-β Sma/Mab but on the insulin receptor DAF-2. We also show that the expression of sma-10 in either hypodermis or intestine fully rescues the wild-type immune response. Our results contribute to understanding the role of SMA-10 as a context-dependent component of TGF-β Sma/Mab, and reveal a function of SMA-10 in immunity in association to the Insulin/insulin-like growth factor signalling (IIS) pathway. Full article
(This article belongs to the Special Issue TGF-Beta Super Family Signaling 3.0)
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