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Transformin Growth Factor-β
Published in Jason Kelley, Cytokines of the Lung, 2022
Transforming growth factor-β is an important immunomodulatory cytokine. In general, it enhances the functions of monocytic cells and suppresses functions mediated by lymphocytes (Roberts and Sporn, 1990). It is an extremely potent immunomodulator that exerts complex actions on many limbs of the immune and hematopoietic systems. In general, TGF-β1 and TGF-β2 inhibit both T and B lymphocytes and augment monocyte functions. It has been pointed out that, as an inhibitor of lymphocytes, TGF-β is 10,000-times more potent than the drug cyclosporine (Kehrl et al., 1986; Roberts and Sporn, 1990). As a potent immunosuppressive agent, TGF-β inhibits IL-1-dependent lymphocyte proliferation (Wahl et al., 1988). It also blocks IL-2-mediated induction of IL-2 receptors on T cells, a critical amplification step in the T-cell response to antigen presentation (Kehrl et al., 1986). Immune functions modulated by TGF-β are summarized in Table 2. Although the dominant or most immediate effects of TGF-β are listed in the table, it is noteworthy that several of the functions listed can be bidirectionally modulated by TGF-β when such conditions as duration of exposure and concentration are taken into account.
Upper Urinary Tract Obstruction
Published in Karl H. Pang, Nadir I. Osman, James W.F. Catto, Christopher R. Chapple, Basic Urological Sciences, 2021
Tubulo-interstitial fibrosisMajor determinant of irreversible loss of renal function post-obstruction.7–14 days: fibroblast recruitment and diffuse accumulation of extracellular matrix (ECM).Mediated by transforming growth factor-β (TGF-β).
Microneedling
Published in Rubina Alves, Ramon Grimalt, Techniques in the Evaluation and Management of Hair Diseases, 2021
Rachita S. Dhurat, Sanober Burzin Daruwalla
The transforming growth factor beta (TGF-β) family forms a group of three isoforms, TGF-β1, TGF-β2, and TGF-β3. TGF-β1 inhibits hair growth through inhibiting keratinocyte growth, TGF-β2 induces catagen phase of murine and human hair follicles through inhibiting cell proliferation or inducing apoptosis of hair matrix keratinocytes and TGF-β3 has no effect on hair formation. TGF-β3 is responsible for inducing epithelial cell adhesion [27].
Design and synthesis of thiazolidine-2,4-diones hybrids with 1,2-dihydroquinolones and 2-oxindoles as potential VEGFR-2 inhibitors: in-vitro anticancer evaluation and in-silico studies
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2022
Mohammed S. Taghour, Hazem Elkady, Wagdy M. Eldehna, Nehal M. El-Deeb, Ahmed M. Kenawy, Eslam B. Elkaeed, Aisha A. Alsfouk, Mohamed S. Alesawy, Ahmed M. Metwaly, Ibrahim. H. Eissa
Overexpression of the Bcl2 gene can inhibit the apoptotic cell death and partially the nonapoptotic cell death, which has a role in arrest of cell cycle. Meanwhile, overexpression of Bcl-xL enhances autophagic cell death60. Moreover, Survivin is a pro-survival protein that is overexpressed in many cancer cells in the G2-M phase. This protein has been linked to tumour progression control and resistance to cancer chemotherapeutics. Furthermore, the transforming growth factor (TGF) is one of various proteins that secreted by transformed cells and stimulate the growth of non-cancerous cells in addition to its role as initiators of the signalling pathway that suppresses the early development of cancer cells61. Dysregulation of TGF-β activation and signalling may result in apoptosis.
Impact of resolvin mediators in the immunopathology of diabetes and wound healing
Published in Expert Review of Clinical Immunology, 2021
David Shofler, Vikrant Rai, Sarah Mansager, Kira Cramer, Devendra K. Agrawal
Transforming growth factor-β (TGF- β) plays a crucial role in different phases of wound healing, particularly in the late-stage of wound healing, and functions as a wound-healing promoting factor [26]. Further, TGF-β1/Smads and TNF-α/NF-κB in macrophages and fibroblasts serve a crucial role in determining the rate and nature of wound healing. The findings of delayed wound healing due to impaired resolution of inflammation mediated by enhanced TNF-α/NF-κB activity through attenuated TGFβ/Smad signaling in diabetes further supports the role of TGF-β in modulating wound healing in diabetes [27]. Increased levels of TGF‐β1 with RvD1in in-vitro [28] and enhanced wound healing with a single injection of TGF β1 in enhancing wound healing in a rat’s tongue [29] support the notion of using RvD1 to enhance wound healing in diabetic wounds. The role of RvD1 in the resolution of inflammation is supported by the fact that RvD1 increases regulatory T (Treg) cell, increases anti-inflammatory macrophages and phagocytosis of apoptotic T cells leading to reduced apoptotic T-cell, and increases TGF-β expression [30]. Further, the findings of enhanced epithelial wound repair, inhibition of TGF-β-induced epithelial-mesenchymal transition, reduction of fibroproliferation and collagen production, and prevention of fibrosis by preventing the over–proliferation of fibroblasts with RvD1support the notion of using RvD1 in the late phase of wound healing [31–33]. Although some of these findings have been observed in different organ systems, the insights may still be valuable.
TGF-beta: a master immune regulator
Published in Expert Opinion on Therapeutic Targets, 2020
Christopher Larson, Bryan Oronsky, Corey A. Carter, Arnold Oronsky, Susan J. Knox, David Sher, Tony R. Reid
Transforming Growth Factor-Beta (TGF-β) is a diverse regulatory and fibrogenic protein with three isoforms, TGF-β1 (the most common), TGF-β2, and TGF-β3. TGF-β is secreted in a precursor form bound to a propeptide, cleaved by furin-type enzymes in the Golgi, transported to the extracellular matrix (ECM) in association with a latency associated peptide (LAP), and activated in the presence of diverse molecules such as thrombospondin-1, integrins, matrix metalloproteinases (MMPs), bone morphogenetic 1 (BMP-1) and reactive oxygen species (ROS) [1]. TGF-β impacts multiple processes including cell growth and differentiation, apoptosis, cell motility, extracellular matrix production, angiogenesis, and immune responsiveness [2–7]. These effects are very dependent upon context, including tumor hypoxia [8,9]. This pleiotropy results from activation of the TGF-β receptor, a heterodimeric complex composed of two transmembrane serine/threonine kinase receptors, TGF-βR1 and TGF-βR2 at the cell surface [10].