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Embryology, Anatomy, and Physiology of the Prostate
Published in Karl H. Pang, Nadir I. Osman, James W.F. Catto, Christopher R. Chapple, Basic Urological Sciences, 2021
Growth factors, suppressors, and signallingEGF (epidermal growth factor), TGF-α (transforming growth factor alpha), and bFGF (basic fibroblast growth factor) − stimulatory growth factors involved in upregulating gene expression.TGF-β (transforming growth factor beta) − inhibitory.IGF (insulin-like growth factor) − required in prostate proliferation, but levels do not drive it.
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].
Regenerative Medicine in Pain Management
Published in Sahar Swidan, Matthew Bennett, Advanced Therapeutics in Pain Medicine, 2020
Sharon McQuillan, Rafael Gonzalez
Transforming growth factor beta (TGF-β) controls many functions in the cellular environment, including growth, propagation, differentiation, and apoptosis. TGF-β possesses both powerful immunosuppressive and neuromodulatory properties. It is thought that TGF-β may reduce chronic pain by inhibiting the activation and propagation of nerve-injury-induced microglia and astrocytes.26 TGF-β also decreases the secretion of pro-inflammatory cytokines. However, the mechanisms of TGF-β inhibition of neuropathic as well as chronic pain need further elucidation.26–28
Activin A backs-up TGF-ß to promote regulatory T cells
Published in OncoImmunology, 2021
Mara De Martino, Camille Daviaud, Claire Vanpouille-Box
Transforming Growth Factor-beta (TGFβ) is a potent immunosuppressive cytokine of the tumor microenvironment (TME) that promote the conversion of naïve CD4 + T cells into CD4 + FoxP3 + T cells (Treg). TGFβ is secreted as an inactivated form in the extracellular matrix awaiting for external stimuli to unleash itself from the latency-associated peptide (LAP). Reactive oxygen species (ROS) generated by radiation therapy (RT) modify the backbone of the LAP-TGFβ complex to release the active cytokine. Consequently, the increase bioavailability of TGFβ within the TME of an irradiated tumor could be responsible for the increase representation of Treg. However, evidence challenge the role of TGFβ in Treg expansion post RT with two publications reporting no effect on Treg representation despite TGFβ inhibition in an irradiated melanoma tumor model2 and in peripheral blood of some metastatic breast cancer patients receiving focal RT with fresolimumab, a human TGFβ blocking antibody.3
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].
Altered Immunity in Endometriosis: What Came First?
Published in Immunological Investigations, 2018
Milena Králíčková, Ludek Fiala, Petr Losan, Pavel Tomes, Vaclav Vetvicka
Transforming growth factor-beta 1 (TGF-β1), an essential growth factor, is responsible for regulating cell proliferation, differentiation, angiogenesis, and immune responses. TGF-β is abundantly and differentially expressed in the endometrium, most likely under hormonal control. The increasing evidences indicate that TGF-β1 expression is high in endometriotic lesions. Many mechanisms must contribute to the development of endometriosis and TGF-β1 was hypothesized to play a key role in endometriotic lesion formation (Omwandho et al., 2010) (Hull et al., 2012). Levels of all three TGF-βs are increased around menstruation, with particular high levels of TGF-β3 in postmenstrual period; it is hypothesized that they might participate in postmenstrual regeneration of endometrium (Omwandho et al., 2010). In addition, TGF-β1 increased the concentration of ID1 mRNA and the VEGF-A-ID1 axis was confirmed by the use of siRNA (Young et al., 2015). The study suggested that ID inhibitors might be beneficial in endometriosis treatment (Fong et al., 2004).