scholarly journals The role of TGF-β2 in cartilage development and diseases

2021 ◽  
Vol 10 (8) ◽  
pp. 474-487
Author(s):  
Mengmeng Duan ◽  
Qingxuan Wang ◽  
Yang Liu ◽  
Jing Xie
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor ◽  
Vital Role ◽  
Cartilage Defects ◽  
Cartilage Development ◽  
Physiological Processes ◽  
Cartilage Diseases ◽  
Autologous Mesenchymal Stem Cells ◽  
Tgf Β1

Transforming growth factor-beta2 (TGF-β2) is recognized as a versatile cytokine that plays a vital role in regulation of joint development, homeostasis, and diseases, but its role as a biological mechanism is understood far less than that of its counterpart, TGF-β1. Cartilage as a load-resisting structure in vertebrates however displays a fragile performance when any tissue disturbance occurs, due to its lack of blood vessels, nerves, and lymphatics. Recent reports have indicated that TGF-β2 is involved in the physiological processes of chondrocytes such as proliferation, differentiation, migration, and apoptosis, and the pathological progress of cartilage such as osteoarthritis (OA) and rheumatoid arthritis (RA). TGF-β2 also shows its potent capacity in the repair of cartilage defects by recruiting autologous mesenchymal stem cells and promoting secretion of other growth factor clusters. In addition, some pioneering studies have already considered it as a potential target in the treatment of OA and RA. This article aims to summarize the current progress of TGF-β2 in cartilage development and diseases, which might provide new cues for remodelling of cartilage defect and intervention of cartilage diseases.

Abstract 17285: A Selective Transforming Growth Factor-β and Growth Differentiation Factor-15 Ligand Trap Attenuates Pulmonary Hypertension

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Lai-Ming Yung ◽  
Samuel D Paskin-Flerlage ◽  
Ivana Nikolic ◽  
Scott Pearsall ◽  
Ravindra Kumar ◽  
...  
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Type I ◽  
Rna Seq ◽  
Differentiation Factor ◽  
Group I ◽  
Tgf Β1

Introduction: Excessive Transforming Growth Factor-β (TGF-β) signaling has been implicated in pulmonary arterial hypertension (PAH), based on activation of TGF-β effectors and transcriptional targets in affected lungs and the ability of TGF-β type I receptor (ALK5) inhibitors to improve experimental PAH. However, clinical use of ALK5 inhibitors has been limited by cardiovascular toxicity. Hypothesis: We tested whether or not selective blockade of TGF-β and Growth Differentiation Factor (GDF) ligands using a recombinant TGFβ type II receptor extracellular domain Fc fusion protein (TGFBRII-Fc) could impact experimental PAH. Methods: Male SD rats were injected with monocrotaline (MCT) and received vehicle or TGFBRII-Fc (15 mg/kg, twice per week, i.p.). C57BL/6 mice were treated with SU-5416 and hypoxia (SUGEN-HX) and received vehicle or TGFBRII-Fc. RNA-Seq was used to profile transcriptional changes in lungs of MCT rats. Circulating levels of GDF-15 were measured in 241 PAH patients and 41 healthy controls. Human pulmonary artery smooth muscle cells were used to examine signaling in vitro . Results: TGFBRII-Fc is a selective ligand trap, inhibiting the ability of GDF-15, TGF-β1, TGF-β3, but not TGF-β2 to activate SMAD2/3 in vitro . In MCT rats, prophylactic treatment with TGFBRII-Fc normalized expression of TGF-β transcriptional target PAI-1, attenuated PAH and vascular remodeling. Delayed administration of TGFBRII-Fc in rats with established PAH at 2.5 weeks led to improved survival, decreased PAH and remodeling at 5 weeks. Similar findings were observed in SUGEN-HX mice. No valvular abnormalities were found with TGFBRII-Fc treatment. RNA-Seq revealed GDF-15 to be the most highly upregulated TGF-β ligand in the lungs of MCT rats, with only modest increases in TGF-β1 and no change in TGF-β2/3 observed, suggesting a dominant role of GDF-15 in the pathophysiology of this model. Plasma levels of GDF-15 were significantly increased in patients with diverse etiologies of WHO Group I PAH. Conclusions: These findings demonstrate that a selective TGF-β/GDF-15 trap attenuates experimental PAH, remodeling and mortality, without causing valvulopathy. These data highlight the potential role of GDF-15 as a pathogenic molecule and therapeutic target in PAH.

scholarly journals Evidence for a Role of Transforming Growth Factor (TGF)-β1 in the Induction of Postglomerular Albuminuria in Diabetic Nephropathy

Diabetes ◽  
2007 ◽  
Vol 56 (2) ◽  
pp. 380-388 ◽  
Author(s):  
Leileata M. Russo ◽  
Elisabetta del Re ◽  
Dennis Brown ◽  
Herbert Y. Lin
Keyword(s):  
Diabetic Nephropathy ◽  
Growth Factor ◽  
Transforming Growth Factor ◽  
Tgf Β1

scholarly journals ROLE OF HUMAN DISKOIDIN DOMAIN RECEPTOR 1 IN THE PROGRESSION OF CHRONIC PYELONEPHRITIS IN CHILDREN

2017 ◽  
pp. 5-20
Author(s):  
N. N. Kaladze ◽  
E. I. Slobodyan
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor ◽  
Inverse Correlation ◽  
Chronic Pyelonephritis ◽  
Clinical Form ◽  
Discoidin Domain Receptors ◽  
Collagen Receptors ◽  
Mediators Of Inflammation ◽  
Tgf Β1

The purpose: to evaluate the role of collagen receptors Human Discoidin Domain Receptors (DDR1) as mediators of inflammation, proliferation and fibrosis in children with chronic pyelonephritis (CP), to reveal their relationship to the clinical form of the disease and the characteristics of its flow. Materials and methods: The levels of DDR1, transforming growth factor (TGF-β1), insulin-like growth factor (IGF-1) in the serum, β2 - microglobulin ( β2- MG) in the serum and urine were identified during the study of 40 children, ages 6 to 16 with CP in a state of clinical and laboratory remission. Results: Clinical and laboratory remission HP was associated with significant increased levels of DDR1 sera from long ill patients with frequent exacerbations, as well as 2-3 degree of activity last exacerbation, with family history. Found a strong inverse correlation between the levels of DDR1 and IGF-1, and the line with TGF-β1 and β2-MG of blood and urine. In patients with obstructive HP DDR1 level was significantly higher than in patients with non-obstructive clinical form. Conclusions: Increased serum DDR1 shows the progression of kidney damage with active fibrogenesis and inflammation in certain categories of patients with CP in a state of clinical and laboratory remission.

scholarly journals CD4+CD25+ Regulatory T Cells Can Mediate Suppressor Function in the Absence of Transforming Growth Factor β1 Production and Responsiveness

2002 ◽  
Vol 196 (2) ◽  
pp. 237-246 ◽  
Author(s):  
Ciriaco A. Piccirillo ◽  
John J. Letterio ◽  
Angela M. Thornton ◽  
Rebecca S. McHugh ◽  
Mizuko Mamura ◽  
...  
Keyword(s):  
T Cells ◽  
Growth Factor ◽  
Regulatory T Cells ◽  
T Cell Activation ◽  
Transforming Growth Factor ◽  
Cell Contact ◽  
Suppressor Function ◽  
Tgf Β1

CD4+CD25+ regulatory T cells inhibit organ-specific autoimmune diseases induced by CD4+CD25−T cells and are potent suppressors of T cell activation in vitro. Their mechanism of suppression remains unknown, but most in vitro studies suggest that it is cell contact–dependent and cytokine independent. The role of TGF-β1 in CD4+CD25+ suppressor function remains unclear. While most studies have failed to reverse suppression with anti–transforming growth factor (TGF)-β1 in vitro, one recent study has reported that CD4+CD25+ T cells express cell surface TGF-β1 and that suppression can be completely abrogated by high concentrations of anti–TGF-β suggesting that cell-associated TGF-β1 was the primary effector of CD4+CD25+-mediated suppression. Here, we have reevaluated the role of TGF-β1 in CD4+CD25+-mediated suppression. Neutralization of TGF-β1 with either monoclonal antibody (mAb) or soluble TGF-βRII-Fc did not reverse in vitro suppression mediated by resting or activated CD4+CD25+ T cells. Responder T cells from Smad3−/− or dominant-negative TGF-β type RII transgenic (DNRIITg) mice, that are both unresponsive to TGF-β1–induced growth arrest, were as susceptible to CD4+CD25+-mediated suppression as T cells from wild-type mice. Furthermore, CD4+CD25+ T cells from neonatal TGF-β1−/− mice were as suppressive as CD4+CD25+ from TGF-β1+/+ mice. Collectively, these results demonstrate that CD4+CD25+ suppressor function can occur independently of TGF-β1.

Role of transforming growth factor-β1 (TGF-β1) in endotoxin-induced hepatic failure after extensive hepatectomy in rats

2005 ◽  
Vol 11 (1) ◽  
pp. 33-39 ◽  
Author(s):  
Noboru Yoshimoto ◽  
Shinji Togo ◽  
Toru Kubota ◽  
Nobuyuki Kamimukai ◽  
Shuji Saito ◽  
...  
Keyword(s):  
Growth Factor ◽  
Hepatic Failure ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Extensive Hepatectomy ◽  
Tgf Β1

Role of tumor-derived transforming growth factor-β1 (TGF-β1) in site-dependent tumorigenicity of murine ascitic lymphosarcoma

2005 ◽  
Vol 54 (9) ◽  
pp. 837-847 ◽  
Author(s):  
V. S. Thakur ◽  
B. Shankar ◽  
S. Chatterjee ◽  
S. Premachandran ◽  
K. B. Sainis
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Tgf Β1

scholarly journals Role of transforming growth factor-β1 (TGF-β1) in endotoxin-induced hepatic failure after extensive hepatectomy in rats

2005 ◽  
Vol 11 (1) ◽  
pp. 33-39 ◽  
Author(s):  
Noboru Yoshimoto ◽  
Shinji Togo ◽  
Toru Kubota ◽  
Nobuyuki Kamimukai ◽  
Shuji Saito ◽  
...  
Keyword(s):  
Growth Factor ◽  
Hepatic Failure ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Extensive Hepatectomy ◽  
Tgf Β1

scholarly journals Role of Transforming Growth Factor-β1 in Regulating Fetal-Maternal Immune Tolerance in Normal and Pathological Pregnancy

2021 ◽  
Vol 12 ◽  
Author(s):  
Dongyong Yang ◽  
Fangfang Dai ◽  
Mengqin Yuan ◽  
Yajing Zheng ◽  
Shiyi Liu ◽  
...  
Keyword(s):  
Growth Factor ◽  
Immune Tolerance ◽  
Immune Cells ◽  
Transforming Growth Factor ◽  
Immune Cell ◽  
Transforming Growth Factor Β ◽  
Normal Pregnancy ◽  
Cell Functions ◽  
Tgf Β1

Transforming growth factor-β (TGF-β) is composed of three isoforms, TGF-β1, TGF-β2, and TGF-β3. TGF-β1 is a cytokine with multiple biological functions that has been studied extensively. It plays an important role in regulating the differentiation of immune cells and maintaining immune cell functions and immune homeostasis. Pregnancy is a carefully regulated process. Controlled invasion of trophoblasts, precise coordination of immune cells and cytokines, and crosstalk between trophoblasts and immune cells play vital roles in the establishment and maintenance of normal pregnancy. In this systematic review, we summarize the role of TGF-β1 in regulating fetal-maternal immune tolerance in healthy and pathological pregnancies. During healthy pregnancy, TGF-β1 induces the production of regulatory T cells (Tregs), maintains the immunosuppressive function of Tregs, mediates the balance of M1/M2 macrophages, and regulates the function of NK cells, thus participating in maintaining fetal-maternal immune tolerance. In addition, some studies have shown that TGF-β1 is dysregulated in patients with recurrent spontaneous abortion or preeclampsia. TGF-β1 may play a role in the occurrence and development of these diseases and may be a potential target for the treatment of these diseases.

scholarly journals Optimizing Platelet-Rich Plasma (PRP) Injections: A Narrative Review

2020 ◽  
Vol 2 (1) ◽  
pp. e31-e47
Author(s):  
Chris Cherian ◽  
Gerard Malanga ◽  
Ken Mautner
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Platelet Rich Plasma ◽  
Vascular Endothelial ◽  
Potential Alternative ◽  
Activating Agent ◽  
Endothelial Growth Factor ◽  
Tgf Β1

Platelet-rich plasma (PRP) is an orthobiologic treatment that has gained popularity as a potential alternative treatment for various musculoskeletal conditions. The physiologic role of platelets in the healing cascade provides clarity regarding its potential as it releases various growth factors such as platelet-derived growth factor (PDGF), transforming growth factor beta-1 (TGF-β1), and vascular endothelial growth factor (VEGF). However, there are various characteristics of PRP treatments including platelet count, presence or absence of leukocytes and red blood cells, as well as the use of an activating agent that introduces heterogeneity among preparations. This aim of this article is to provide clarity, where available, regarding the optimal characteristics for PRP treatments regarding tendon and ligament injuries as well as articular and muscular pathology.

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