Transforming growth factor (TGF)-β is a group of cytokines with anti-inflammatory effects in the TGF family, which participates in the development of stress and depression-related mechanisms, and plays roles in the regulation of inflammatory response in depression and the recovery of various cytokine imbalances. The core symptoms of depression is associated with TGF-β level, and the psychological symptoms of depression are related to TGF-β gene polymorphism. Various antidepressants may up-regulate TGF-β level through the complex interaction between neurotransmitters and inflammatory factors, inhibiting inflammatory response and regulating cytokine imbalance to improve depressive symptoms. Studies have shown that recombinant TGF-β1 protein has beneficial effects in mouse depression models, indicating TGF-β1 might be a potential therapeutic target for depression and nasal sprays having the advantage of being fast acting delivery method. This article reviews the research progress on dynamic changes of TGF-β level before and after depression treatment and the application of TGF-β level as an indicator for the improvement of depressive symptoms. We provide ideas for the development of new antidepressants and for the evaluation of the treatment efficacy in depression.
Animals ; Mice ; Transforming Growth Factor beta/metabolism* ; Transforming Growth Factor beta1 ; Depression ; Cytokines ; Antidepressive Agents/therapeutic use* ; Transforming Growth Factors

OBJECTIVETo explore the possible effect of transforming growth factor-beta(1) (TGF -beta(1)) on the development of renal fibrosis in human mesengial proliferative glomerulonephritis (MsPGN).

METHODSImmunohistochemistry method, sirius red staining polarization microscopy and the computer imaging analysis system were used to detect the expression of TGF-beta(1), the distribution of collagen I, collagen III and collagen IV.

RESULTIn MsPGN with renal fibrosis, collagen IV was increased markedly,and collagen I and collagen III appeared in the expanded mesengial matrix abnormally. Collagen III and collagen IV were increased markedly in tubulointerstitium. TGF-beta(1) expression was positively correlated with the expression of collagen I, collagen III and collagen IV in tubulointerstitium (r=0.82 0.92,P<0.01), and negatively correlated with I/III, I/IV and III/IV (r=-0.83,-0.92, P<0.001).

CONCLUSIONAbnormal increase of TGF-beta(1) may be one of the important factors associated with glomerular sclerosis and tubulointerstitial fibrosis through the increment and abnormal distribution of collagen I, collagen III and collagen IV.

Collagen ; analysis ; Fibrosis ; Glomerulonephritis, Membranoproliferative ; metabolism ; pathology ; Humans ; Immunohistochemistry ; Kidney ; pathology ; Transforming Growth Factor beta ; analysis ; Transforming Growth Factor beta1

OBJECTIVE: To investigate the effect of TGF-β1 on Shh signaling pathway during the transformation of meningeal fibroblasts into myofibroblasts. METHODS: Primary meningeal fibroblasts were isolated from neonatal (24 h) SD rats and purified using type Ⅳ collagenase. The isolated cells were treated with 10 ng/mL TGF-β1 alone or in combination with 20 μmol/L SB-431542 (a TGF-β1 receptor inhibitor) for 72 h, and the changes in proliferation and migration abilities of the fibroblasts were assessed with CCK-8 assay and cell scratch test. The expression of fibronectin (Fn) was detected with immunofluorescence assay, and Western blotting was performed to examine the expressions of Fn, α-SMA and Shh protein in the cells; the expression of Shh mRNA was detected with real-time fluorescence quantitative PCR. RESULTS: TGF-β1 treatment obviously enhanced the proliferation and migration of primary meningeal fibroblasts (P < 0.05), and promoted the transformation of meningeal fibroblasts into myofibroblasts and the secretion of Fn (P < 0.05). TGF-β1 treatment also upregulated the expression of Shh at both protein and mRNA levels (P < 0.05). Treatment with SB-431542 partially blocked the effect of TGF-β1 on the transformation of meningeal fibroblasts (P < 0.05). CONCLUSION TGF-β1 can induce the transformation of meningeal fibroblasts into myofibroblasts by up-regulating Shh expression in Sonic Hedgehog signaling pathway.
Animals ; Fibroblasts/metabolism* ; Hedgehog Proteins ; Myofibroblasts/metabolism* ; Rats ; Rats, Sprague-Dawley ; Transforming Growth Factor beta1/metabolism*

Humans ; Pulmonary Fibrosis ; metabolism ; pathology ; Signal Transduction ; physiology ; Transforming Growth Factor beta1 ; metabolism ; Wound Healing ; physiology

Chronic rhinosinusitis is a common health problem of otorhinolaryngology head and neck surgery, and is characterized by persistent inflammation of the nasal and paranasal mucosal linings. In recent years, tissue remodeling has been demonstrated to play an important role in the development of chronic rhinosinusitis, and furthermore transforming growth factor-beta1 (TGF-beta1) may play a pivotal role in this progress. This review will summarize the current knowledge on the roles of tissue remodeling in chronic rhinosinusitis, therefore to offer reference to the research and help to make diagnosis and give treatment for this disease.
Airway Remodeling ; Chronic Disease ; Humans ; Inflammation ; Sinusitis ; metabolism ; pathology ; Transforming Growth Factor beta1 ; metabolism

Objective: miR-663a has been reported to be downregulated by X-ray irradiation and participates in radiation-induced bystander effect via TGF-β1. The goal of this study was to explore the role of miR-663a during radiation-induced Epithelium-to-mesenchymal transition (EMT). Methods: TGF-β1 or IR was used to induce EMT. After miR-663a transfection, cell migration and cell morphological changes were detected and the expression levels of miR-663a, TGF-β1, and EMT-related factors were quantified. Results: Enhancement of cell migration and promotion of mesenchymal changes induced by either TGF-β1 or radiation were suppressed by miR-663a. Furthermore, both X-ray and carbon ion irradiation resulted in the upregulation of TGF-β1 and downregulation of miR-663a, while the silencing of TGF-β1 by miR-663a reversed the EMT process after radiation. Conclusion Our findings demonstrate an EMT-suppressing effect by miR-663a via TGF-β1 in radiation-induced EMT.
Down-Regulation ; Epithelial-Mesenchymal Transition ; Epithelium/metabolism* ; MicroRNAs/metabolism* ; Transforming Growth Factor beta1/pharmacology*

As a crucial regulatory molecule in the context of vascular stenosis, transforming growth factor-β (TGF-β), plays a pivotal role in its initiation and progression. TGF-β, a member of the TGF-β superfamily, can bind to the TGF-β receptor and transduce extracellular to intracellular signals through canonical Smad dependent or noncanonical signaling pathways to regulate cell growth, proliferation, differentiation, and apoptosis. Restenosis remains one of the most challenging problems in cardiac, cerebral, and peripheral vascular disease worldwide. The mechanisms for occurrence and development of restenosis are diverse and complex. The TGF-β pathway exhibits diversity across various cell types. Hence, clarifying the specific roles of TGF-β within different cell types and its precise impact on vascular stenosis provides strategies for future research in the field of stenosis.
Humans ; Transforming Growth Factor beta/metabolism* ; Constriction, Pathologic ; Signal Transduction ; Cell Differentiation ; Vascular Diseases ; Transforming Growth Factors ; Transforming Growth Factor beta1

OBJECTIVETo probe into periostin's role in the pathological mechanism of hyperplasic scars, by examining the expression of periostin in hyperplasic scar tissues. To investigate the correlations between periostin and TGF-beta1, TGF-beta R I, TGF-beta R II.

METHODSRT-PCR was used to assess the mRNA expression levels of TGF-beta1, TGF-beta R I, TGF-beta R II in three kinds of tissues, which are keloid (K), hypertrophic scar (HS) and normal skin (SK). The protein expression of periostin was measured with Western blotting.

RESULTSThe mRNA level of periostin in K was higher than that in SK. The mRNA expression of TGF-beta1 in K was higher than that in HS and SK. The mRNA level of TGF-beta R I in K was higher than that in HS and SK. The significances above all was at P < 0.01. The protein expression level of periostin in HS increased, compared with that in SK (P < 0.05). Periostin was related to TGF-beta1 positively (P <0.01).

CONCLUSIONSThe periostin's expression is increased in keloids. Periostin is a cicatrix specific gene. Periostin appears to play an important role in the formation of keloids, which is related to TGF-beta1 closely.

Adult ; Cell Adhesion Molecules ; metabolism ; Cicatrix, Hypertrophic ; metabolism ; pathology ; Female ; Humans ; Keloid ; metabolism ; pathology ; Male ; Receptors, Transforming Growth Factor beta ; metabolism ; Transforming Growth Factor beta1 ; metabolism

OBJECTIVETo investigate the functions of human periodontal myofibroblast (MFB) in vitro.

METHODSHuman periodontal fibroblast (hPDLFs) was cultured and induced to MFB by transforming growth factor-β1 (TGF-β1). MFB was denoted as the experimental group, whereas the hPDLFs was the control group. The groups were continuously cultured and harvested at 0, 12, 24, 48, and 72 h. The MFB marker α-smooth muscle actin (α-SMA) was examined by immunocytochemistry. The expression of fibronectin (FN) between MFB was examined by immunocytochemistry to detect the MFB contact relationship. The mRNA expression levels of α-SMA, collagen (Col) I, and Col III were measured by reverse transcription-polymerase chain reaction (RT-PCT) to analyze extracellular matrix secretion. The protein expression levels of α-SMA and Col I were also assessed by Western blot.

RESULTSThe experimental group had significantly higher α-SMA expression than the control group at 0 h (P < 0.001). A positive expression of FN was found between MFB. The experimental group had significantly higher expression levels of Col I and Col III than the control group at 24 h (P < 0.001).

CONCLUSIONHuman periodontal MFB presents a continuous, high expression of α-SMA. MFB could interact through FN. MFB is significantly capable of extracellular matrix secretion.

Actins ; Epithelial Cells ; Extracellular Matrix ; Fibroblasts ; Fibronectins ; Humans ; Jaw ; metabolism ; Myofibroblasts ; Transforming Growth Factor beta1

This study explored the usefulness of two-dimensional shear wave elastography (2D-SWE) in the early assessment of corpora cavernosa fibrosis (CCF). New Zealand male rabbits were randomly assigned to an experimental group or a control group. Recombinant human transforming growth factor beta 1 (TGF-β1) was injected into the dorsal penis tissue of rabbits in the experimental group. Conventional ultrasound and 2D-SWE examinations were performed before and 20 days after injection. Penile histological analysis was performed by hematoxylin-eosin staining, sirius red staining, and immunohistochemistry. Measurement of 2D-SWE examination results was performed using shear wave elastography quantitative measurement (SWQ). Histological analysis outcomes were the proportion of smooth muscle cells (SMCs), collagen fibers (CFs), collagen type I (Col I), and collagen type III (Col III), as well as the SMCs/CFs ratio, measured by sirius red staining. Other histological analysis outcomes were the positive area proportion (PAP) of TGF-β1 (PAP_T), fibronectin (PAP_F), and Col III (PAP_C), measured by immunohistochemistry. After recombinant human TGF-β1 injection, SWQ was higher in the experimental group than that in the control group (P < 0.001); however, there were no differences in conventional ultrasound results. There were significant differences in histological outcomes between the two groups (all P < 0.05). These results indicated that 2D-SWE was superior for identifying early histological changes in CCF.
Animals ; Elasticity Imaging Techniques/methods* ; Fibrosis ; Male ; Penis/pathology* ; Rabbits ; Transforming Growth Factor beta1/metabolism*