No abstract available.
Chitosan* ; Osteoblasts* ; Transforming Growth Factor beta1 ; Transforming Growth Factors*

The main cause of failure in glaucoma filtering surgery is obstruction of aqueous outflow due to subconjunctival fibrosis. Transforming growth factor-beta(TGF-beta) is known to be a growth factor for subconjunctival fibroblast. Recently, mannose-6-phosphate(M-6-P) is reported to be an inhibitor of TGF-beta activity. In this study, we evaluated the effects of TGF-betas and M-6-P on the proliferation of cultured subconjunctival fibroblast of white rabbit in vitro. Cell proliferation was determined by 3H-thymidine DNA incorporation method. TGF-beta1, 2, 3 all promoted proliferation of subconjunctival fibroblast in a concentration dependent fashion and the effect of TGF-beta1 was most prominent among 3 types. Low concentration (0.01mM) of M-6-P paradoxically increased cell proliferation, but with the concentration of 1.0mM, the inhibitory effects were varied in the range of 45% to 7%.
Cell Proliferation ; DNA ; Fibroblasts* ; Fibrosis ; Filtering Surgery ; Glaucoma ; Transforming Growth Factor beta ; Transforming Growth Factor beta1

BACKGROUND AND OBJECTIVES: Transforming growth factor-beta1 (TGF-beta1) is a multifunctional regulator of cellular differentiation, motility and growth. Loss of sensitivity to the growth inhibitory effects by TGF-beta1 plays important roles in neoplastic progression. So expression of TGF-beta1 has been described in several tumors, but little is known about the role of TGF-beta1 in neoplastic progression of human larynx. The aim of this study was to investigate the role of TGF-beta1 in the neoplastic progression of human larynx. MATERIALS AND METHODS: We evaluated the expression of TGF-beta1 using immunohistochemical study in 6 cases of normal laryngeal mucosa, 6 cases of laryngeal dysplasia, 20 cases of laryngeal carcinoma. RESULTS: The results were as follows: 1) Normal laryngeal mucosa has no expression of TGF-beta1. 2) The expression of TGF-beta was 16.7% in laryngeal dysplasia, 50.0% in laryngeal carcinoma. CONCLUSION: The TGF-beta1 expression rate was correlated to the progression of laryngeal lesions when compared to normal laryngeal mucosa, laryngeal dysplasia and laryngeal carcinoma.
Humans ; Laryngeal Mucosa* ; Larynx ; Transforming Growth Factor beta ; Transforming Growth Factor beta1

BACKGROUND: In vitro experimental studies have reported that transforming growth factor-beta1 (TGF-beta1) stimulates the production of alpha-smooth muscle actin (alpha-SMA) in porcine valves. However, the relation between TGF-beta1 and alpha-SMA in myxomatous valves has not been elucidated. METHODS: We classified 27 subjects into two groups: 1) myxomatous group (M:F=11:12, mean age=55+/-15 years) and 2) rheumatic group (M:F=3:1, mean age=41+/-17 years) according to preoperative echocardiographic and postoperative histologic findings. Twenty-seven valve specimens from the patients who underwent valve replacement were obtained. Tissue samples were analyzed by immunohistochemistry for TGF-beta1 and alpha-SMA. The positively stained areas were measured using an image analysis program (Image Pro-Plus 4.5), and then the TGF-beta1 volume fraction (TGF-VF) and alpha-SMA volume fraction (alpha-SMA-VF) were calculated. RESULTS: TGF-VF in myxomatous valves was higher than in rheumatic valves (2,759+/-2,294 vs 864+/-276, p=0.04). alpha-SMA-VF in myxomatous valves was higher than in rheumatic valves (4,122+/-2,275 vs 2,421+/-844, p=0.002). There was a significant correlation between TGF-beta1 and alpha-SMA in myxomatous valves (r=0.38, p=0.04). There was no significant correlation between TGF-beta1 and alpha-SMA in rheumatic valves (r=-0.50, p=0.67). CONCLUSIONS: TGF-beta1 and alpha-SMA may be related to the pathogenesis of myxomatous valves. The activation of TGF-beta1 might increase the expression of alpha-SMA in human myxomatous valves.
Actins ; Humans ; Immunohistochemistry ; Muscles ; Transforming Growth Factor beta1

The present study investigates the role of TGF-beta1 as one of possible etiologic factors of glaucoma by studying the effect of TGF-beta1 on the secretion of matrix metalloproteinase and tissue inhibitor of matrix metalloproteinase. The cultured samples of trabecular meshwork cells were treated with TGF-beta1 in concentrations of 0, 100, 1000 and 10000 pg/ml. The samples were analysed for the secretion of MMP2 and timp2 through electrophoresis, western blot and TGF-beta1 increased, the secretions of MMP2 and TIMP2 were not significantly changed after 24 hours. But the secretion of MMP2 was decreased while the secretion of TIMP2 was increased after 72 hours. The results suggest that TGFbeta1 may be one of the etilogic factors of glaucoma.
Blotting, Western ; Electrophoresis ; Glaucoma ; Trabecular Meshwork ; Transforming Growth Factor beta1

BACKGROUND: In our previous study, we demonstrated that transforming growth factor-beta 1 receptor II (TGF-beta1RII) may have a role in the formation of bullae. In this study, we investigated if expression of transforming growth factor-beta 1 (TGF-beta1) ligand was altered in a bullous lung tissue by immunohistochemical staining of bullous tissues from patients with primary spontaneous pneumothorax. MATERIAL AND METHOD: Bullous lung tissues were obtained from 36 patients with primary spontaneous pneumothorax, including 34 males and 2 females aged 14 to 38 years old. RESULT: Of the 36 patients, 19 were TGF-beta1 positive and 24 were transforming growth factor-beta 1 receptor II (TGF-beta1RII) positive. Among the 19 TGF-beta1 positives, 15 were also TGF-beta1RII positive, observation at high magnification showed that strong immunohistochemical stain was detected in the boundary region between the bullous and normal lung tissues. CONCLUSION: These results suggest that overexpression of TGF-beta1 may be involved in the formation of a bulla as well as the alteration of TGF-beta1RII expression. Further molecular studies are needed to elucidate the more detailed molecular mechanisms of the bulla formation.
Adult ; Female ; Humans ; Lung ; Male ; Pneumothorax* ; Transforming Growth Factor beta1*

As a common soft tissue disease, the mechanism of tendinopathy has not been clarified and is lack of effective treatment method. Change of tissue fibrosis is the one of the main pathological features. Transforming growth factor beta 1 (TGF-β1), which is one of the important factor, participated in fibrosis. Inconsonant expressions of TGF-β1 could be found in tendinopathy. The studies are still controversial, but the vast majority of studies had showed that TGF-β1 was abnormal, and it is given priority to increase, which means that TGF-β1 plays an important role in the process of tendinopathy. In the process of tendon injuries and repairs, the time of TGF-β1 increasing is inconsistent. The time for TGF-β1 plays a significant role has not been determined. TGF-β1 has abnormal expressions in both tendinopathy and tendon repairs, which are two opposite processes. Thus, it may not be a one-way adjustment factor, but has a pleiotropic. Recent studies showed that TGF-β1 was considered as binding to receptor and transferring signal into the cell. Now there are three different receptors are found. The classical pathway of TGF-β1 in intracellular signal transduction is mainly through activation of Smad pathway. In the same time, there are also some non-classical pathways. TGF-β1 could break balance of extracellular matrix, which may be a reason to cause tendinopathy. But the regulations of TGF-β1 on the extracellular matrix are complex and diverse, further studies are required. Existing researches showed that the performance of treatments on tendinopathy is unsatisfied by blocking TGF-β1 downstream pathway. Therefore, it is a good way to study the upstream mechanism of produce TGF-β1. It may be an effective method to find new targets to inhibit the development of tendinopathy better by finding the original source of TGF-β1.
Fibrosis ; Humans ; Signal Transduction ; Tendinopathy ; Transforming Growth Factor beta1

Gap junction (GJ) has been indicated to have an intimate correlation with adhesion junction. However, the direct interaction between them partially remains elusive. In the current study, we aimed to elucidate the role of N-cadherin, one of the core components in adhesion junction, in mediating connexin 43, one of the functional constituents in gap junction, via transforming growth factor-β1(TGF-β1) induction in osteoblasts. We first elucidated the expressions of N-cadherin induced by TGF-β1 and also confirmed the upregulation of Cx43, and the enhancement of functional gap junctional intercellular communication (GJIC) triggered by TGF-β1 in both primary osteoblasts and MC3T3 cell line. Colocalization analysis and Co-IP experimentation showed that N-cadherin interacts with Cx43 at the site of cell-cell contact. Knockdown of N-cadherin by siRNA interference decreased the Cx43 expression and abolished the promoting effect of TGF-β1 on Cx43. Functional GJICs in living primary osteoblasts and MC3T3 cell line were also reduced. TGF-β1-induced increase in N-cadherin and Cx43 was via Smad3 activation, whereas knockdown of Smad3 signaling by using siRNA decreased the expressions of both N-cadherin and Cx43. Overall, these data indicate the direct interactions between N-cadherin and Cx43, and reveal the intervention of adhesion junction in functional gap junction in living osteoblasts.
Cadherins ; Cell Communication ; Connexin 43 ; Osteoblasts ; Transforming Growth Factor beta1

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

BACKGROUND: Transforming growth factor-beta (TGF-beta), a multifunctional growth factor, has three isoforms: TGF-beta1, TGF-beta2, and TGF-beta3. Different isoforms of TGF-beta are associated with different proliferation and differentiation states of the epidermis. Narrow band ultraviolet B (NBUVB) emits a concentrated UVB source of 311 nm. NBUVB 1,000 mJ/cm2 induces apoptosis in approximately 50% of keratinocytes. OBJECTIVE: The purpose of this study was to evaluate whether irradiation with NBUVB would alter the expression and production of TGF-beta1, 2, and 3. METHODS: We measured TGF-beta1, 2, and 3 mRNA and TGF-beta1 and 2 protein levels at 800, 1,000, and 1,200 mJ/cm2 for 24 hours and 48 hours. RESULTS: TGF-beta1 mRNA levels were increased at both 24 hr and 48 hr, TGF-beta2 mRNA levels were decreased at both 24 hr and 48 hr, and TGF-beta3 mRNA levels were increased at 24 hr and similar to control at 48 hr. TGF-beta1 protein levels were increased at 48 hr but decreased at 24 hr. TGF-beta2 protein levels were decreased at both 24 hr and 48 hr. CONCLUSION: The results suggest a possible role for TGF-beta1 after NBUVB irradiation and opposing roles for TGF-beta1 and TGF-beta2 isoforms in NBUVB irradiation.
Apoptosis ; Enzyme Multiplied Immunoassay Technique ; Epidermis ; Humans ; Keratinocytes ; Protein Isoforms ; RNA, Messenger ; Transforming Growth Factor beta ; Transforming Growth Factor beta1 ; Transforming Growth Factor beta2 ; Transforming Growth Factor beta3