scholarly journals Cloning of Transforming Growth Factor-β1 (TGF-β1) and Its Type II Receptor from Zebrafish Ovary and Role of TGF-β1 in Oocyte Maturation

Endocrinology ◽  
2003 ◽  
Vol 144 (5) ◽  
pp. 1931-1941 ◽  
Author(s):  
Gurneet Kohli ◽  
Siqin Hu ◽  
Eric Clelland ◽  
Tamara Di Muccio ◽  
Jeffrey Rothenstein ◽  
...  
Keyword(s):  
Oocyte Maturation ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Kinase Domain ◽  
Dependent Manner ◽  
Type Ii ◽  
Downstream Signaling ◽  
High Level ◽  
Tgf Β1

TGF-β is a multifunctional factor involved in regulating a variety of cellular activities. In mammals, TGF-β is known to regulate reproduction, including ovarian functions. The role of TGF-β in lower vertebrates, such as fish, is poorly understood. To examine the role of TGF-β in fish reproduction, cDNAs encoding TGF-β1 and the type II TGF-β receptor (TβRII) were cloned from the zebrafish ovary using PCR- based strategies. The mature peptide region of the zebrafish TGF-β1 shows 70–85% identity with TGF-β1 from other species. The zebrafish TβRII cDNA sequence is the first to be reported from a fish species, and it shows a high level of conservation at the kinase domain. Using RT-PCR, we have detected mRNA expression of TGF-β1, TβRII, as well as its downstream signaling molecules Smad2, 3, and 4 in ovarian follicles at different stages of development. In addition, we have examined the effect of TGF-β1 on oocyte maturation. TGF-β1 significantly inhibited both gonadotropin- and 17α, 20β-dihydroxyprogesterone-induced oocyte maturation in a dose- and time-dependent manner. These findings demonstrate, for the first time, that TGF-β1 plays a role in regulating oocyte maturation in fish and suggest that a TGF-β/Smad signaling pathway is present in the zebrafish ovary.

Regulation of extracellular matrix synthesis by TNF-α and TGF-β1 in type II cells exposed to coal dust

1998 ◽  
Vol 275 (4) ◽  
pp. L637-L644 ◽  
Author(s):  
Yu-Chen Lee ◽  
D. Eugene Rannels
Keyword(s):  
Extracellular Matrix ◽  
Cell Cultures ◽  
Transforming Growth Factor ◽  
Coal Dust ◽  
Transforming Growth Factor Β1 ◽  
Type Ii ◽  
Tnf Α ◽  
Type Ii Cell ◽  
Primary Type ◽  
Tgf Β1

Type II pulmonary epithelial cells respond to anthracite coal dust PSOC 867 with increased synthesis of extracellular matrix (ECM) components. Alveolar macrophages modulate this response by pathways that may involve soluble mediators, including tumor necrosis factor-α (TNF-α) or transforming growth factor-β1 (TGF-β1). The effects of TNF-α (10 ng/ml) and/or TGF-β1 (2 ng/ml) were thus investigated in dust-exposed primary type II cell cultures. In control day 1 or day 3 cultures, TNF-α and/or TGF-β1 had little or no effect on the synthesis of type II cellular proteins, independent of whether the cells were exposed to dust. With PSOC 867 exposure, where ECM protein synthesis is elevated, TNF-α and TGF-β1 further increased both the absolute and relative rates of ECM synthesis on day 3 but had little effect on day 1. Each mediator increased expression of fibronectin mRNA, as well as of ECM fibronectin content, in a manner qualitatively similar to their effects on synthesis. Thus TNF-α and TGF-β1 modulate both ECM synthesis and fibronectin content in coal dust-exposed type II cell cultures.

scholarly journals Studies on the Biological Effects of Ozone: 10. Release of Factors from Ozonated Human Platelets

1999 ◽  
Vol 8 (4-5) ◽  
pp. 205-209 ◽  
Author(s):  
G. Valacchi ◽  
Velio Bocci
Keyword(s):  
Platelet Aggregation ◽  
Growth Factor ◽  
Transforming Growth Factor ◽  
Platelet Rich Plasma ◽  
Biological Effects ◽  
Transforming Growth Factor Β1 ◽  
Human Platelets ◽  
Dependent Manner ◽  
Dose Dependent ◽  
Tgf Β1

In a previous work we have shown that heparin, in the presence of ozone (O3), promotes a dose-dependent platelet aggregation, while after Ca2+chelation with citrate, platelet aggregation is almost negligible. These results led us to think that aggregation may enhance the release of platelet components. We have here shown that indeed significantly higher amount of platelet-derived growth factor (PDGF), transforming growth factor β1 (TGF-β1) and interleukin-8(IL-8) are released in a dose-dependent manner after ozonation of heparinised platelet-rich plasma samples. These findings may explain the enhanced healing of torpid ulcers in patients with chronic limbischemia treated with O3autohaemoteraphy (O3-AHT).

scholarly journals Targeted DNA oxidation by LSD1–SMAD2/3 primes TGF-β1/ EMT genes for activation or repression

2020 ◽  
Vol 48 (16) ◽  
pp. 8943-8958 ◽  
Author(s):  
Antonio Pezone ◽  
Maria Letizia Taddei ◽  
Alfonso Tramontano ◽  
Jacopo Dolcini ◽  
Francesca Ludovica Boffo ◽  
...  
Keyword(s):  
Epithelial To Mesenchymal Transition ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Dna Oxidation ◽  
Mesenchymal Transition ◽  
Kinase C ◽  
Histone Lysine ◽  
Lysine Specific Demethylase ◽  
Tgf Β1

Abstract The epithelial-to-mesenchymal transition (EMT) is a complex transcriptional program induced by transforming growth factor β1 (TGF-β1). Histone lysine-specific demethylase 1 (LSD1) has been recognized as a key mediator of EMT in cancer cells, but the precise mechanism that underlies the activation and repression of EMT genes still remains elusive. Here, we characterized the early events induced by TGF-β1 during EMT initiation and establishment. TGF-β1 triggered, 30–90 min post-treatment, a nuclear oxidative wave throughout the genome, documented by confocal microscopy and mass spectrometry, mediated by LSD1. LSD1 was recruited with phosphorylated SMAD2/3 to the promoters of prototypic genes activated and repressed by TGF-β1. After 90 min, phospho-SMAD2/3 downregulation reduced the complex and LSD1 was then recruited with the newly synthesized SNAI1 and repressors, NCoR1 and HDAC3, to the promoters of TGF-β1-repressed genes such as the Wnt soluble inhibitor factor 1 gene (WIF1), a change that induced a late oxidative burst. However, TGF-β1 early (90 min) repression of transcription also required synchronous signaling by reactive oxygen species and the stress-activated kinase c-Jun N-terminal kinase. These data elucidate the early events elicited by TGF-β1 and the priming role of DNA oxidation that marks TGF-β1-induced and -repressed genes involved in the EMT.

scholarly journals Expression and Clinical Significance of Mucin Gene in Chronic Rhinosinusitis

2020 ◽  
Vol 20 (11) ◽  
Author(s):  
Jiaxin Tong ◽  
Qingjia Gu
Keyword(s):  
Chronic Rhinosinusitis ◽  
Transforming Growth Factor ◽  
Critical Role ◽  
Transforming Growth Factor Β1 ◽  
Inflammatory Factors ◽  
Human Neutrophil Elastase ◽  
Mucin Expression ◽  
Nasal Disease ◽  
Tgf Β1

Abstract Purpose of Review This review highlights the expression and regulation of mucin in CRS and discusses its clinical implications. Recent Findings Chronic rhinosinusitis (CRS) is common chronic nasal disease; one of its main manifestations and important features is mucus overproduction. Mucin is the major component of mucus and plays a critical role in the pathophysiological changes in CRS. The phenotype of CRS affects the expression of various mucins, especially in nasal polyps (NP). Corticosteroids(CS), human neutrophil elastase (HNE), and transforming growth factor-β1 (TGF-β1) are closely related to the tissue remodeling of CRS and regulate mucin expression, mainly MUC1, MUC4, MUC5AC, and MUC5B. “It is expected that CS, HNE and TGF - β could be used to regulate the expression of mucin in CRS.” However, at present, the research on mucin is mainly focused on mucin 5AC and mucin 5B, which is bad for finding new therapeutic targets. Summary Investigating the expression and location of mucin in nasal mucosa and understanding the role of various inflammatory factors in mucin expression are helpful to figure out regulatory mechanisms of airway mucin hypersecretion. It is of great significance for the treatment of CRS.

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

Transcriptional regulation of the TGF-β1 promoter by androgen receptor

2008 ◽  
Vol 416 (3) ◽  
pp. 453-462 ◽  
Author(s):  
Wei Qi ◽  
Shen Gao ◽  
Zhengxin Wang
Keyword(s):  
Prostate Cancer ◽  
Androgen Receptor ◽  
Cancer Cells ◽  
Transforming Growth Factor ◽  
Prostate Gland ◽  
Transforming Growth Factor Β1 ◽  
Prostate Cancer Cells ◽  
Level Of Activity ◽  
High Level ◽  
Tgf Β1

TGF (transforming growth factor)-β1 is a multifunctional cytokine that influences homoeostatic processes of various tissues. TGF-β1 expression is inhibited by androgens in the prostate gland, whereas its expression is enhanced by androgens in highly metastatic prostate cancer cells. Here, we examined regulation of human TGF-β1 promoter activity by androgen in prostate cancer cells. The full-length (−3363 to +110) promoter showed a high level of activity in response to androgen in PC3mm2 cells expressing AR (androgen receptor). Further deletion analysis revealed three distal and three proximal AREs (androgen-response elements) in the promoter. Gel-shift and footprint assays show that these AREs physically interact with the DNA-binding domain of AR. Chromatin immunoprecipitation assays revealed the androgen-dependent recruitment of AR to the ARE-containing regions of the TGF-β1 gene. More importantly, a negative ARE was detected in the TGF-β1 promoter. Both positive and negative AREs are functional in the androgen-regulated transcription of the TGF-β1 promoter. These findings imply that androgen signalling may positively or negatively regulate TGF-β1 expression in response to various signals or under different environmental conditions.

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

The role of macrophage-derived TGF-β1 on SiO2-induced pulmonary fibrosis: A review

2021 ◽  
pp. 074823372198989
Author(s):  
Zhao-qiang Zhang ◽  
Hai-tao Tian ◽  
Hu Liu ◽  
Ruining Xie
Keyword(s):  
Pulmonary Fibrosis ◽  
Molecular Mechanisms ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Silica Dust ◽  
Molecular Events ◽  
Fibrotic Lung Disease ◽  
Different Sources ◽  
Tgf Β1

Silicosis is an occupational fibrotic lung disease caused by inhaling large amounts of crystalline silica dust. Transforming growth factor-β1 (TGF-β1), which is secreted from macrophages, has an important role in the development of this disease. Macrophages can recognize and capture silicon dust, undergo M2 polarization, synthesize TGF-β1 precursors, and secrete them out of the cell where they are activated. Activated TGF-β1 induces cells from different sources, transforming them into myofibroblasts through autocrine and paracrine mechanisms, ultimately causing silicosis. These processes involve complex molecular events, which are not yet fully understood. This systematic summary may further elucidate the location and development of pulmonary fibrosis in the formation of silicosis. In this review, we discussed the proposed cellular and molecular mechanisms of production, secretion, activation of TGF-β1, as well as the mechanisms through which TGF-β1 induces cells from three different sources into myofibroblasts during the pathogenesis of silicosis. This study furthers the medical understanding of the pathogenesis and theoretical basis for diagnosing silicosis, thereby promoting silicosis prevention and treatment.

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