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           Search results for: Human Transforming Growth Factor beta 1 TGF-β 1   

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#29044208   2017/10/18 Save this To Up

Growth factors regulate phospholipid biosynthesis in human fibroblast-like synoviocytes obtained from osteoarthritic knees.

Elevated levels of growth factors and phospholipids (PLs) have been found in osteoarthritic synovial fluid (SF), although the metabolic regulation of PLs is currently unknown. This study aimed to determine the effects of growth factors on the biosynthesis of PLs by fibroblast-like synoviocytes (FLS) obtained from human osteoarthritic knee joints. Electrospray ionization tandem mass spectrometry was applied to analyse the newly synthesized PLs. In the presence of stable isotope-labelled PL precursors, cultured FLS were treated with either transforming growth factor-β1 (TGF-β1), bone morphogenetic protein (BMP)-2, BMP-4, BMP-7 or insulin-like growth factor-1 (IGF-1) alone or in combination with specific inhibitors of cell signalling pathways. TGF-β1 and IGF-1 markedly stimulated the biosynthesis of phosphatidylcholine (PC) before sphingomyelin (SM) and lysophosphatidylcholine (LPC) species were stimulated. BMPs elaborated less pronounced effects. The BMPs tested have different potentials to induce the biosynthesis of phosphatidylethanolamine (PE) and PE-based plasmalogens. Our study shows for the first time that TGF-β1 and IGF-1 substantially regulate the biosynthesis of PC, SM and LPC in human FLS. The functional consequences of elevated levels of PLs require additional study. The BMPs tested may be joint protective in that they upregulate PE-based plasmalogens that function as endogenous antioxidants against reactive oxygen species.

1913 related Products with: Growth factors regulate phospholipid biosynthesis in human fibroblast-like synoviocytes obtained from osteoarthritic knees.

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#29044189   2017/10/18 Save this To Up

TGF-β signalling and PEG10 are mutually exclusive and inhibitory in chondrosarcoma cells.

Histological distinction between enchondroma and chondrosarcoma is difficult because of a lack of definitive biomarkers. Here, we found highly active transforming growth factor-β (TGF-β) and bone morphogenetic protein (BMP) signalling in human chondrosarcomas compared with enchondromas by immunohistochemistry of phosphorylated SMAD3 and SMAD1/5. In contrast, the chondrogenic master regulator SOX9 was dramatically down-regulated in grade 1 chondrosarcoma. Paternally expressed gene 10 (PEG10) was identified by microarray analysis as a gene overexpressed in chondrosarcoma SW1353 and Hs 819.T cells compared with C28/I2 normal chondrocytes, while TGF-β1 treatment, mimicking higher grade tumour conditions, suppressed PEG10 expression. Enchondroma samples exhibited stronger expression of PEG10 compared with chondrosarcomas, suggesting a negative association of PEG10 with malignant cartilage tumours. In chondrosarcoma cell lines, application of the TGF-β signalling inhibitor, SB431542, increased the protein level of PEG10. Reporter assays revealed that PEG10 repressed TGF-β and BMP signalling, which are both SMAD pathways, whereas PEG10 knockdown increased the level of phosphorylated SMAD3 and SMAD1/5/9. Our results indicate that mutually exclusive expression of PEG10 and phosphorylated SMADs in combination with differentially expressed SOX9 is an index to distinguish between enchondroma and chondrosarcoma, while PEG10 and TGF-β signalling are mutually inhibitory in chondrosarcoma cells.

1213 related Products with: TGF-β signalling and PEG10 are mutually exclusive and inhibitory in chondrosarcoma cells.

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#29042658   2017/10/18 Save this To Up

Exosomes secreted by human adipose mesenchymal stem cells promote scarless cutaneous repair by regulating extracellular matrix remodelling.

Scar formation is an intractable medical problem that appears after skin wounds have healed. Recent research has shown that exosomes secreted by human adipose mesenchymal stem cells (ASC-Exos) can benefit wound healing. To further explore the therapeutic potential of ASC-Exos, we investigated their effects on mitigating scar formation, and the underlying mechanisms of these effects. We found that intravenous injection of ASC-Exos decreased the size of scars and increased the ratio of collagen III to collagen I in murine incisional wounds. Exosome treatment also prevented the differentiation of fibroblasts into myofibroblasts and increased the ratio of transforming growth factor-β3 (TGF-β3) to TGF-β1 in vivo. Additionally, we found that ASC-Exos increased the matrix metalloproteinases-3 (MMP3) expression of skin dermal fibroblasts by activating the ERK/MAPK pathway, leading to a high ratio of MMP3 to tissue inhibitor of matrix metalloproteinases-1 (TIMP1), which is also beneficial for the remodelling of extracellular matrix (ECM). In conclusion, our results demonstrated that ASC-Exos promote ECM reconstruction in cutaneous wound repair by regulating the ratios of collagen type III: type I, TGF-β3:TGF-β1 and MMP3:TIMP1, and by regulating fibroblast differentiation to mitigate scar formation. Therefore, the application of ASC-Exos may be a novel therapeutic approach for scarless wound repair.

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#29039466   2017/10/17 Save this To Up

RACK1 silencing attenuates renal fibrosis by inhibiting TGF-β signaling.

The receptor for activated C-kinase 1 (RACK1) is a member of the WD40-repeat family of proteins and has been reported to be implicated in the development of liver fibrosis. However, the role of RACK1 in renal fibrosis remains unclear. Therefore, in this study, we investigated the effects of RACK1 on transforming growth factor-β1 (TGF-β1)-treated human proximal tubular epithelial cells and aimed to elucidate the possible mechanisms responsible for its anti-fibrotic effects. Our results revealed that RACK1 was highly expressed in the renal fibrotic tissues and TGF-β1-treated HK-2 cells. RACK1 silencing inhibited TGF-β1‑induced α-smooth muscle actin and connective tissue growth factor expression in the HK-2 cells. Furthermore, RACK1 silencing inhibited the expression of phosphorylated Smad3 in the TGF-β1-treated HK-2 cells. To the best of our knowledge, these data demonstrate for the first time the role of RACK1 in renal fibrosis. The present findings indicate that RACK1 silencing attenuates renal fibrosis by suppressing the activation of TGF-β1/Smad3 signaling pathway in HK-2 cells. Thus, RACK1 may serve as a novel regulator of renal fibrosis.

1955 related Products with: RACK1 silencing attenuates renal fibrosis by inhibiting TGF-β signaling.

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#29031615   2017/10/16 Save this To Up

The leukotriene receptor antagonist pranlukast attenuates airway remodeling by suppressing TGF-β signaling.

Asthma is a chronic airway disease characterized by airway eosinophilic inflammation and remodeling, which are associated with a loss in lung function. Although both contribute significantly to asthma pathogenesis, mechanistic studies and drug discovery have focused on inflammatory targets. In this study, we investigated the effect of the leukotriene receptor antagonist pranlukast on allergic airway inflammation and remodeling in vivo and in vitro.

1870 related Products with: The leukotriene receptor antagonist pranlukast attenuates airway remodeling by suppressing TGF-β signaling.

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#29024711   2017/10/12 Save this To Up

Fluoride potentiates tubulointerstitial nephropathy caused by unilateral ureteral obstruction.

The contamination of ground water by fluoride has been reported worldwide. Most fluoride (approximately 70%) is filtered by the kidneys; humans or experimental animals with renal damage therefore may be more affected by fluoride exposure than those with normal kidney function. Tubulointerstitial fibrosis, which involves macrophage-promoted extracellular matrix production and myofibroblast migration, can be induced in rats by unilateral ureteral obstruction (UUO). We examined the effects of fluoride exposure on tubulointerstitial fibrosis in the obstructed kidney of UUO rats. The left ureters of 6-week-old male rats were ligated using silk sutures. Fluoride was then administered for 2 weeks at doses of 0, 75, and 150ppm in the drinking water. Real-time polymerase chain reaction was performed to analyze transforming growth factor beta 1 (TGF-β1) transcription; histological and immunohistochemical staining were used to identify positive areas within the renal cortex and staining-positive cells by image analysis. Significant increases were observed in the obstructed kidneys of UUO rats exposed to 150ppm fluoride (compared to 0ppm) for areas or number of cells that stained with Masson trichrome or with antibodies against collagen type I, alpha-smooth muscle actin (α-SMA, a myofibroblast marker), ED1, ED2, and ED3 (macrophage markers), and TGF-β1. Taken together, these observations suggested that fluoride exacerbates tuburointerstitial nephropathy resulting from UUO, and that this effect occurs via activation of the M2 macrophage-TGF-β1-fibroblast/myofibroblast-collagen synthesis pathway.

2209 related Products with: Fluoride potentiates tubulointerstitial nephropathy caused by unilateral ureteral obstruction.

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#28993461   2017/10/10 Save this To Up

Brucella abortus promotes a fibrotic phenotype in hepatic stellate cells with concomitant autophagy pathway activation.

The liver is frequently affected in patients with active brucellosis. The present study demonstrates that B. abortus infection induces the activation of the autophagic pathway in hepatic stellate cells to create a microenvironment that promote a profibrogenic phenotype through the induction of transforming growth factor-β1 (TGF-β1), collagen deposition and inhibition of matrix metalloproteinase-9 (MMP-9) secretion. Autophagy was revealed by up-regulation of the LC3II/LC3I ratio and beclin-1 expression as well as inhibition of p62 expression in infected cells. The above findings were dependent on the type IV secretion system (VirB) and the secreted BPE005 protein; which were partially corroborated using the pharmacological inhibitors wortmannin - a PI3-kinase inhibitor - and leupeptin plus E64 (inhibitors of lysosomal proteases). Activation of the autophagic pathway in hepatic stellate cells during Brucella infection could have an important contribution in attenuating inflammatory hepatic injury by inducing fibrosis. However, with time, B. abortus infection induced beclin-1 cleavage with concomitant cleavage of caspase-3 indicating the onset of apoptosis of LX-2 cells, as was confirmed by the TUNEL assay and Hoechst staining. These results demonstrate that the crosstalk of LX-2 cells and B. abortus induces autophagy and fibrosis with concomitant apoptosis of LX-2 cells, which may explain some potential mechanisms of liver damage observed in human brucellosis.

1413 related Products with: Brucella abortus promotes a fibrotic phenotype in hepatic stellate cells with concomitant autophagy pathway activation.

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#28991210   2017/10/09 Save this To Up

A Central Bioactive Region of LTBP-2 Stimulates the Expression of TGF-β1 in Fibroblasts via Akt and p38 Signalling Pathways.

Latent transforming growth factor-β-1 binding protein-2 (LTBP-2) belongs to the LTBP-fibrillin superfamily of extracellular proteins. Unlike other LTBPs, LTBP-2 does not covalently bind transforming growth factor-β1 (TGF-β1) but appears to be implicated in the regulation of TGF-β1 bioactivity, although the mechanisms are largely unknown. In experiments originally designed to study the displacement of latent TGF-β1 complexes from matrix storage, we found that the addition of exogenous LTBP-2 to cultured human MSU-1.1 fibroblasts caused an increase in TGF-β1 levels in the medium. However, the TGF-β1 increase was due to an upregulation of TGF-β1 expression and secretion rather than a displacement of matrix-stored TGF-β1. The secreted TGF-β1 was mainly in an inactive form, and its concentration peaked around 15 h after addition of LTBP-2. Using a series of recombinant LTBP-2 fragments, the bioactivity was identified to a small region of LTBP-2 consisting of an 8-Cys motif flanked by four epidermal growth factor (EGF)-like repeats. The LTBP-2 stimulation of TGF-β expression involved the phosphorylation of both Akt and p38 mitogen-activated protein kinase (MAPK) signalling proteins, and specific inactivation of each protein individually blocked TGF-β1 increase. The search for the cell surface receptor mediating this LTBP-2 activity proved inconclusive. Inhibitory antibodies to integrins β1 and αVβ5 showed no reduction of LTBP-2 stimulation of TGF-β1. However, TGF-β1 upregulation was partially inhibited by anti-αVβ3 integrin antibodies, suggestive of a direct or indirect role for this integrin. Overall, the study indicates that LTBP-2 can directly upregulate cellular TGF-β1 expression and secretion by interaction with cells via a short central bioactive region. This may be significant in connective tissue disorders involving aberrant TGF-β1 signalling.

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#28984468   2017/10/06 Save this To Up

TGF-β1 Evokes Human Airway Smooth Muscle Cell Shortening and Hyperresponsiveness via Smad3.

Transforming growth factor beta 1 (TGF-β1), a cytokine whose levels are elevated in the airways of patients with asthma, perpetuates airway inflammation and modulates airway structural cell remodeling. However, the role of TGF-β1 in excessive airway narrowing in asthma, or airway hyperresponsiveness (AHR), remains unclear. In this study, we set out to investigate the direct effects of TGF-β1 on human airway smooth muscle (HASM) cell shortening and hyperresponsiveness. The dynamics of AHR and single-cell excitation-contraction (E-C) coupling were measured in human precision-cut lung slices (hPCLS) and in isolated HASM cells using supravital microscopy and magnetic twisting cytometry (MTC), respectively. In hPCLS, overnight treatment with TGF-β1 significantly augmented basal and carbachol-induced bronchoconstriction. In isolated HASM cells, TGF-β1 increased basal and methacholine-induced cytoskeletal stiffness in a dose- and time-dependent manner. TGF-β1-induced single-cell contraction was corroborated by concomitant increases in myosin light chain (MLC) and myosin phosphatase target subunit 1 (MYPT1) phosphorylation levels, which were attenuated by siRNA-mediated knockdown of Smad3 and pharmacological inhibition of Rho kinase. Strikingly, these physiologic effects of TGF-β1 occurred through a RhoA-independent mechanism with little effect on HASM cell [Ca2+]i levels. Together, our data suggest that TGF-β1 enhances HASM E-C coupling pathways to induce HASM cell shortening and hyperresponsiveness. These findings reveal a potential link between airway injury-repair responses and bronchial hyperreactivity in asthma, and define TGF-β1 signaling as a potential target to reduce AHR in asthma.

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#28959347   2017/09/29 Save this To Up

Gene Regulation Network Based Analysis Associated with TGF-βeta Stimulation in Lung Adenocarcinoma Cells.

Transforming growth factor (TGF)-β is over-expressed in a wide variety of cancers such as lung adenocarcinoma. TGF-β plays a major role in cancer progression through regulating cancer cell proliferation and remodeling of the tumor micro-environment. However, it is still a great challenge to explain the phenotypic effects caused by TGF-β stimulation and the effect of TGF-β stimulation on tumor micro-environment.

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