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Pamrevlumab, an anti-connective tissue growth factor therapy, for idiopathic pulmonary fibrosis (PRAISE): a phase 2, randomised, double-blind, placebo-controlled trial.

Connective tissue growth factor (CTGF) is a secreted glycoprotein that has a central role in the process of fibrosis. This study was designed to assess the safety, tolerability, and efficacy of pamrevlumab (FG-3019), a fully recombinant human monoclonal antibody against CTGF, in idiopathic pulmonary fibrosis. The aim was to establish whether pamrevlumab could slow, stop, or reverse progression of idiopathic pulmonary fibrosis.

2580 related Products with: Pamrevlumab, an anti-connective tissue growth factor therapy, for idiopathic pulmonary fibrosis (PRAISE): a phase 2, randomised, double-blind, placebo-controlled trial.

Mouse Anti-Ca19.9 Sialyl Rabbit Polyclonal Antibod Goat Anti-Human Tissue Fa Rat monoclonal anti mouse Rabbit Polyclonal Antibod Anti-ADAMTS-13 (A Disinti Goat Anti-Human Fibroblas Sheep Polyclonal Antibody Rat monoclonal anti mouse Rat monoclonal anti mouse Rabbit Polyclonal Antibod Rat monoclonal anti mouse

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Down-regulation of interferon regulatory factor 2 binding protein 2 suppresses gastric cancer progression by negatively regulating connective tissue growth factor.

Interferon regulatory factor 2 binding protein 2 (IRF2BP2) is a transcriptional repressor involved in regulating gene expression and other biological processes, including tumorigenesis. However, the clinical significance and roles of IRF2BP2 in human gastric cancer (GC) remain uncertain. Clinical GC tissues were obtained from GC patients at the First Affiliated Hospital of Nanchang University. Immunohistochemistry (IHC) was conducted to detect the IRF2BP2 protein in clinical paraffin specimens. Cell proliferation, migration and invasion were evaluated by MTT, colony formation assays and transwell assays. Co-immunoprecipitation was conducted to detect the interaction between TEA domain family members 4 (TEAD4) and vestigial-like family member 4 (VGLL4) or Yes-associated protein 1 (YAP1). Dual-luciferase reporter assay was used to confirm the binding of miR-101-3p to the 3'-UTR. The expression of IRF2BP2 was significantly higher in GC tissues than in normal tissues. Patients with higher IRF2BP2 protein expression had lower survival. IRF2BP2 knockdown inhibited proliferation, migration, invasion and epithelial-mesenchymal transition in GC cells. IRF2BP2 knockdown decreased the mRNA and protein levels of connective tissue growth factor (CTGF). The interaction between IRF2BP2 and VGLL4 increased the binding of TEAD4 to YAP1, resulting in the transcriptional coactivation of CTGF. In addition, miR-101-3p suppressed the expression of CTGF by directly targeting the 3'-UTR of IRF2BP2. Taken together, these findings provide a model for the role of miR-101-3p-IRF2BP2-CTGF signalling axis in GC and a novel insight into the mechanism of GC progression and metastasis.

2027 related Products with: Down-regulation of interferon regulatory factor 2 binding protein 2 suppresses gastric cancer progression by negatively regulating connective tissue growth factor.

Rat monoclonal anti mouse Rat monoclonal anti mouse Rat monoclonal anti mouse Recombinant Human Factor Rat monoclonal anti mouse Human Insulin-like Growth Human Connective Tissue G Anti PDX1 Polyclonal Anti Human, Connective Tissue Rat monoclonal anti mouse anti-Vitamin D binding pr Rabbit Anti-Human Interfe

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The Role of CTGF in Inflammatory Responses Induced by Silica Particles in Human Bronchial Epithelial Cells.

Prolonged exposure to crystalline silica leads to persistent pulmonary inflammation and progressive fibrosis. Connective tissue growth factor (CTGF) has emerged as a potent proinflammatory and profibrotic regulator to participate in a variety of chronic inflammatory diseases. However, the role of CTGF in silica-induced pulmonary inflammation remains poorly understood.

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Human Macrophage Inflamma Human Epstein-Barr Virus Anti AGO2 Human, Monoclon GFP Expressing Human Inte Human Macrophage Inflamma Human Small Intestine Mic TGF beta induced factor 2 Human, Allograft Inflamma Human Macrophage Inflamma Human Gro g Macrophage In Human Internal Mammary Ar Macrophage Colony Stimula

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Transforming growth factor (TGF)-β1-induced miR-133a inhibits myofibroblast differentiation and pulmonary fibrosis.

Transforming growth factor (TGF)-β1, a main profibrogenic cytokine in the progression of idiopathic pulmonary fibrosis (IPF), induces differentiation of pulmonary fibroblasts to myofibroblasts that produce high levels of collagen, leading to concomitantly loss of lung elasticity and function. Recent studies implicate the importance of microRNAs (miRNAs) in IPF but their regulation and individual pathological roles remain largely unknown. We used both RNA sequencing and quantitative RT-PCR strategies to systematically study TGF-β1-induced alternations of miRNAs in human lung fibroblasts (HFL). Our data show that miR-133a was significantly upregulated by TGF-β1 in a time- and concentration-dependent manner. Surprisingly, miR-133a inhibits TGF-β1-induced myofibroblast differentiation whereas miR-133a inhibitor enhances TGF-β1-induced myofibroblast differentiation. Interestingly, quantitative proteomics analysis indicates that miR-133a attenuates myofibroblast differentiation via targeting multiple components of TGF-β1 profibrogenic pathways. Western blot analysis confirmed that miR-133a down-regulates TGF-β1-induced expression of classic myofibroblast differentiation markers such as ɑ-smooth muscle actin (ɑ-SMA), connective tissue growth factor (CTGF) and collagens. miRNA Target Searcher analysis and luciferase reporter assays indicate that TGF-β receptor 1, CTGF and collagen type 1-alpha1 (Col1a1) are direct targets of miR-133a. More importantly, miR-133a gene transferred into lung tissues ameliorated bleomycin-induced pulmonary fibrosis in mice. Together, our study identified TGF-β1-induced miR-133a as an anti-fibrotic factor. It functions as a feed-back negative regulator of TGF-β1 profibrogenic pathways. Thus, manipulations of miR-133a expression may provide a new therapeutic strategy to halt and perhaps even partially reverse the progression of IPF.

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Epidermal Growth Factor ( Growth Differentiation Fa Human Growth and Differen Human Growth and Differen Human Transforming Growth Growth Differentiation Fa Rat transforming growth f Human Growth and Differen Epidermal Growth Factor ( Human Transforming Growth Rabbit Placenta Growth Fa CELLKINES PLATELET DERIVE

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Jiadifenolide induces the expression of cellular communication network factor (CCN) genes, and CCN2 exhibits neurotrophic activity in neuronal precursor cells derived from human induced pluripotent stem cells.

Jiadifenolide has been reported to have neurotrophin-like activity in primary rat cortical neurons, and also possesses neurotrophic effects in neuronal precursor cells derived from human induced pluripotent stem cells (hiPSCs), as we have previously reported. However, the molecular mechanisms by which jiadifenolide exerts its neurotrophic effects in rat and human neurons are unknown. Thus, we aimed to investigate the molecular mechanisms and pathways by which jiadifenolide promotes neurotrophic effects. Here, we found that jiadifenolide activated cellular communication network factor (CCN) signaling pathways by up-regulating mRNA level expression of CCN genes in human neuronal cells. We also found that CCN2 (also known as connective tissue growth factor, CTGF) protein promotes neurotrophic effects through activation of the p44/42 mitogen-activated protein kinase signaling pathway. This is the first discovery which links neurotrophic activity with CCN signaling.

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Macrophage Colony Stimula Macrophage Colony Stimula Human Glial Derived Neuro Stemez hN2 Human Neuron D Human Large Intestine Mic Epidermal Growth Factor ( MarkerGene™ Cellular Se MarkerGeneTM in vivo lacZ thymic dendritic cell-der LumiSTEM 96 iPS MSC deriv Anti Human Brain Derived GFP Expressing Human Inte

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A CTGF-RUNX2-RANKL Axis in Breast and Prostate Cancer cells Promotes Tumor Progression in Bone.

Metastasis to bone is a frequent occurrence in patients with breast and prostate cancers and inevitably threatens the patient's quality of life and survival. Identification of cancer-derived mediators of bone metastasis and osteolysis may lead to novel therapeutic strategies. In this study, we established highly bone-metastatic PC3 prostate and MDA-MB-231 (MDA) breast cancer cell sublines by in vivo selection in mice. In bone-metastatic cancer cells, the expression and secretion of connective tissue growth factor (CTGF) were highly upregulated. CTGF knockdown in bone-metastatic cells decreased invasion activity and MMP expression. RUNX2 overexpression in the CTGF knockdown cells restored the invasion activity and MMP expression. In addition, CTGF increased RUNX2 protein stability by inducing its acetylation via p300 acetyl transferase. The integrin αvβ3 receptor mediated these effects of CTGF. Furthermore, CTGF promoted RUNX2 recruitment to the RANKL promoter, resulting in increased RANKL production from the tumor cells and subsequent stimulation of osteoclastogenesis from precursor cells. In addition, animal model with injection of CTGF knockdowned prostate cancer cells into 6-week old BALB/c male mice showed reduced osteolytic lesions. More importantly, the expression levels of CTGF and RANKL showed a strong positive correlation in human primary breast tumor tissues and were higher in bone metastases than in other site metastases. These findings indicate that CTGF plays crucial roles for osteolytic bone metastasis both by enhancing invasiveness of tumor cells and by producing RANKL for osteoclastogenesis. Targeting CTGF may lead to the development of effective preventive and therapeutic strategies for osteolytic metastasis. This article is protected by copyright. All rights reserved.

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Top 4 types of cancer (co Breast cancer tissue arra Prostate cancer, hyperpla Breast cancer tissue arra Breast cancer tissue arra Breast cancer and matched Pancreatic disease spectr Breast cancer, carcinoma Prostate cancer test tiss Prostate cancer, adjacent Late stage breast cancer Breast tumor survey tissu

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Insulin-like growth factor binding protein-4 exerts antifibrotic activity by reducing levels of connective tissue growth factor and the C-X-C chemokine receptor 4.

The Insulin-like growth factor (IGF) system plays an important role in variety cellular biological functions; we previously reported levels of IGF binding proteins (IGFBP) -3 and -5 are increased in dermal and pulmonary fibrosis associated with the prototypic fibrosing disease systemic sclerosis (SSc), induce extracellular matrix (ECM) production, and promote fibrosis. We sought to examine the effects of another member of the family, IGFBP-4, on ECM production and fibrosis using cell-based, organ culture and mouse lung fibrosis models. IGFBP-4 mRNA levels were significantly decreased in pulmonary fibroblasts of patients with SSc. ECM components were significantly reduced by endogenous and exogenous IGFBP-4. IGFBP-4 also blocked TGFβ-induced ECM production, and inhibited ECM production in human lung and skin in organ culture. , IGFBP-4 reduced bleomycin-induced collagen production and histologic evidence of fibrosis. Silencing IGFBP-4 expression to mimic levels observed in SSc lung fibroblasts resulted in increased ECM production. IGFBP-4 reduced mRNA and protein levels of the chemokine receptor CXCR4 and the pro-fibrotic factor CTGF. Further, CTGF silencing potentiated the anti-fibrotic effects of IGFBP-4. Reduced IGFBP-4 levels in SSc lung fibroblasts may contribute to the fibrotic phenotype via loss of IGFBP-4 anti-fibrotic activity.

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Human Connective Tissue G Rat monoclonal anti mouse IGF-1R Signaling Phospho- Human, Connective Tissue Rat monoclonal anti mouse Rat monoclonal anti mouse Rat monoclonal anti mouse Rat monoclonal anti mouse RABBIT ANTI HUMAN SDF-1 A IGF1, Insulin-like growth Human Insulin-like Growth CELLKINES PLATELET DERIVE

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induces connective tissue growth factor expression through the TLR2-JNK-AP-1 pathway in human lung fibroblasts.

() infection in lung causes pulmonary fibrosis, which leads to the irreversible reduction of pulmonary function. Fibrotic protein connective tissue growth factor (CTGF) expression has been confirmed to play a crucial role in lung fibrosis. However, the underlying signal pathway and effect of on CTGF expression in human lung fibroblasts are unclear. Our results revaled that caused time- and concentration-dependent increases in CTGF expression in human lung fibroblasts. A mechanistic investigation revealed that induced CTGF expression through TLR2 but not TLR4. The promoter activity assay indicated that -induced CTGF activity was mainly controlled by the promoter region at -747 to -184 bp, which contained signal transducer and activator of transcription 3 and activator protein 1 (AP-1) binding sites. Moreover, curcumin (AP-1 inhibitor) restrained -induced CTGF expression. also induced increases in AP-1 luciferase activity and DNA binding activity of c-Jun and c-Fos on the CTGF promoter. Furthermore, the knockdown of c-Jun by small interfering RNA attenuated -induced CTGF expression and AP-1 luciferase activity. A JNK inhibitor (SP600125) and a JNK dominant-negative mutant suppressed -induced CTGF expression. We also discovered that could induce the phosphorylation of JNK and c-Jun. Furthermore, SP600125 inhibited -induced c-Jun phosphorylation and AP-1- luciferase activity. -induced fibronectin expression was inhibited by anti-CTGF antibody. These results demonstrate that is activated through TLR2 to induce JNK activation, further increasing the DNA binding activity of c-Jun and c-Fos and finally inducing CTGF expression and extracellular matrix production.-Lee, H.-S., Hua, H.-S., Wang, C.-H., Yu, M.-C., Chen, B.-C., Lin, C.-H. induces connective tissue growth factor expression through the TLR2-JNK-AP-1 pathway in human lung fibroblasts.

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Goat Anti-Human Tissue Fa Human Connective Tissue G Human Insulin-like Growth Human, Connective Tissue Growth Differentiation Fa TGF beta induced factor 2 Human Fibroblast Growth F Human Fibroblast Growth F Human Insulin-like Growth Human Insulin-like Growth Rat Insulin-like Growth F Goat Anti-Human Fibroblas

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Connective tissue growth factor is correlated with peritoneal lymphangiogenesis.

Lymphatic absorption in the peritoneal cavity may contribute to ultrafiltration failure in peritoneal dialysis (PD). Lymphatic vessels develop during PD-related peritoneal fibrosis. Connective tissue growth factor (CTGF, also called CCN2) is an important determinant of fibrotic tissue remodeling, but little is known about its possible involvement in lymphangiogenesis. In this study, we investigated the relationship between CTGF and peritoneal lymphangiogenesis. A positive correlation was observed between vascular endothelial growth factor-C (VEGF-C), a major lymphangiogenic growth factor, and the CTGF concentration in human PD effluents. CTGF expression was positively correlated with expression of lymphatic markers and VEGF-C in human peritoneal biopsies. We found a positive correlation between the increase in CTGF and the increase in VEGF-C in cultured human peritoneal mesothelial cells (HPMCs) treated with transforming growth factor-β1 (TGF-β1). The diaphragm is a central player in peritoneal lymphatic absorption. CTGF expression was also correlated with expression of VEGF-C and lymphatics in a rat diaphragmatic fibrosis model induced by chlorhexidine gluconate (CG). Furthermore, CTGF gene deletion reduced VEGF-C expression and peritoneal lymphangiogenesis in the mouse CG model. Inhibition of CTGF also reduced VEGF-C upregulation in HPMCs treated with TGF-β1. Our results suggest a close relationship between CTGF and PD-associated lymphangiogenesis.

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Human Connective Tissue G Human, Connective Tissue Mouse Anti-Insulin-Like G Bacillus anthracis (Anthr Mouse Epidermal Growth Fa Rabbit Anti-Factor VII Po Rabbit anti-Placenta Grow Human Growth Hormone anti IGF-1R Signaling Phospho- Rabbit Anti-Factor VII Po anti-Complement factor B, Human Platelet Derived Gr

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Mitochondrial-Targeted Antioxidants Attenuate TGF-β2 Signaling in Human Trabecular Meshwork Cells.

POAG is a progressive optic neuropathy that is currently the leading cause of irreversible blindness worldwide. While the underlying cause of POAG remains unclear, TGF-β2-dependent remodeling of the extracellular matrix (ECM) within the trabecular meshwork (TM) microenvironment is considered an early pathologic consequence associated with impaired aqueous humor (AH) outflow and elevated IOP. Early studies have also demonstrated markedly elevated levels of oxidative stress markers in AH from POAG patients along with altered expression of antioxidant defenses. Here, using cultured primary or transformed human TM cells, we investigated the role oxidative stress plays at regulating TGF-β2-mediated remodeling of the ECM.

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Human Internal Mammary Ar Macrophage Colony Stimula Human Large Intestine Mic Macrophage Colony Stimula GFP Expressing Human Inte Human Small Intestine Mic Recombinant Human Interle Cytokine (Human) Antibody Goat Anti-Human GOT1 (aa Goat Anti-Human TOM1L1 SR Goat Anti-Human ABCB5, (i glial cells missing homol

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