Search results for: Human Connective Tissue Growth Factor CTGF
#32447983 2020/05/23 To Up
Pamrevlumab for the treatment of idiopathic pulmonary fibrosis.The two available therapies for idiopathic pulmonary fibrosis (IPF), pirfenidone and nintedanib, slow down but do not halt IPF progression. Hence, in the last few years, several agents with specific molecular targets have been investigated to find a cure for IPF. Pamrevlumab, a recombinant human antibody that binds to connective tissue growth factor (CTGF) has emerged as a potential therapy for IPF and has advanced to phase 3 clinical trials. Because CTGF plays a central role in tumorigenesis and abnormal tissue repair processes, this could represent a more targeted therapeutic approach.
Giacomo Sgalla, Claudia Franciosa, Jacopo Simonetti, Luca Richeldi96 Well200 mg2000 rxn0.1 mg25 g250 ml500IUeach 100ul10
#32428986 2020/05/19 To Up
Liposome-encapsulated statins reduce hypertrophic scarring through topical application.Hypertrophic scar is an important clinical problem with limited therapeutic options. Aside from their roles as 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors, statins have also been demonstrated to decrease scarring by reducing connective tissue growth factor (CTGF) expression. However, poor penetrative ability limits their utility as topical treatments for hypertrophic scar. Here, we aim to develop novel statin formulations using liposomes to enhance dermal penetrative ability and to evaluate their efficacy against formation of hypertrophic scar utilizing our validated rabbit ear hypertrophic scar model. Liposomal simvastatin or pravastatin were compounded using a novel, flexible liposomal formulation and applied topically to rabbit ear hypertrophic scars daily from postoperation day (POD) 14 until POD 25. Scar color, including erythema and melanin, was measured using reflectance spectrophotometry on POD 28, and scar tissue was harvested for evaluation of scar elevation index as well as gene and protein expression. Human foreskin fibroblasts were also treated with statin formulations and CCN2 expression was determined by quantitative PCR. Both simvastatin and pravastatin were efficiently encapsulated in liposomes, forming nanometer-scale particles possessing highly negative charges. Topical treatment with liposomal simvastatin and pravastatin at 6.5% concentration significantly reduced scar elevation index and decreased type I/III collagen content and myofibroblast persistence in the wound. The erythema/vascularity of scars was reduced by liposomal statin treatment, with concomitant decrease of CD31 expression as measured histologically. Expression levels of transcripts encoding CTGF, collagen I, and collagen III collagen in scar tissue were also decreased by liposomal pravastatin treatment, as were myofibroblast persistence and the type I/III collagen ratio as assessed by immunofluorescence and picrosirus red staining, respectively. Treatment of human foreskin fibroblasts with simvastatin or with liposome-encapsulated pravastatin resulted in decreased expression of transcript encoding CTGF. Overall, our novel statin formulations encapsulated in liposomes were successfully delivered through topical application, significantly reducing hypertrophic scarring in a rabbit ear model.
Ping Xie, David M Dolivo, Shengxian Jia, XingGuo Cheng, John Salcido, Robert D Galiano, Seok Jong Hong, Thomas A Mustoe
2300 related Products with: Liposome-encapsulated statins reduce hypertrophic scarring through topical application.100ul50ul 100ul 100ul 100ul 100ul 100ul 100ul100ug Lyophilized100ug Lyophilized100ug Lyophilized50ul
#32377718 2020/04/29 To Up
The JAK2/STAT3 pathway inhibitor, AG490, suppresses the abnormal behavior of keloid fibroblasts in vitro.AG490 is a selective inhibitor of the Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) signaling pathway. The present study examined its effects on the abnormal behavior of human keloid fibroblasts (HKFs) and evaluated its potential use in the treatment of keloids. Human normal fibroblasts (HNFs) and HKFs were treated with increasing concentrations of AG490. The proliferation of HNFs and HKFs was inhibited by AG490 in both a time‑ and concentration‑dependent manner by increasing apoptosis and inducing G1 cell cycle arrest. The downregulation of cyclin D1 and connective tissue growth factor (CTGF) expression was associated with a decrease in STAT3 expression in response to AG490. The effects of AG490 on TGF‑β‑stimulated fibroblasts, including HNFs, HKFs and hypertrophic scar fibroblasts (HSFs) were also evaluated. The TGF‑β1‑stimulated excessive proliferation and CTGF production were markedly inhibited by the application of AG490 in the HNFs, HSFs and HKFs. In addition, the STAT3‑specific decoy oligodeoxynucleotides (SODNs) were transfected into HKFs. The invasive ability of the SODN‑transfected HKFs was determined and the expression of extracellular matrix components was quantified. Similarly, SODNs blocked the constitutive activation of STAT3. SODNs inhibited the invasion and progression of HKFs, possibly via the upregulation of the expression of tissue inhibitor of metalloproteinase‑2 (TIMP‑2), and the downregulation of the expression of matrix metalloproteinase‑2 (MMP‑2) and vascular endothelial growth factor (VEGF). On the whole, the findings of the present study demonstrate that STAT3‑specific elimination, such as the application of AG490 and decoy ODNs, may serve as promising therapeutic strategies for the treatment of keloids.
Ying Zhou, Yuexin Sun, Wenjun Hou, Liwen Ma, Yue Tao, Dan Li, Cui Xu, Jun Bao, Weixin Fan
1507 related Products with: The JAK2/STAT3 pathway inhibitor, AG490, suppresses the abnormal behavior of keloid fibroblasts in vitro.200 units100 500IUmin 2 cartons5 mg100.00 ul 100 G15mg14 inhibitors
#32319650 2020/04/09 To Up
HDGF enhances VEGF‑dependent angiogenesis and FGF‑2 is a VEGF‑independent angiogenic factor in non‑small cell lung cancer.Non‑small cell lung cancer (NSCLC) accounts for over 80% of all diagnosed lung cancer cases. Lung cancer is the leading cause of cancer‑related deaths worldwide. Most NSCLC cells overexpress vascular endothelial growth factor‑A (VEGF‑A) which plays a pivotal role in tumour angiogenesis. Anti‑angiogenic therapies including VEGF‑A neutralisation have significantly improved the response rates, progression‑free survival and overall survival of patients with NSCLC. However, the median survival of these patients is shorter than 18 months, suggesting that NSCLC cells secrete VEGF‑independent angiogenic factors, which remain unknown. We aimed to explore these factors in human NSCLC cell lines, A549, Lu99 and EBC‑1 using serum‑free culture, to which only EBC‑1 cells could adapt. By mass spectrometry, we identified 1,007 proteins in the culture supernatant derived from EBC‑1 cells. Among the identified proteins, interleukin‑8 (IL‑8), macrophage migration inhibitory factor (MIF), galectin‑1, midkine (MK), IL‑18, galectin‑3, VEGF‑A, hepatoma‑derived growth factor (HDGF), osteopontin (OPN), connective tissue growth factor (CTGF) and granulin (GRN) are known to be involved in angiogenesis. Tube formation, neutralisation and RNA interference assays revealed that VEGF‑A and HDGF function as angiogenic factors in EBC‑1 cells. To confirm whether VEGF‑A and HDGF also regulate angiogenesis in the other NSCLC cell lines, we established a novel culture method. NSCLC cells were embedded in collagen gel and cultured three‑dimensionally. Tube formation, neutralisation and RNA interference assays using the three‑dimensional (3D) culture supernatant showed that VEGF‑A and HDGF were not angiogenic factors in Lu99 cells. By gene microarray in EBC‑1 and Lu99 cells, we identified 61 mRNAs expressed only in Lu99 cells. Among these mRNAs, brain‑derived neurotrophic factor (BDNF), fibroblast growth factor‑2 (FGF‑2) and FGF‑5 are known to be involved in angiogenesis. Tube formation and neutralisation assays clarified that FGF‑2 functions as an angiogenic factor in Lu99 cells. These results indicate that HDGF enhances VEGF‑dependent angiogenesis and that FGF‑2 is a VEGF‑independent angiogenic factor in human NSCLC cells.
Ryoji Eguchi, Ichiro Wakabayashi
2726 related Products with: HDGF enhances VEGF‑dependent angiogenesis and FGF‑2 is a VEGF‑independent angiogenic factor in non‑small cell lung cancer.100ug Lyophilized100ug Lyophilized
#32279070 2020/04/12 To Up
The YAP signaling pathway promotes the progression of lymphatic malformations through the activation of lymphatic endothelial cells.To investigate whether the YAP/TAZ (Yes-associated protein/transcriptional coactivator with PDZ binding motif) pathway contributes to the pathogenesis of lymphatic malformations (LMs).
Wenqun Zhong, Hao Jiang, Yanping Zou, Jiangang Ren, Zhizheng Li, Kefei He, Jihong Zhao, Xiaoshun Zhou, Dongsheng Mou, Yu Cai
2979 related Products with: The YAP signaling pathway promotes the progression of lymphatic malformations through the activation of lymphatic endothelial cells.1.00 flask1.00 flask0.1 mg100 IU 100 G500 Units121
#32239869 // To Up
[Construction of eukaryotic expression plasmid of pcDNA3.1(+)- CTGF and its expression in human osteoblast-like cells SaOS-2].To construct pcDNA3.1(+) eukaryotic expression plasmid of connective tissue growth factor(CTGF), and detected its expression in human osteoblast-like cells SaOS-2, which provides a technical support for further research on the mechanism of CTGF gene in bone development and bone repair process. ;Methods: The whole sequence of CTGF gene was cloned in vitro by polymerase chain reaction(PCR) method and connected to the linear pcDNA3.1(+) vector for constructing pcDNA3.1(+)-CTGF eukaryotic expression plasmid by homologous recombination technology. The plasmid was identified by sequencing. After identification, it was transfected into SaOS-2 cells and its expression was detected at 48 h. ;Results: pcDNA3.1(+)-CTGF eukaryotic expression recombinant plasmid was successfully constructed, which was confirmed by sequencing. Compared with the control group, CTGF expression level was significantly up-regulated after transfection of SaOS-2 cells for 48 h, up to five times as much as the control group. ;Conclusion: pcDNA3.1(+)-CTGF eukaryotic expression plasmid was successfully constructed and could be stably expressed in human osteoblasts-like cell SaOS-2, which laid a foundation for further study on the regulatory mechanism of CTGF gene on bone formation.
Ke-Feng Ma, Shu-Guang Yang, Shao-Jun Liu
2708 related Products with: [Construction of eukaryotic expression plasmid of pcDNA3.1(+)- CTGF and its expression in human osteoblast-like cells SaOS-2].1.00 flask1.00 flask
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#32134425 2020/03/05 To Up
RNAi nanotherapy for fibrosis: highly durable knockdown of CTGF/CCN-2 using siRNA-DegradaBALL (LEM-S401) to treat skin fibrotic diseases.Skin fibrosis occurs in a variety of human diseases but the current anti-fibrosis treatments are not sufficient. One major cause of fibrotic diseases shared across diverse organ fibrosis is uncontrolled overexpression of the connective tissue growth factor (CTGF, also known as CCN2). Here, we examine the anti-fibrotic activity of RNAi therapy utilizing siRNA against CTGF with a new drug delivery system (DDS), 'DegradaBALL', which is based on porous nanoparticles, for durable CTGF gene silencing. DegradaBALL is a modular DDS having many favorable properties for RNA delivery such as effective intracellular uptake, convenient drug loading, biocompatibility, sustained release profile and biodegradability. DegradaBALL loaded with siCTGF, named 'LEM-S401', showed highly durable and effective CTGF gene-silencing in TGF-β induced lung fibrosis and skin fibrosis model cells, A549 and HaCaT, respectively. In addition, LEM-S401 induced knockdown of collagen types I and III, which are excess extracellular matrix components in fibrotic skin in addition to CTGF in the mouse wound healing model. Most importantly, we showed that LEM-S401 effectively inhibited the formation of hypertrophic scars in wound-associated dermal fibrosis mouse models, during both the epidermis recovery and tissue remodeling process. Our findings suggest that LEM-S401 could be a highly potent therapeutic option for skin fibrotic diseases.
Seounghun Kang, Jun Kim, Minchul Ahn, Jungho Kim, Myeong-Gang Heo, Dal-Hee Min, Cheolhee Won
2792 related Products with: RNAi nanotherapy for fibrosis: highly durable knockdown of CTGF/CCN-2 using siRNA-DegradaBALL (LEM-S401) to treat skin fibrotic diseases.600 Tests / Kit200assays 5 G250ul 2x5L2000 rxn5/200 Packing /sleeve/bo5 per Sleeve, 100 Flasks/25ul250ul100 mg
#32092752 2020/02/24 To Up
Investigation of the Effect of Secreted Factors from Mesenchymal Stem Cells on Disc Cells from Degenerated Discs.Low back pain is experienced by a large number of people in western countries and may be caused and influenced by many different pathologies and psychosocial factors including disc degeneration. Disc degeneration involves the increased expression of proinflammatory cytokines and matrix metalloproteinases (MMPs) in the disc environment, which leads to the loss of extracellular matrix (ECM) and the viability of the native disc cells (DCs). Treatment approaches using growth factors and cell therapy have been proposed due to the compelling results that growth factors and mesenchymal stem cells (MSCs) can influence the degenerated discs. The aim of this study was to investigate the effects of conditioned media (CM) from human MSCs (hMSCs) and connective tissue growth factor (CTGF) and TGF-β on disc cells, and hMSCs isolated from patients with degenerative discs and severe low back pain. The aim was also to examine the constituents of CM in order to study the peptides that could bring about intervertebral disc (IVD) regeneration. DCs and hMSC pellets (approx.. 200,000 cells) were cultured and stimulated with hMSC-derived CM or CTGF and TGF-β over 28 days. The effects of CM and CTGF on DCs and hMSCs were assessed via cell viability, proteoglycan production, the expression of ECM proteins, and chondrogenesis in 3D pellet culture. To identify the constituents of CM, CM was analyzed with tandem mass spectrometry. The findings indicate that CM enhanced the cellular viability and ECM production of DCs while CTGF and the control exhibited nonsignificant differences. The same was observed in the hMSC group. Mass spectrometry analysis of CM identified >700 peptides, 129 of which showed a relative abundance of ≥2 (CTGF among them). The results suggest that CM holds potential to counter the progression of disc degeneration, likely resulting from the combination of all the substances released by the hMSCs. The soluble factors released belong to different peptide families. The precise mechanism underlying the regenerative effect needs to be investigated further, prior to incorporating peptides in the development of new treatment strategies for low back pain that is potentially caused by IVD degeneration.
Daphne Hingert, Phonphan Nawilaijaroen, Jonathan Aldridge, Adad Baranto, Helena Brisby
2796 related Products with: Investigation of the Effect of Secreted Factors from Mesenchymal Stem Cells on Disc Cells from Degenerated Discs.10 ug5 x 10A5 cells/vial11 mg96 tests96 tests1 x 10^6 cells/vial1 vial5 x 200ul/Unit5 Modulators 1 kit(s) 50ml
#32059976 2020/02/12 To Up
Exosomes derived from platelet-rich plasma activate YAP and promote the fibrogenic activity of Müller cells via the PI3K/Akt pathway.The purpose of this study was to investigate the role of exosomes derived from platelet-rich plasma (PRP-Exos) in the regulation of the fibrogenic activity of Müller cells and the underlying mechanism. We studied the effects of PRP-Exos on the fibrogenic activity of human retinal Müller cells (hMCs) in vitro. PRP-Exos were isolated from the plasma of diabetic rats (DM-PRP-Exos) and normal control rats (Nor-PRP-Exos) and then observed by transmission electron microscopy. After treatment with DM-PRP-Exos or Nor-PRP-Exos, the proliferation and migration of hMCs were measured in vitro. Western blotting was conducted to assess the levels of fibrogenic molecules and activation of Yes-associated protein (YAP) and the PI3K-Akt signalling pathway. In cultured hMCs, DM-PRP-Exos but not Nor-PRP-Exos effectively increased the proliferative and migratory activities and improved connective tissue growth factor (CTGF) and fibronectin expression. Genetic and pharmacological suppression of YAP could reduce the proliferative and migratory activities of hMCs induced by DM-PRP-Exo. Additionally, YAP knockdown inhibited the DM-PRP-Exo-induced up-regulation of CTGF and fibronectin. Furthermore, DM-PRP-Exo-induced PI3K-Akt signalling mediated YAP activation and the expression of CTGF and fibronectin. In summary, DM-PRP-Exos, through YAP activation, enhance both the proliferation and fibrogenic activity of Müller cells via the PI3K/Akt pathway.
Wei Zhang, Hao Jiang, Yichun Kong
2264 related Products with: Exosomes derived from platelet-rich plasma activate YAP and promote the fibrogenic activity of Müller cells via the PI3K/Akt pathway.1 mg1100 ug/vial100 U1mg1 x 10^6 cells/vial2ug2000 IU
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