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https://www.readbyqxmd.com/read/27910859/t-cell-programming-in-pancreatic-adenocarcinoma-a-review
#1
REVIEW
Y D Seo, V G Pillarisetty
Despite recent advancements in multimodal therapy, pancreatic ductal adenocarcinoma (PDA) continues to have a dismal prognosis. In the era of burgeoning immune therapies against previously difficult-to-treat malignancies, there has been growing interest in activating the immune system against PDA; however, unlike in other cancers such as melanoma and lymphoma, immunotherapy has not yielded many clinically significant results. To harness these mechanisms for therapeutic use, an in-depth understanding of T-cell programming in the immune microenvironment of PDA must be achieved...
December 2, 2016: Cancer Gene Therapy
https://www.readbyqxmd.com/read/27880803/wdr68-mediates-dorsal-and-ventral-patterning-events-for-craniofacial-development
#2
Estibaliz Alvarado, Mina Yousefelahiyeh, Greg Alvarado, Robin Shang, Taryn Whitman, Andrew Martinez, Yang Yu, Annie Pham, Anish Bhandari, Bingyan Wang, Robert M Nissen
Birth defects are among the leading causes of infant mortality and contribute substantially to illness and long-term disability. Defects in Bone Morphogenetic Protein (BMP) signaling are associated with cleft lip/palate. Many craniofacial syndromes are caused by defects in signaling pathways that pattern the cranial neural crest cells (CNCCs) along the dorsal-ventral axis. For example, auriculocondylar syndrome is caused by impaired Endothelin-1 (Edn1) signaling, and Alagille syndrome is caused by defects in Jagged-Notch signaling...
2016: PloS One
https://www.readbyqxmd.com/read/27866969/overexpression-of-cd109-in-the-epidermis-differentially-regulates-alk1-versus-alk5-signaling-and-modulates-extracellular-matrix-synthesis-in-the-skin
#3
Joshua Vorstenbosch, Christopher M Nguyen, Shufeng Zhou, You Jung Seo, Aya Siblini, Kenneth W Finnson, Albane A Bizet, Simon D Tran, Anie Philip
Transforming growth factor-beta (TGF-β) is a multifunctional growth factor involved in many physiological processes including wound healing and inflammation. Excessive TGF-β signaling in the skin has been implicated in fibrotic skin disorders such as keloids and scleroderma. We have previously identified CD109 as a TGF- β co-receptor and inhibitor of TGF-ß signaling, and have shown that transgenic mice overexpressing CD109 in the epidermis display decreased scarring. In certain cell types, in addition to the canonical type I receptor, ALK5 which activates Smad2/3, TGF-β can signal through another type I receptor ALK1 which activates Smad1/5...
November 17, 2016: Journal of Investigative Dermatology
https://www.readbyqxmd.com/read/27865848/retinol-dehydrogenase-13-deficiency-diminishes-carbon-tetrachloride-induced-liver-fibrosis-in-mice
#4
Xiaofang Cui, Suying Dang, Yan Wang, Yan Chen, Jia Zhou, Chunling Shen, Ying Kuang, Jian Fei, Lungen Lu, Zhugang Wang
Retinol dehydrogenase 13 (RDH13) is a mitochondrion-localized member of the short-chain dehydrogenases/reductases (SDRs) superfamily that participates in metabolism of some compounds. Rdh13 mRNA is most highly expressed in mouse liver. Rdh13 deficiency reduces the extent of liver injury and fibrosis, reduces hepatic stellate cell (HSC) activation, attenuates collagen I (II), tissue inhibitor of metalloproteinase 1 (TIMP-1) and transforming growth factor beta 1 (Tgf-β1) expression. The results indicate an important role of Rdh13 and suggest RDH13 as a possible new therapeutic target for CCl4-induced fibrosis...
November 16, 2016: Toxicology Letters
https://www.readbyqxmd.com/read/27863384/a-novel-highly-potent-trivalent-tgf-%C3%AE-receptor-trap-inhibits-early-stage-tumorigenesis-and-tumor-cell-invasion-in-murine-pten-deficient-prostate-glands
#5
Tai Qin, Lindsey Barron, Lu Xia, Haojie Huang, Maria M Villarreal, John Zwaagstra, Cathy Collins, Junhua Yang, Christian Zwieb, Ravindra Kodali, Cynthia S Hinck, Sun Kyung Kim, Robert L Reddick, Chang Shu, Maureen D O'Connor-McCourt, Andrew P Hinck, Lu-Zhe Sun
The effects of transforming growth factor beta (TGF-β) signaling on prostate tumorigenesis has been shown to be strongly dependent on the stage of development, with TGF-β functioning as a tumor suppressor in early stages of disease and as a promoter in later stages. To study in further detail the paradoxical tumor-suppressive and tumor-promoting roles of the TGF-β pathway, we investigated the effect of systemic treatment with a TGF-β inhibitor on early stages of prostate tumorigenesis. To ensure effective inhibition, we developed and employed a novel trivalent TGF-β receptor trap, RER, comprised of domains derived from the TGF-β type II and type III receptors...
November 14, 2016: Oncotarget
https://www.readbyqxmd.com/read/27814632/implication-of-cd38-gene-in-autophagic-degradation-of-collagen-i-in-mouse-coronary-arterial-myocytes
#6
Jun-Xiang Bao, Qin-Fang Zhang, Mi Wang, Min Xia, Krishna M Boini, Erich Gulbins, Yang Zhang, Pin-Lan Li
Collagen deposition is a hallmark of atherosclerosis. Although compromised collagen I degradation has been implied in the pathogenesis of atherosclerosis, the molecular mechanisms are still unclear. Thus, we determined the role of CD38, an enzyme involved in cellular calcium modulation and autophagic flux, in the regulation of collagen I degradation in coronary arterial myocytes (CAMs).In primary cultured CAMs from CD38(-/-) mice, collagen I protein accumulation but not mRNA abundance was significantly increased compared with cells from CD38(+/+) mice either under control or upon TGF-Beta stimulation...
January 1, 2017: Frontiers in Bioscience (Landmark Edition)
https://www.readbyqxmd.com/read/27814572/tgf-beta1-wnt-and-shh-signaling-in-tumor-progression-and-in-fibrotic-diseases
#7
Maria D Castellone, Mikko O Laukkanen
Activation of resting fibroblasts to myofibroblasts characterizes several physiological and pathological conditions, from wound healing to aggressive metastatic cancers. In tissue damage, including wound healing, fibroblasts are activated in response to injury for a limited period of time to stimulate the healing process. Similar biological mechanisms are maintained in pathological conditions, e.g., scleroderma and cancer, where myofibroblasts persist in producing cytokines and growth factors to drive the development of fibrosis and the progression of disease...
January 1, 2017: Frontiers in Bioscience (Scholar Edition)
https://www.readbyqxmd.com/read/27803787/anti-inflammatory-effect-of-yu-ping-feng-san-via-tgf-%C3%AE-1-signaling-suppression-in-rat-model-of-copd
#8
Zhong-Shan Yang, Jin-Yuan Yan, Ni-Ping Han, Wei Zhou, Yu Cheng, Xiao-Mei Zhang, Ning Li, Jia-Li Yuan
OBJECTIVES: Yu-Ping-Feng-San (YPFS) is a classical traditional Chinese medicine that is widely used for treatment of the diseases in respiratory systems, including chronic obstructive pulmonary disease (COPD) recognized as chronic inflammatory disease. However, the molecular mechanism remains unclear. Here we detected the factors involved in transforming growth factor beta 1 (TGF-β1)/Smad2 signaling pathway and inflammatory cytokines, to clarify whether YPFS could attenuate inflammatory response dependent on TGF-β1/Smad2 signaling in COPD rats or cigarette smoke extract (CSE)-treated human bronchial epithelial (Beas-2B) cells...
September 2016: Iranian Journal of Basic Medical Sciences
https://www.readbyqxmd.com/read/27769861/activin-a-smads-signaling-pathway-negatively-regulates-oxygen-glucose-deprivation-induced-autophagy-via-suppression-of-jnk-and-p38-mapk-pathways-in-neuronal-pc12-cells
#9
Long-Xing Xue, Zhong-Hang Xu, Jiao-Qi Wang, Cui Yang, Hong-Yu Liu, Wen-Zhao Liang, Qiu-Ye Ji, Jin-Ting He, Yan-Kun Shao, Jing Mang, Zhong-Xin Xu
Activin A (Act A), a member of the transforming growth factor-beta (TGF-β), reduces neuronal apoptosis during cerebral ischemia through Act A/Smads signaling pathway. However, little is known about the effect of Act A/Smads pathway on autophagy in neurons. Here, we found that oxygen-glucose deprivation (OGD)-induced autophagy was suppressed by exogenous Act A in a concentration-dependent manner and enhanced by Act A/Smads pathway inhibitor (ActRIIA-Ab) in neuronal PC12 cells. These results indicate that Act A/Smads pathway negatively regulates autophagy in OGD-treated PC12 cells...
October 18, 2016: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/27763636/znf32-contributes-to-the-induction-of-multidrug-resistance-by-regulating-tgf-%C3%AE-receptor-2-signaling-in-lung-adenocarcinoma
#10
Jun Li, Jie Ao, Kai Li, Jie Zhang, Yanyan Li, Le Zhang, Yuyan Wei, Di Gong, Junping Gao, Weiwei Tan, Lugang Huang, Lunxu Liu, Ping Lin, Yuquan Wei
Multidrug resistance (MDR) is one of the most important contributors to the high mortality of cancer and remains a major concern. We previously found that zinc finger protein 32 (ZNF32), an important transcription factor associated with cancer in Homo sapiens, protects tumor cells against cell death induced by oxidative stress and other stimuli. We thus hypothesized that ZNF32 might enable the tolerance of cancer cells to anti-tumor drugs because higher ZNF32 expression has been found in cancer tissues and in drug-resistant lung adenocarcinoma (AC) cells...
October 20, 2016: Cell Death & Disease
https://www.readbyqxmd.com/read/27742777/pnpla3-overexpression-results-in-reduction-of-proteins-predisposing-to-fibrosis
#11
Piero Pingitore, Paola Dongiovanni, Benedetta Maria Motta, Marica Meroni, Saverio Massimo Lepore, Rosellina Margherita Mancina, Serena Pelusi, Cristina Russo, Andrea Caddeo, Giorgio Rossi, Tiziana Montalcini, Arturo Pujia, Olov Wiklund, Luca Valenti, Stefano Romeo
Liver fibrosis is a pathological scarring response to chronic hepatocellular injury and hepatic stellate cells (HSCs) are key players in this process. PNPLA3 I148M is a common variant robustly associated with liver fibrosis but the mechanisms underlying this association are unknown.We aimed to examine a) the effect of fibrogenic and proliferative stimuli on PNPLA3 levels in HSCs and b) the role of wild type and mutant PNPLA3 overexpression on markers of HSC activation and fibrosis.Here we show that PNPLA3 is upregulated by the fibrogenic cytokine transforming growth factor-beta (TGF-β), but not by platelet-derived growth factor (PDGF), and is involved in the TGF-β-induced reduction in lipid droplets in primary human HSCs...
October 13, 2016: Human Molecular Genetics
https://www.readbyqxmd.com/read/27720345/transforming-growth-factor-beta-1-increases-collagen-content-and-stimulates-procollagen-i-and-tissue-inhibitor-of-metalloproteinase-1-production-of-dental-pulp-cells-role-of-mek-erk-and-activin-receptor-like-kinase-5-smad-signaling
#12
Po-Shuen Lin, Hsiao-Hua Chang, Chien-Yang Yeh, Mei-Chi Chang, Chiu-Po Chan, Han-Yueh Kuo, Hsin-Cheng Liu, Wan-Chuen Liao, Po-Yuan Jeng, Sin-Yuet Yeung, Jiiang-Huei Jeng
BACKGROUND/PURPOSE: In order to clarify the role of transforming growth factor beta 1 (TGF-β1) in pulp repair/regeneration responses, we investigated the differential signaling pathways responsible for the effects of TGF-β1 on collagen turnover, matrix metalloproteinase-3 (MMP-3), and tissue inhibitor of metalloproteinase-1 (TIMP-1) production in human dental pulp cells. METHODS: Pulp cells were exposed to TGF-β1 with/without pretreatment and coincubation by 1,4-diamino-2,3-dicyano-1,4-bis(o-aminophenyl mercapto)butadiene (U0126; a mitogen-activated protein kinase kinase [MEK]/extracellular signal-regulated kinase [ERK] inhibitor) and 4-(5-benzol[1,3]dioxol-5-yl-4-pyrldin-2-yl-1H- imidazol-2-yl)-benzamide hydrate (SB431542; an activin receptor-like kinase-5/Smad signaling inhibitor)...
October 6, 2016: Journal of the Formosan Medical Association, Taiwan Yi Zhi
https://www.readbyqxmd.com/read/27714812/dact1-a-wnt-pathway-inhibitor-mediates-human-mesangial-cell-tgf-%C3%AE-1-induced-apoptosis
#13
Daniele Pereira Jardim, Paula Cristina Eiras Poço, Alexandre Holthausen Campos
Chronic kidney disease (CKD) is a worldwide public health problem that affects millions of men and women of all ages and racial groups. Loss of mesangial cells (MC) represents an early common feature in the pathogenesis of CKD. Transforming growth factor-β1 (TGF-β1) is a key inducer of kidney damage and triggers several pathological changes in renal cells, notably MC apoptosis. However, the mechanism of MC apoptosis induced by TGF-β1 remains elusive. Here we demonstrate for the first time a novel regulatory pathway in which the disheveled-binding antagonist of beta-catenin 1 (Dact1) gene is upregulated by TGF-β1, inducing MC apoptosis...
October 7, 2016: Journal of Cellular Physiology
https://www.readbyqxmd.com/read/27702653/ucn-enhances-tgf-beta-mediated-mitoinhibition-of-vsmcs-via-counteracting-tgf-beta-induced-cpla2-expression-and-activation
#14
Chao Zhu, Changchun Cao, Xiaofei Wang, Jie Yuan, Lai Jin, Shengnan Li
Urocortins (UCNs) and transforming growth factor-beta (TGF-beta) have been demonstrated to participate in various cardiovascular diseases, many of which involve vascular smooth muscle cells (VSMCs) proliferation. Cytosolic phospholipase A2 (cPLA2)-mediated arachidonic acid (AA) release is an important cause of VSMCs proliferation. The work was to investigate the regulation of VSMCs proliferation by UCN/TGF-beta and whether cPLA2 was a link between their signaling pathways. VSMCs proliferation was measured by colorimetric assay and immunofluorescence microscopy...
October 1, 2016: International Journal of Biochemistry & Cell Biology
https://www.readbyqxmd.com/read/27679717/cardiovascular-renal-complications-and-the-possible-role-of-plasminogen-activator-inhibitor-a-review
#15
John A D'Elia, George Bayliss, Ray E Gleason, Larry A Weinrauch
Since angiotensin increases the expression of plasminogen activator inhibitor (PAI), mechanisms associated with an actively functioning renin-angiotensin-aldosterone system can be expected to be associated with increased PAI-1 expression. These mechanisms are present not only in common conditions resulting in glomerulosclerosis associated with aging, diabetes or genetic mutations, but also in autoimmune disease (like scleroderma and lupus), radiation injury, cyclosporine toxicity, allograft nephropathy and ureteral obstruction...
October 2016: Clinical Kidney Journal
https://www.readbyqxmd.com/read/27673327/roles-of-hdac2-and-hdac8-in-cardiac-remodeling-in-renovascular-hypertensive-rats-and-the-effects-of-valproic-acid-sodium
#16
Rui-Fang Li, Shan-Shan Cao, Wei-Jin Fang, Ying Song, Xue-Ting Luo, Hong-Yun Wang, Jian-Gang Wang
Recent studies indicate that histone deacetylases (HDACs) activity is associated with the development and progression of cardiac hypertrophy. In this study, we investigated the effects of a HDACs inhibitor, valproic acid sodium (VPA), on cardiac remodeling and the differential expression of HDACs in left ventricles (LVs) of renovascular hypertensive rats. Renovascular hypertension was induced in rats by the two-kidney two-clip (2K2C) method. Cardiac remodeling, heart function and the differential expression of HDACs were examined at different weeks after 2K2C operation...
September 27, 2016: Pharmacology
https://www.readbyqxmd.com/read/27649383/testing-for-the-erythropoiesis-stimulating-agent-sotatercept-ace-011-actriia-fc-in-serum-by-means-of-western-blotting-and-lc-hrms
#17
Katja Walpurgis, Andreas Thomas, Matthias Vogel, Christian Reichel, Hans Geyer, Wilhelm Schänzer, Mario Thevis
Sotatercept (formerly ACE-011) is a glycosylated, dimeric fusion protein composed of the extracellular domain of the human activin receptor type IIA (ActRIIA) and the Fc region of human IgG1. The protein-based drug candidate acts as a ligand trap which competitively binds to activin A and other members of the transforming growth factor beta superfamily, thus blocking signalling through ActRIIA. Since the inhibition of activin A was found to significantly increase bone formation and quality, Sotatercept was originally developed for the treatment of diseases involving bone loss...
September 20, 2016: Drug Testing and Analysis
https://www.readbyqxmd.com/read/27640434/the-possible-role-of-ns3-protease-activity-of-hepatitis-c-virus-on-fibrogenesis-and-mir-122-expression-in-hepatic-stellate-cells
#18
S Khanizadeh, M Ravanshad, S Y Hosseini, P Davoodian, A N Zadeh, F Sabahi, J Sarvari, Z Khanlari, M Hasani-Azad
The various roles of hepatitis C virus (HCV) NS3 protein in viral pathogenesis are emphasized, especially in the progression of fibrosis and tumors. The levels of miR-122 have been widely accepted as a critical factor in viral pathogenesis and disease progression. However, the possible correlation between miR-122 levels and fibrosis state has been less investigated. Therefore, in this study, plasmids expressing protease competent and protease mutated non-structural proteins 3 (NS3) were transfected into LX-2 cell line...
2016: Acta Virologica
https://www.readbyqxmd.com/read/27602954/hypoxia-promotes-glioma-associated-macrophage-infiltration-via-periostin-and-subsequent-m2-polarization-by-upregulating-tgf-beta-and-m-csfr
#19
Xiaofan Guo, Hao Xue, Qianqian Shao, Jian Wang, Xing Guo, Xi Chen, Jinsen Zhang, Shugang Xu, Tong Li, Ping Zhang, Xiao Gao, Wei Qiu, Qinglin Liu, Gang Li
Tumor-associated macrophages (TAMs) are enriched in gliomas and help create a tumor-immunosuppressive microenvironment. A distinct M2-skewed type of macrophages makes up the majority of glioma TAMs, and these cells exhibit pro-tumor functions. Gliomas contain large hypoxic areas, and the presence of a correlation between the density of M2-polarized TAMs and hypoxic areas suggests that hypoxia plays a supportive role during TAM recruitment and induction. Here, we investigated the effects of hypoxia on human macrophage recruitment and M2 polarization...
September 2, 2016: Oncotarget
https://www.readbyqxmd.com/read/27596071/nickel-oxide-nanoparticles-induced-pulmonary-fibrosis-via-tgf-%C3%AE-1-activation-in-rats
#20
X H Chang, A Zhu, F F Liu, L Y Zou, L Su, S K Liu, H H Zhou, Y Y Sun, A J Han, Y F Sun, S Li, J Li, Y B Sun
Nano nickel oxide (NiO), widely used in industry, has recently been discovered to have pulmonary toxicity. However, no subchronic exposure studies about nano NiO-induced pulmonary fibrosis have been reported. The objective of this study was to investigate pulmonary fibrosis induced by nano NiO and its potential mechanism in rats. Male Wistar rats (n = 40, 200-240 g) were randomized into control group, nano NiO groups (0.015, 0.06, and 0.24 mg/kg), and micro NiO group (0.024 mg/kg). All rats were killed to collect lung tissue after intratracheal instillation of NiO particles twice a week for 6 weeks...
September 5, 2016: Human & Experimental Toxicology
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