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Journal articles on the topic 'Collagen Type 1 CTGF'

Author: Grafiati

Published: 9 March 2023

Last updated: 31 July 2025

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1

Takeuchi, H., S. Kubota, E. Murakashi, et al. "Nicotine-induced CCN2: from Smoking to Periodontal Fibrosis." Journal of Dental Research 89, no. 1 (2009): 34–39. http://dx.doi.org/10.1177/0022034509353403.

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Since fibrosis is observed in smokers’ gingiva, it was hypothesized that fibrosis was caused by nicotine in the periodontium. Therefore, in this study, we investigated the effects of nicotine on the induction of a profibrotic molecule, connective tissue growth factor (CCN2/CTGF), in human gingival fibroblasts (HGFs) and periodontal ligament (PDL) cells. With 1 μg/mL nicotine, vacuolization and attenuated proliferation were observed. Interestingly, 1 μg/mL nicotine increased the production of CCN2/CTGF protein in both cells without increasing mRNA expression. Furthermore, type I collagen mRNA a

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2

Romero, Jose R., Dennis A. Ricupero, Alicia Rivera, Ronald H. Goldstein, and Paul R. Conlin. "Activation of Na + /Ca 2+ Exchanger in Kinin B 1 Receptor-Stimulated Human Fibroblast Is Associated with Collagen Production." Hypertension 36, suppl_1 (2000): 710–20. http://dx.doi.org/10.1161/hyp.36.suppl_1.710.

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P148 The arterial wall in hypertension is characterized by thickening of the media, in part due to increased deposition of connective tissue. Autocrine and paracrine factors may participate in this process; including products of the kallikrein-kinin system. We evaluated early signal transduction events and effects on collagen formation in B 1 -stimulated human myofibroblast cells (IMR-90). We measured cytosolic calcium (Ca cyt ) levels in cells loaded with FURA-2AM. Gene expression of connective tissue growth factor (CTGF) and α1(I) collagen was determined by estimating mRNA levels using North

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3

Chen, Chung-Ming, Hsiu-Chu Chou, Leng-Fang Wang, and Yaw-Dong Lang. "Experimental Oligohydramnios Decreases Collagen in Hypoplastic Fetal Rat Lungs." Experimental Biology and Medicine 233, no. 11 (2008): 1334–40. http://dx.doi.org/10.3181/0803-rm-99.

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Neonates with premature rupture of the membrane and oligohydramnios have an increased risk of acute respiratory morbidity. The aims of this study are to investigate the effects of experimental oligohydramnios on transforming growth factor (TGF)-β1 and connective tissue growth factor (CTGF) expressions and collagen level in fetal rat lungs. On day 16 of gestation, we anesthetized timed pregnant Sprague-Dawley dams, punctured the uterine wall and fetal membranes of each amniotic sac which resulted in oligohydramnios. Fetuses in the opposite uterine horn served as controls. On days 19 and 21 of g

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Zhou, Hong, Caixia Fang, Lihui Zhang, Yonggui Deng, Mian Wang, and Fengling Meng. "Fasudil hydrochloride hydrate, a Rho-kinase inhibitor, ameliorates hepatic fibrosis in rats with type 2 diabetes." Chinese Medical Journal 127, no. 2 (2014): 225–31. http://dx.doi.org/10.3760/cma.j.issn.0366-6999.20131917.

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Background Hyperglycemia may accelerate liver fibrosis. Currently, there is no effective treatment for liver fibrosis induced by type 2 diabetes. The study aim was to investigate whether RhoA/Rho kinase (ROCK) pathway is involved in liver fibrosis in the rats with type 2 diabetes and define the protective effects of fasudil on livers. Methods A rat model of type 2 diabetes was established by high fat diet combined with streptozotocin (30 mg/kg, intraperitoneal injection). Animals were randomly assigned to 3 groups: control rats, untreated diabetic rats that received vehicle and fasudil-treated

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Wang, Shinong, та Raimund Hirschberg. "BMP7 antagonizes TGF-β-dependent fibrogenesis in mesangial cells". American Journal of Physiology-Renal Physiology 284, № 5 (2003): F1006—F1013. http://dx.doi.org/10.1152/ajprenal.00382.2002.

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Exogenous administration of recombinant human bone morphogenetic protein (BMP)-7 was recently shown to ameliorate renal glomerular and interstitial fibrosis in rodents with experimental renal diseases. We tested the hypothesis that BMP7 functions by antagonizing profibrogenic events that are induced by transforming growth factor (TGF)-β in cultured mesangial cells. Incubation of murine mesangial cells with TGF-β (50–200 pM) increased cell-associated collagen type IV and fibronectin, soluble collagen type IV, thrombospondin, and connective tissue growth factor (CTGF). Coincubation with recombin

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Chaqour, Brahim, Catherine Whitbeck, Ji-Soo Han, et al. "Cyr61 and CTGF are molecular markers of bladder wall remodeling after outlet obstruction." American Journal of Physiology-Endocrinology and Metabolism 283, no. 4 (2002): E765—E774. http://dx.doi.org/10.1152/ajpendo.00131.2002.

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Cysteine-rich protein (Cyr61) and connective tissue growth factor (CTGF) are key immediate early growth factors with functions in cell proliferation, differentiation, and extracellular matrix synthesis. Studies were performed to assess the gene expression profile of Cyr61 and CTGF in rat urinary bladder during growth in response to partial outlet obstruction. The mRNA levels of Cyr61 as determined by ribonuclease protection assay increased sharply after 1 day and remained elevated throughout the time period of the obstruction. This correlates well with increased bladder weight. The CTGF mRNA l

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7

Zhang, Lin, Jin Tan, Yi-Ping Liu, Xun Liu та Mang Luo. "Curcumin relieves the arecoline-induced fibrosis of oral mucosal fibroblasts via inhibiting HIF-1α/TGF-β/CTGF signaling pathway: an in vitro study". Toxicology Research 10, № 3 (2021): 631–38. http://dx.doi.org/10.1093/toxres/tfab046.

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Abstract Oral submacosal fibrosis (OSF) has been recognized as one of the oral potentially malignant disorders. Areca nut chewing is implicated in this pathological fibrosis. The current treatments for OSF have failed to achieve the desired curative effect. Here, we propose that curcumin has excellent therapeutic effect on OSF and explore its specific mechanism. Transwell assay was performed to detected cell migration. Flow cytometry was used to measured apoptosis. And MTT assay was performed to test cell viability. Gene and protein levels were detected by quantitative real-time polymerase cha

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Hillege, Michèle, Ricardo Galli Caro, Carla Offringa, Gerard de Wit, Richard Jaspers та Willem Hoogaars. "TGF-β Regulates Collagen Type I Expression in Myoblasts and Myotubes via Transient Ctgf and Fgf-2 Expression". Cells 9, № 2 (2020): 375. http://dx.doi.org/10.3390/cells9020375.

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Transforming Growth Factor β (TGF-β) is involved in fibrosis as well as the regulation of muscle mass, and contributes to the progressive pathology of muscle wasting disorders. However, little is known regarding the time-dependent signalling of TGF-β in myoblasts and myotubes, as well as how TGF-β affects collagen type I expression and the phenotypes of these cells. Here, we assessed effects of TGF-β on gene expression in C2C12 myoblasts and myotubes after 1, 3, 9, 24 and 48 h treatment. In myoblasts, various myogenic genes were repressed after 9, 24 and 48 h, while in myotubes only a reductio

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9

McDonald, Emily A., Ling Cheng, Blanca Jarilla, et al. "Maternal Infection with Schistosoma japonicum Induces a Profibrotic Response in Neonates." Infection and Immunity 82, no. 1 (2013): 350–55. http://dx.doi.org/10.1128/iai.01060-13.

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ABSTRACTThe global burden of schistosomiasis is significant, with fibrosis a major associated morbidity and the primary cause of mortality. We have previously shown that schistosomiasis during pregnancy upregulates proinflammatory cytokines in the cord blood. In this study, we extend these findings to include a large panel of fibrosis-associated markers. We developed a multiplex bead-based assay to measure the levels of 35 proteins associated with fibrosis. Cord blood from 109 neonates born to mothers residing in an area ofSchistosoma japonicumendemicity was assessed for these molecules. Ten m

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Roestenberg, Peggy, Frans A. van Nieuwenhoven, Jaap A. Joles, et al. "Temporal expression profile and distribution pattern indicate a role of connective tissue growth factor (CTGF/CCN-2) in diabetic nephropathy in mice." American Journal of Physiology-Renal Physiology 290, no. 6 (2006): F1344—F1354. http://dx.doi.org/10.1152/ajprenal.00174.2005.

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Connective tissue growth factor (CTGF) is overexpressed in diabetic nephropathy (DN) and has therefore been implicated in its pathogenesis. The objective of the present study was to determine the tissue distribution of increased CTGF expression and the relationship of plasma, urinary, and renal CTGF levels to the development and severity of DN. We studied the relationship between CTGF and renal pathology in streptozotocin (STZ)-induced diabetes in C57BL/6J mice. Diabetic and age-matched control mice were killed after 1, 2, 4, and 9 wk of diabetes. In addition, key parameters of diabetes and DN

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Ploeg, Meike C., Chantal Munts, Tayeba Seddiqi та ін. "Culturing of Cardiac Fibroblasts in Engineered Heart Matrix Reduces Myofibroblast Differentiation but Maintains Their Response to Cyclic Stretch and Transforming Growth Factor β1". Bioengineering 9, № 10 (2022): 551. http://dx.doi.org/10.3390/bioengineering9100551.

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Isolation and culturing of cardiac fibroblasts (CF) induces rapid differentiation toward a myofibroblast phenotype, which is partly mediated by the high substrate stiffness of the culture plates. In the present study, a 3D model of Engineered Heart Matrix (EHM) of physiological stiffness (Youngs modulus ~15 kPa) was developed using primary adult rat CF and a natural hydrogel collagen type 1 matrix. CF were equally distributed, viable and quiescent for at least 13 days in EHM and the baseline gene expression of myofibroblast-markers alfa-smooth muscle actin (Acta2), and connective tissue growth

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Wu, Shi-Bei, Tzu-Yu Hou, Hui-Chuan Kau та Chieh-Chih Tsai. "Effect of Pirfenidone on TGF-β1-Induced Myofibroblast Differentiation and Extracellular Matrix Homeostasis of Human Orbital Fibroblasts in Graves’ Ophthalmopathy". Biomolecules 11, № 10 (2021): 1424. http://dx.doi.org/10.3390/biom11101424.

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Pirfenidone is a pyridinone derivative that has been shown to inhibit fibrosis in animal models and in patients with idiopathic pulmonary fibrosis. Its effect on orbital fibroblasts remains poorly understood. We investigated the in vitro effect of pirfenidone in transforming growth factor-β1 (TGF-β1)-induced myofibroblast transdifferentiation and extracellular matrix (ECM) homeostasis in primary cultured orbital fibroblasts from patients with Graves’ ophthalmopathy (GO). The expression of fibrotic proteins, including α-smooth muscle actin (α-SMA), connective tissue growth factor (CTGF), fibron

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Liu, Mengxuan, Megumi Honjo, Reiko Yamagishi, and Makoto Aihara. "Effects of Brimonidine, Latanoprost, and Omidenepag on Tunicamycin-Induced Endoplasmic Reticulum Stress and Fibrosis in Human Trabecular Meshwork Cells." Biomolecules 15, no. 3 (2025): 389. https://doi.org/10.3390/biom15030389.

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This study evaluated the effects of α2-adrenergic agonist, prostaglandin F2α analog, and EP2 receptor agonist on tunicamycin-induced endoplasmic reticulum (ER) stress and fibrosis in human trabecular meshwork (TM) cells. Human TM cells were treated with tunicamycin for 24 h, followed by cotreatment with brimonidine (BRI), latanoprost (LAT), or omidenepag (OMD). Immunocytochemistry was used to assess expressions of collagen type I alpha 1 chain (COL1A1), fibronectin, F-actin, and alpha-smooth muscle actin (α-SMA). Western blotting was performed to evaluate levels of C/EBP homologous protein (CH

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Yang, Guimin, Yupeng Deng, Guangming Cao, and Chongdong Liu. "Galectin-3 promotes fibrosis in ovarian endometriosis." PeerJ 12 (February 14, 2024): e16922. http://dx.doi.org/10.7717/peerj.16922.

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Objective This study aimed to investigate the potential role of galectin-3 (Gal-3) in the pathogenesis of fibrotic alterations in ovarian endometriosis (OVE). Methods In this study, we collected the ectopic endometrial tissues and eutopic endometrial tissues from 31 OVE patients treated by laparoscopy, and the eutopic endometrial tissues from 23 non-OVE patients with leiomyoma or other benign diseases were used as control. Hematoxylin and eosin (H&E) and Masson’s trichrome staining were utilized for histopathological assessment. The primary normal endometrial stromal cells (NESC), ectopic

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15

García-Bañuelos, Jesús, Edén Oceguera-Contreras, Ana Sandoval-Rodríguez, et al. "AdhMMP8 Vector Administration in Muscle: An Alternate Strategy to Regress Hepatic Fibrosis." Cells 12, no. 17 (2023): 2127. http://dx.doi.org/10.3390/cells12172127.

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The development of several vaccines against the SARS-CoV2 virus and their application in millions of people have shown efficacy and safety in the transfer of genes to muscle turning this tissue into a protein-producing factory. Established advanced liver fibrosis, is characterized by replacement of hepatic parenchyma by tissue scar, mostly collagen type I, with increased profibrogenic and proinflammatory molecules gene expression. Matrix metalloproteinase 8 (MMP-8) is an interstitial collagen-degrading proenzyme acting preferentially on collagen type I when activated. This study was carried ou

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16

DU, Li-qun, Hong-ling YANG, Xin-yi WU, Shen-guo WANG, and Yun LI. "Effect of poly(DL-lactide-co-glycolide) on scar formation after glaucoma filtration surgery." Chinese Medical Journal 126, no. 23 (2013): 4528–35. http://dx.doi.org/10.3760/cma.j.issn.0366-6999.20131766.

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Background Glaucoma filtering surgery (GFS) is the most common procedure performed in the treatment of glaucoma. Although antiscarring agents help prevent postsurgical scarring and improve glaucoma surgical outcomes, they may be associated with an increased incidence of severe and potentially blinding complications. Poly(DL-lactide-co-glycolide) (PDLLA/GA) is a bioresorbable polymer, which can be prepared with a large range of physical, mechanical, and biological properties and has been widely used in medicine, including as an absorbable suture and a drug carrier and especially as a scaffold i

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Correll, Kelly A., Karen E. Edeen, Rachel L. Zemans, et al. "Transitional human alveolar type II epithelial cells suppress extracellular matrix and growth factor gene expression in lung fibroblasts." American Journal of Physiology-Lung Cellular and Molecular Physiology 317, no. 2 (2019): L283—L294. http://dx.doi.org/10.1152/ajplung.00337.2018.

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Epithelial-fibroblast interactions are thought to be very important in the adult lung in response to injury, but the specifics of these interactions are not well defined. We developed coculture systems to define the interactions of adult human alveolar epithelial cells with lung fibroblasts. Alveolar type II cells cultured on floating collagen gels reduced the expression of type 1 collagen (COL1A1) and α-smooth muscle actin (ACTA2) in fibroblasts. They also reduced fibroblast expression of hepatocyte growth factor (HGF), fibroblast growth factor 7 (FGF7, KGF), and FGF10. When type II cells wer

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Sheykhhasan, Mohsen, Hoda Fazaeli, Azar Sheikholeslami, Seyed Abbas Seyedebrahimi, Seyed Jalal Eshagh Hoseini, and Naser Kalhor. "Identification of Diagnostic Biomarkers by Bioinformatics Analysis in the Inflamed and Non-inflamed Intestinal Mucosa of Patients With Crohn’s Disease." Research in Molecular Medicine 9, no. 3 (2021): 209–20. http://dx.doi.org/10.32598/rmm.9.3.1069.4.

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Background: Crohn’s Disease (CD) is a type of inflammatory bowel disease that, despite its unknown etiology, is generally associated with genetics, immune system, and environmental factors. In this study, we uncover transcriptional signatures in patients with CD and subsequently explain the putative molecular pathways in the inflamed and non-inflamed intestinal mucosa. Materials and Methods: We obtain GSE83448 gene expression profiles from the Omnibus gene expression database. Also, for the Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis of Differentially Express

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Trundle, Jessica, Viktorija Cernisova, Alexis Boulinguiez, Ngoc Lu-Nguyen, Alberto Malerba, and Linda Popplewell. "Expression of the Pro-Fibrotic Marker Periostin in a Mouse Model of Duchenne Muscular Dystrophy." Biomedicines 12, no. 1 (2024): 216. http://dx.doi.org/10.3390/biomedicines12010216.

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Duchenne muscular dystrophy (DMD) is characterised by fibrotic tissue deposition in skeletal muscle. We assessed the role of periostin in fibrosis using mdx mice, an established DMD murine model, for which we conducted a thorough examination of periostin expression over a year. RNA and protein levels in diaphragm (DIA) muscles were assessed and complemented by a detailed histological analysis at 5 months of age. In dystrophic DIAs, periostin (Postn) mRNA expression significantly exceeded that seen in wildtype controls at all timepoints analysed, with the highest expression at 5 months of age (

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Xu, Xuefeng, Sa Luo, Biyun Li, Huaping Dai, and Jinglan Zhang. "IL-25 contributes to lung fibrosis by directly acting on alveolar epithelial cells and fibroblasts." Experimental Biology and Medicine 244, no. 9 (2019): 770–80. http://dx.doi.org/10.1177/1535370219843827.

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Interleukin (IL)-25 is shown to potentiate type-2 immunity and contribute to chronic airway inflammation and remodeling in allergic airway diseases. However, the role of IL-25 in idiopathic pulmonary fibrosis (IPF), dominated by nonatopic type-2 immunity, still remains largely unclear. Herein, we detected the expression levels of IL-25 and IL-17BR (IL-25’s receptor) by using lung tissue samples gained from IPF patients and normal subjects. Also, by directly intranasal (IN) instillation of IL-25 to mice, we examined the potential roles and mechanisms of IL-25 in the development of lung fibrosis

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McCurdy, Sarah M., Qiuxia Dai, Jianhua Zhang, et al. "SPARC mediates early extracellular matrix remodeling following myocardial infarction." American Journal of Physiology-Heart and Circulatory Physiology 301, no. 2 (2011): H497—H505. http://dx.doi.org/10.1152/ajpheart.01070.2010.

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Secreted protein, acidic, and rich in cysteine (SPARC) is a matricellular protein that functions in the extracellular processing of newly synthesized collagen. Collagen deposition to form a scar is a key event following a myocardial infarction (MI). Because the roles of SPARC in the early post-MI setting have not been defined, we examined age-matched wild-type (WT; n=22) and SPARC-deficient (null; n=25) mice at day 3 post-MI. Day 0 WT ( n=28) and null ( n=20) mice served as controls. Infarct size was 52 ± 2% for WT and 47 ± 2% for SPARC null ( P=NS), indicating that the MI injury was comparabl

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Wu, Qiuqian, and Jason H. Huang. "Ectopic expression of Smurf2 and acceleration of age-related intervertebral disc degeneration in a mouse model." Journal of Neurosurgery: Spine 27, no. 1 (2017): 116–26. http://dx.doi.org/10.3171/2016.11.spine16901.

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OBJECTIVELumbar intervertebral disc degeneration, an age-related process, is a major cause of low-back pain. Although low-back pain is a very common clinical problem in the aging population, no effective treatment is available, largely owing to lack of understanding of the molecular mechanisms underlying disc degeneration. The goal of this study was to characterize how ectopic expression of Smurf2 driven by the collagen Type II alpha 1 (Col2a1) promoter alters disc cell phenotype and associated cellular events, matrix synthesis, and gene expression during disc degeneration in mice.METHODSTo ch

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Morinaga, Jun, Yutaka Kakizoe, Taku Miyoshi, et al. "The antifibrotic effect of a serine protease inhibitor in the kidney." American Journal of Physiology-Renal Physiology 305, no. 2 (2013): F173—F181. http://dx.doi.org/10.1152/ajprenal.00586.2012.

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Interstitial fibrosis is a final common pathway for the progression of chronic kidney diseases. Activated fibroblasts have an extremely important role in the progression of renal fibrosis, and transforming growth factor (TGF)-β1 is a major activator of fibroblasts. Since previous reports have indicated that serine protease inhibitors have a potential to inhibit TGF-β1 signaling in vitro, we hypothesized that a synthetic serine protease inhibitor, camostat mesilate (CM), could slow the progression of renal fibrosis. TGF-β1 markedly increased the phosphorylation of TGF-β type I receptor, ERK 1/2

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Yang, Ru, Jawaria Amir, Haibo Liu, and Brahim Chaqour. "Mechanical strain activates a program of genes functionally involved in paracrine signaling of angiogenesis." Physiological Genomics 36, no. 1 (2008): 1–14. http://dx.doi.org/10.1152/physiolgenomics.90291.2008.

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Studies were performed to examine the extent to which mechanical stimuli mediate control of angiogenesis in bladder cells both in vitro and in vivo. Differential gene expression between control nonstretched and cyclically stretched bladder smooth muscle cells was assessed using oligonucleotide microarrays and pathway analysis by the web tool Fast Assignment and Transference of Information (FatiGO). Data showed that a substantial proportion (33 of 86) of mechanically responsive genes were angiogenesis-related and include cytokines, growth-related factors, adhesion proteins, and matricellular, s

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Zhou, Xuan, Jun Xiong, Shi Lu, et al. "Inhibitory Effect of Corilagin on miR-21-Regulated Hepatic Fibrosis Signaling Pathway." American Journal of Chinese Medicine 47, no. 07 (2019): 1541–69. http://dx.doi.org/10.1142/s0192415x19500794.

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Corilagin is a polyphenol that can be extracted from many medicinal plants and shows multiple pharmacological effects. We aimed to investigate the role of corilagin on miR-21-regulated hepatic fibrosis, especially miR-21-regulated TGF-[Formula: see text]1/Smad signaling pathway, in hepatic stellate LX2 cell line and Sprague–Dawley rats. The mRNA or protein levels of miR-21, Smad7, connective tissue growth factor (CTGF), [Formula: see text]-smooth muscle actin ([Formula: see text]-SMA), tissue inhibitor of metalloproteinase-1 (TIMP-1), matrix metalloproteinase-9 (MMP-9), collagen type I alpha 1

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Huang, Xiao R., Arthur C. K. Chung, Xiao J. Wang, Kar Neng Lai та Hui Y. Lan. "Mice overexpressing latent TGF-β1 are protected against renal fibrosis in obstructive kidney disease". American Journal of Physiology-Renal Physiology 295, № 1 (2008): F118—F127. http://dx.doi.org/10.1152/ajprenal.00021.2008.

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Transforming growth factor (TGF)-β1, once activated, binds to its receptors and mediates renal fibrosis via the downstream Smad signaling pathway. We reported here that mice overexpressing latent TGF-β1 in keratinocytes were protected against renal fibrosis in a model of obstructive kidney disease. In normal mice, both transgenic (Tg) and wild-type (WT) mice had normal renal histology and function, despite a 10-fold increase in plasma latent TGF-β1 in Tg mice. A severe renal fibrosis was developed in WT mice at 7 days after urinary obstruction. Unexpectedly, renal fibrosis was prevented in Tg

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Lee, Da-Young, Sun-Mi Yun, Moon-Young Song, Sang-Deok Ji, Jong-Gon Son та Eun-Hee Kim. "Administration of Steamed and Freeze-Dried Mature Silkworm Larval Powder Prevents Hepatic Fibrosis and Hepatocellular Carcinogenesis by Blocking TGF-β/STAT3 Signaling Cascades in Rats". Cells 9, № 3 (2020): 568. http://dx.doi.org/10.3390/cells9030568.

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Hepatocellular carcinoma (HCC) is the leading cause of cancer-related deaths worldwide and the majority of HCC patients occur with a background of hepatic fibrosis and cirrhosis. We have previously reported the hepatoprotective effects of steamed and freeze-dried mature silkworm larval powder (SMSP) in a chronic ethanol-treated rat model. Here, we assessed the anti-fibrotic and anti-carcinogenic effects of SMSP on diethylnitrosamine (DEN)-treated rats. Wistar rats were intraperitoneally injected with DEN once a week for 12 or 16 weeks with or without SMSP administration (0.1 and 1 g/kg). SMSP

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van Beusekom, Cyrina D., and Tanja M. Zimmering. "Profibrotic effects of angiotensin II and transforming growth factor beta on feline kidney epithelial cells." Journal of Feline Medicine and Surgery 21, no. 8 (2018): 780–87. http://dx.doi.org/10.1177/1098612x18805862.

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Objectives The aim of this study was to evaluate the role of angiotensin II (AT-II) and its main mediator, transforming growth factor beta 1 (TGF-β1), in the development of feline renal fibrosis. Methods Expression of marker genes indicating epithelial-to-mesenchymal transition (EMT), profibrotic mediators and matricellular proteins was measured in feline kidney epithelial cells (Crandell Rees feline kidney [CRFK] cells) after incubation with AT-II and/or TGF-β1. Results Cells incubated with TGF-β1 or the combination of TGF-β1 with AT-II showed clear EMT with more stretched fibroblastic cells,

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Lubel, John S., Chandana B. Herath, Jorge Tchongue, et al. "Angiotensin-(1–7), an alternative metabolite of the renin–angiotensin system, is up-regulated in human liver disease and has antifibrotic activity in the bile-duct-ligated rat." Clinical Science 117, no. 11 (2009): 375–86. http://dx.doi.org/10.1042/cs20080647.

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Ang-(1–7) (angiotensin-1–7), a peptide product of the recently described ACE (angiotensin-converting enzyme) homologue ACE2, opposes the harmful actions of AngII (angiotensin II) in cardiovascular tissues, but its role in liver disease is unknown. The aim of the present study was to assess plasma levels of Ang-(1–7) in human liver disease and determine its effects in experimental liver fibrosis. Angiotensin peptide levels were measured in cirrhotic and non-cirrhotic patients with hepatitis C. The effects of Ang-(1–7) on experimental fibrosis were determined using the rat BDL (bile-duct ligatio

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Schrör and Hohlfeld. "Mechanisms of anti-ischemic action of prostaglandin E1 in peripheral arterial occlusive disease." Vasa 33, no. 3 (2004): 119–24. http://dx.doi.org/10.1024/0301-1526.33.3.119.

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The mechanisms of anti-ischemic effects of PGE1 in patients with peripheral arterial occlusive disease (PAD) are probably complex and clearly not limited to a direct vasodilator action. In addition to the known effects on blood flow, viscosity, fibrinolysis and platelet aggregation, the compound also inhibits monocyte and neutrophil function, suggesting that PGE1 will also have anti-inflammatory effects. Recent research has detected additional actions of PGE1 and prostacyclin analogs which might be relevant to its clinical efficacy. This includes inhibition of expression of adhesion molecules

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Qiu, Ming, Huanyu Shu, Lu Li та ін. "Interleukin 10 Attenuates Angiotensin II-Induced Aortic Remodelling by Inhibiting Oxidative Stress-Induced Activation of the Vascular p38 and NF-κB Pathways". Oxidative Medicine and Cellular Longevity 2022 (26 квітня 2022): 1–15. http://dx.doi.org/10.1155/2022/8244497.

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Interleukin 10 (IL-10) is a probable anti-inflammatory factor that can attenuate hypertrophic remodelling caused by overloaded pressure and improve cardiac function. In this study, IL-10 was decreased in both the plasma of hypertensive patients and the aortic vessels of angiotensin II (Ang II)-induced hypertensive mice. IL-10 was unable to alter blood pressure in the case of Ang II-induced hypertension. The aortic thickness, collagen deposition, and the levels of fibrosis-associated markers, including collagen type I α 1 (Col1α1), connective tissue growth factor (CTGF), transforming growth fac

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Qiu, Ming, Huanyu Shu, Lu Li та ін. "Interleukin 10 Attenuates Angiotensin II-Induced Aortic Remodelling by Inhibiting Oxidative Stress-Induced Activation of the Vascular p38 and NF-κB Pathways". Oxidative Medicine and Cellular Longevity 2022 (26 квітня 2022): 1–15. http://dx.doi.org/10.1155/2022/8244497.

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Interleukin 10 (IL-10) is a probable anti-inflammatory factor that can attenuate hypertrophic remodelling caused by overloaded pressure and improve cardiac function. In this study, IL-10 was decreased in both the plasma of hypertensive patients and the aortic vessels of angiotensin II (Ang II)-induced hypertensive mice. IL-10 was unable to alter blood pressure in the case of Ang II-induced hypertension. The aortic thickness, collagen deposition, and the levels of fibrosis-associated markers, including collagen type I α 1 (Col1α1), connective tissue growth factor (CTGF), transforming growth fac

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Peterson, Joshua M., Anesh Prasai, Jayson W. Jay, Steven E. Wolf, and Amina El Ayadi. "143 Galunisertib Exerts Targeted Anti-Fibrotic Effects in In Vitro Models of Burn Wound Healing." Journal of Burn Care & Research 42, Supplement_1 (2021): S95. http://dx.doi.org/10.1093/jbcr/irab032.147.

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Abstract Introduction Inhibition of TGF-β has shown promising in vitro and in vivo results for reduction of hypertrophic scarring after burn injury. However, TGF-β regulates diverse cellular pathways apart from fibrosis, including physiologic wound healing, cell cycle control, and homeostasis. Galunisertib, a novel small molecular tyrosine kinase inhibitor of TGF-beta receptor type 1, specifically targets downstream pro-fibrotic pathways of TGF-β signaling, has an excellent adverse effect profile, and minimal off-target effects. We hypothesized that galunisertib diminishes fibrotic phenotypes

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Lu, H. K., H. P. Chou, C. L. Li, M. Y. Wang та L. F. Wang. "Stimulation of Cells Derived from Nifedipine-induced Gingival Overgrowth with Porphyromonas gingivalis, Lipopolysaccharide, and Interleukin-1β". Journal of Dental Research 86, № 11 (2007): 1100–1104. http://dx.doi.org/10.1177/154405910708601115.

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The purpose of this study was to clarify the main contributory factor of nifedipine-induced gingival overgrowth either by Porphyromonas gingivalis lipopolysaccharide ( Pg-LPS) or interleukin-1beta (IL-1β). Human gingival fibroblasts from healthy tissues and nifedipine-induced gingival overgrowth tissues were stimulated with nifedipine, IL-1β, Escherichia coli lipopolysaccharide ( Ec-LPS), and Pg-LPS, and the gene expressions were analyzed by RT-PCR. Analysis of the data showed no strong evidence of a synergistic effect of nifedipine and Pg-LPS on IL-6, connective tissue growth factor (CTGF), a

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Trink, Jackie, Renzhong Li, Yaseelan Palarasah, et al. "Activated Alpha 2-Macroglobulin Is a Novel Mediator of Mesangial Cell Profibrotic Signaling in Diabetic Kidney Disease." Biomedicines 9, no. 9 (2021): 1112. http://dx.doi.org/10.3390/biomedicines9091112.

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Diabetic kidney disease (DKD) is caused by the overproduction of extracellular matrix proteins (ECM) by glomerular mesangial cells (MCs). We previously showed that high glucose (HG) induces cell surface translocation of GRP78 (csGRP78), mediating PI3K/Akt activation and downstream ECM production. Activated alpha 2-macroglobulin (α2M*) is a ligand known to initiate this signaling cascade. Importantly, increased α2M was observed in diabetic patients’ serum, saliva, and glomeruli. Primary MCs were used to assess HG responses. The role of α2M* was assessed using siRNA, a neutralizing antibody and

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Castillero, Estibaliz, Hirokazu Akashi, Marc Najjar, et al. "Activin type II receptor ligand signaling inhibition after experimental ischemic heart failure attenuates cardiac remodeling and prevents fibrosis." American Journal of Physiology-Heart and Circulatory Physiology 318, no. 2 (2020): H378—H390. http://dx.doi.org/10.1152/ajpheart.00302.2019.

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Myostatin (MSTN) is a transforming growth factor (TGF)-β superfamily member that acts as a negative regulator of muscle growth and may play a role in cardiac remodeling. We hypothesized that inhibition of activin type II receptors (ACTRII) to reduce MSTN signaling would reduce pathological cardiac remodeling in experimental heart failure (HF). C57BL/6J mice underwent left anterior descending coronary artery ligation under anesthesia to induce myocardial infarction (MI) or no ligation (sham). MI and sham animals were each randomly divided into groups ( n ≥ 10 mice/group) receiving an ACTRII or

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Yoon, Jung Joo, Yun Jung Lee, Dae Gill Kang, and Ho Sub Lee. "Protective Role of Oryeongsan Against Renal Inflammation and Glomerulosclerosis in db/db Mice." American Journal of Chinese Medicine 42, no. 06 (2014): 1431–52. http://dx.doi.org/10.1142/s0192415x14500906.

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Diabetic nephropathy is characterized by renal hardening and interstitial fibrosis caused by extracellular matrix (ECM) accumulation. The most distinctive diabetic lesion in the glomeruli is mesangial expansion and hyperplasia, which ultimately leads to diabetic nephrosclerosis. Oryeongsan (ORS), a traditional Chinese herbal medication, is widely used to treat nephrosis, dropsy, and uremia. In this study, type 2 diabetic animals (db/db mice) were administered ORS (100 mg/kg/day) for 8 weeks to examine the potential beneficial effects on metabolic abnormalities and diabetic nephropathy progress

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Subramanian, Umadevi, Chandramohan Ramasamy, Samivel Ramachandran, Joshua M. Oakes, Jason D. Gardner та Kailash N. Pandey. "Genetic Disruption of Guanylyl Cyclase/Natriuretic Peptide Receptor-A Triggers Differential Cardiac Fibrosis and Disorders in Male and Female Mutant Mice: Role of TGF-β1/SMAD Signaling Pathway". International Journal of Molecular Sciences 23, № 19 (2022): 11487. http://dx.doi.org/10.3390/ijms231911487.

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The global targeted disruption of the natriuretic peptide receptor-A (NPRA) gene (Npr1) in mice provokes hypertension and cardiovascular dysfunction. The objective of this study was to determine the mechanisms regulating the development of cardiac fibrosis and dysfunction in Npr1 mutant mice. Npr1 knockout (Npr1−/−, 0-copy), heterozygous (Npr1+/−, 1-copy), and wild-type (Npr1+/+, 2-copy) mice were treated with the transforming growth factor (TGF)-β1 receptor (TGF-β1R) antagonist GW788388 (2 µg/g body weight/day; ip) for 28 days. Hearts were isolated and used for real-time quantitative reverse

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Scavo, Maria Principia, Giuseppe Lisco, Nicoletta Depalo, et al. "Semaglutide Modulates Extracellular Matrix Production of LX-2 Cells via Exosomes and Improves Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD)." International Journal of Molecular Sciences 25, no. 3 (2024): 1493. http://dx.doi.org/10.3390/ijms25031493.

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Metabolic dysfunction-associated steatotic liver disease (MASLD) is closely related to some metabolic disorders, such as central obesity and type 2 diabetes (T2D). Glucagon-like peptide 1 receptor agonists (GLP-1RAs), such as semaglutide, may have therapeutic roles in MASLD associated with T2D. This study aims to investigate the molecular mechanisms underlying the effectiveness of semaglutide on MASLD in terms of progression from liver steatosis to fibrosis. We characterized exosomes from ten patients with type 2 diabetes (T2D) before (T0) and after 12 months (T12) of treatment with once-weekl

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Sánchez-López, Elsa, Juan Rodriguez-Vita, Cecile Cartier та ін. "Inhibitory effect of interleukin-1β on angiotensin II-induced connective tissue growth factor and type IV collagen production in cultured mesangial cells". American Journal of Physiology-Renal Physiology 294, № 1 (2008): F149—F160. http://dx.doi.org/10.1152/ajprenal.00129.2007.

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Connective tissue growth factor (CTGF) is overexpressed in kidney diseases associated with extracellular matrix accumulation. Angiotensin II (ANG II) participates in renal fibrosis by the upregulation of growth factors, including CTGF, and extracellular matrix proteins, such as type IV collagen. During renal injury, ANG II and the macrophage-produced cytokine interleukin-1β (IL-1β) may be present simultaneously in the glomerular environment. However, there are no studies about the interaction between ANG II and IL-1β in renal fibrosis. For this reason, in cultured mesangial cells (MC), we inve

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Kennedy, David, Fatimah Khalaf, Brendan Sheehy, et al. "Telocinobufagin, a Novel Cardiotonic Steroid, Promotes Renal Fibrosis via Na+/K+-ATPase Profibrotic Signaling Pathways." International Journal of Molecular Sciences 19, no. 9 (2018): 2566. http://dx.doi.org/10.3390/ijms19092566.

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Cardiotonic steroids (CTS) are Na+/K+-ATPase (NKA) ligands that are elevated in volume-expanded states and associated with cardiac and renal dysfunction in both clinical and experimental settings. We test the hypothesis that the CTS telocinobufagin (TCB) promotes renal dysfunction in a process involving signaling through the NKA α-1 in the following studies. First, we infuse TCB (4 weeks at 0.1 µg/g/day) or a vehicle into mice expressing wild-type (WT) NKA α-1, as well as mice with a genetic reduction (~40%) of NKA α-1 (NKA α-1+/−). Continuous TCB infusion results in increased proteinuria and

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Ding, Luo-Bin, Yao Li, Guang-Yuan Liu та ін. "Long non-coding RNA PVT1, a molecular sponge of miR-26b, is involved in the progression of hyperglycemia-induced collagen degradation in human chondrocytes by targeting CTGF/TGF-β signal ways". Innate Immunity 26, № 3 (2019): 204–14. http://dx.doi.org/10.1177/1753425919881778.

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The current study was conducted to investigate the role of long non-coding RNA PVT1 in hyperglycemia-triggered human osteoarthritis (OA) chondrocytes. Cartilage from knee OA patients with and without diabetes, as well as normal cartilage, was obtained. Isolated human chondrocytes were treated with 30 nM of Glc with or without pioglitazone. The expression levels of PVT1, miR-26b, and type II collagen were determined by RT-PCR. Type II collagen was detected by immunocytochemistry and chondrocytes were stained with Alcian blue. Moreover, the interaction among PVT1, miR-26b, and CTGF was examined

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Chiu, Y. H., J. Spierings, J. M. Van Laar, J. De Vries-Bouwstra, M. Van Dijk, and R. Goldschmeding. "POS0469 ENDOTHELIAL TO MESENCHYMAL TRANSITION AND SENESCENCE ARE PART OF THE FIBROTIC PATHOGENESIS IN SYSTEMIC SCLEROSIS." Annals of the Rheumatic Diseases 81, Suppl 1 (2022): 488.3–489. http://dx.doi.org/10.1136/annrheumdis-2022-eular.76.

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BackgroundSystemic sclerosis (SSc) is a systemic autoimmune disease characterised by inflammation, vasculopathy and fibrosis. Several mechanisms, including endothelial to mesenchymal transition (EndMT) and cellular senescence, may be included in the fibrosis process, especially in response to inflammation and vasculopathy.ObjectivesOur study aimed to identify how EndMT and cellular senescence manifest in SSc skin fibrosis.MethodsWe performed a cross-sectional biobank study on formalin-fixed, paraffin-embedded skin biopsies from patients meeting the ACR/EULAR 2013 classification criteria for SS

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Wasson, C., E. Clavane, R. Ross та ін. "OP0113 THE BETA SECRETASE BACE1 DRIVES SYSTEMIC SCLEROSIS FIBROBLASTS ACTIVATION THROUGH Β-CATENIN AND NOTCH SIGNALLING". Annals of the Rheumatic Diseases 82, Suppl 1 (2023): 75.1–75. http://dx.doi.org/10.1136/annrheumdis-2023-eular.2236.

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BackgroundThe beta-amyloid precursor protein cleaving enzyme 1 (BACE1) is well known for its role in the development of Alzheimer’s disease via the generation of β-amyloid. Recent publications, including our own, have demonstrated a role for this enzyme in other chronic inflammatory diseases, including type 2 diabetes and cardiovascular disease. However, to date there has been no studies looking into the role of BACE1 in the autoimmune condition Systemic Sclerosis (SSc).ObjectivesThe aim of this study was to assess the expression profile of BACE1 in SSc patient samples and investigate the effe

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Ouyang, Xiaosen, Thu H. Le, Carlos Roncal, et al. "Th1 inflammatory response with altered expression of profibrotic and vasoactive mediators in AT1A and AT1B double-knockout mice." American Journal of Physiology-Renal Physiology 289, no. 4 (2005): F902—F910. http://dx.doi.org/10.1152/ajprenal.00141.2005.

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AT1 double receptor (AT1A and AT1B) knockout mice have lower blood pressure, impaired growth, and develop early renal microvascular disease and tubulointerstitial injury. We hypothesized that there would be an increased expression of vasoactive, profibrotic, and inflammatory mediators expressed in the kidneys of AT1 double-knockout mice. We examined the renal expression of various mediator systems in control ( n = 6) vs. double-knockout mice ( n = 6) at 3–5 mo of age by real-time PCR, immunohistochemistry, and Western blot analysis. AT1 double-knockout mice show activation of Th1-dependent pat

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Meng, YH, C. Tian, L. Liu, L. Wang, and Q. Chang. "Elevated expression of connective tissue growth factor, osteopontin and increased collagen content in human ascending thoracic aortic aneurysms." Vascular 22, no. 1 (2013): 20–27. http://dx.doi.org/10.1177/1708538112472282.

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Little is known about the molecular mechanisms of ascending thoracic aortic aneurysms (ATAAs). Abnormal extracellular matrix changes and variations of vascular smooth muscle cells (VSMCs) have been implicated in abdominal aortic aneurysm formation. Our objective was to investigate the alterations of collagen, stimulators of collagen synthesis and synthetic VSMCs in patients with ATAA. Surgical samples from ATAA were taken from 20 patients, and 18 control aortas were obtained during coronary artery bypass surgery. All aortic wall specimens were fixed for histology and immunohistochemistry for c

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Del Papa, N., M. Lorini, V. Carbonelli, et al. "AB0153 ADIPOSE-DERIVED STROMAL/STEM CELLS FROM SYSTEMIC SCLEROSIS PATIENTS SUCCESSFULLY EXERT A PARACRINE ANTI-FIBROTIC ACTIVITY AND INDUCE A PRO-ANGIOGENIC PHENOTYPE OF SCLERODERMA FIBROBLASTS IN VITRO." Annals of the Rheumatic Diseases 79, Suppl 1 (2020): 1377.2–1377. http://dx.doi.org/10.1136/annrheumdis-2020-eular.3248.

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Background:Adipose-derived stromal/stem cells (ADSCs) are multipotential non-hematopoietic progenitor cells with anti-inflammatory, immunomodulatory and regenerative effects. They have the advantage of accessibility and potent pro-angiogenic effects when compared with other stem cells, such as bone-marrow derived stem cells. Recent studies have shown that autologous fat grafting may be effective in the treatment of fibrotic and vascular complications in systemic sclerosis (SSc), despite a pro-fibrotic signature.Objectives:Aim of the study was to better characterize the proliferative and secret

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Ong, V., X. Shiwen, F. Zhang, et al. "POS0145 CLINICAL AND PATHOGENIC SIGNIFICANCE OF S100A4 OVEREXPRESSION IN SYSTEMIC SCLEROSIS." Annals of the Rheumatic Diseases 82, Suppl 1 (2023): 293–94. http://dx.doi.org/10.1136/annrheumdis-2023-eular.581.

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BackgroundS100A4 belongs to a family of proteins originally defined by solubility of the prototypic members in 100% saturated ammonium sulphate. Preclinical studies suggest that extracellular S100A4 as a Damage Associated Molecular Pattern (DAMP) protein is upregulated upon stress or injury and may be a target for antifibrotic therapy.ObjectivesWe explored expression and function of S100A4 as a driver of fibroblast activation in systemic sclerosis (SSc).MethodsS100A4 protein concentration was measured by ELISA in serum of SSc (n=94) and healthy controls (n=15). Association of serum level with

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Dean, Rachael G., Leanne C. Balding, Riccardo Candido, et al. "Connective Tissue Growth Factor and Cardiac Fibrosis after Myocardial Infarction." Journal of Histochemistry & Cytochemistry 53, no. 10 (2005): 1245–56. http://dx.doi.org/10.1369/jhc.4a6560.2005.

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The temporal and spatial expression of transforming growth factor (TGF)-β1 and connective tissue growth factor (CTGF) was assessed in the left ventricle of a myocardial infarction (MI) model of injury with and without angiotensin-converting enzyme (ACE) inhibition. Coronary artery ligated rats were killed 1, 3, 7, 28, and 180 days after MI. TGF-β1, CTGF, and procollagen α1(I) mRNA were localized by in situ hybridization, and TGF-β1 and CTGF protein levels by immunohistochemistry. Collagen protein was measured using picrosirius red staining. In a separate group, rats were treated for 6 months w

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Qi, W., S. Twigg, X. Chen та ін. "Integrated actions of transforming growth factor-β1 and connective tissue growth factor in renal fibrosis". American Journal of Physiology-Renal Physiology 288, № 4 (2005): F800—F809. http://dx.doi.org/10.1152/ajprenal.00179.2004.

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Matrix accumulation in the renal tubulointerstitium is predictive of a progressive decline in renal function. Transforming growth factor-β1 (TGF-β1) and, more recently, connective tissue growth factor (CTGF) are recognized to play key roles in mediating the fibrogenic response, independently of the primary renal insult. Further definition of the independent and interrelated effects of CTGF and TGF-β1 is critical for the development of effective antifibrotic strategies. CTGF (20 ng/ml) induced fibronectin and collagen IV secretion in primary cultures of human proximal tubule cells (PTC) and cor

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