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Journal articles on the topic 'CTGF'

Author: Grafiati

Published: 4 June 2021

Last updated: 26 July 2025

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1

Gerritsen, Karin G., Hilde P. Peters, Tri Q. Nguyen, et al. "Renal proximal tubular dysfunction is a major determinant of urinary connective tissue growth factor excretion." American Journal of Physiology-Renal Physiology 298, no. 6 (2010): F1457—F1464. http://dx.doi.org/10.1152/ajprenal.00694.2009.

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Connective tissue growth factor (CTGF) plays a key role in renal fibrosis. Urinary CTGF is elevated in various renal diseases and may have biomarker potential. However, it is unknown which processes contribute to elevated urinary CTGF levels. Thus far, urinary CTGF was considered to reflect renal expression. We investigated how tubular dysfunction affects urinary CTGF levels. To study this, we administered recombinant CTGF intravenously to rodents. We used both full-length CTGF and the NH2-terminal fragment, since the NH2-fragment is the predominant form detected in urine. Renal CTGF extractio

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2

Boes, Mary, Brian L. Dake, Barbara A. Booth, et al. "Connective Tissue Growth Factor (IGFBP-rP2) Expression and Regulation in Cultured Bovine Endothelial Cells*." Endocrinology 140, no. 4 (1999): 1575–80. http://dx.doi.org/10.1210/endo.140.4.6633.

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Abstract Media from large vessel endothelial cells (pulmonary artery, aorta) contained intact connective tissue growth factor (CTGF) and a dominant 19-kDa band. N-terminal analysis of the 19-kDa band showed sequence corresponding to CTGF amino acid 181–190, suggesting that the 19-kDa band represented a proteolytic fragment of CTGF. Intact CTGF was increased by cAMP but not by transforming growth factor-β (TGFβ). CTGF messenger RNA (mRNA) was not changed by cAMP nor TGFβ. In two microvessel endothelial cells, mRNA was found at low levels by PCR and Northern analysis, but no CTGF protein was see

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3

Lu, Hongbo, Venkata Lokesh Battula, Yuexi Shi, et al. "Role of Connective Tissue Growth Factor (CTGF) in Survival and Chemosensitivity of Acute Lymphoblastic Leukemia." Blood 118, no. 21 (2011): 2593. http://dx.doi.org/10.1182/blood.v118.21.2593.2593.

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Abstract Abstract 2593 Connective tissue growth factor (CTGF/CCN2) is a member of the CCN family of proteins involved in extracellular matrix production, tumor cell proliferation, adhesion, migration, and metastasis. Recent studies have shown that CTGF expression is elevated in 75% of acute lymphoblastic leukemia (Br J Haematol, 2007; 138(6):740–8), and that increased expression of CTGF is associated with inferior outcome in B-ALL (Blood, 2007; 109(7):3080–3). In this study, we characterized the functional role and downstream signaling pathways of CTGF in ALL cells. First, we utilized lentivir

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4

Canalis, Ernesto, Stefano Zanotti, Wesley G. Beamer, Aris N. Economides, and Anna Smerdel-Ramoya. "Connective Tissue Growth Factor Is Required for Skeletal Development and Postnatal Skeletal Homeostasis in Male Mice." Endocrinology 151, no. 8 (2010): 3490–501. http://dx.doi.org/10.1210/en.2010-0145.

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Connective tissue growth factor (CTGF), a member of the cysteine-rich 61 (Cyr 61), CTGF, nephroblastoma overexpressed (NOV) (CCN) family of proteins, is synthesized by osteoblasts, and its overexpression inhibits osteoblastogenesis and causes osteopenia. The global inactivation of Ctgf leads to defective endochondral bone formation and perinatal lethality; therefore, the consequences of Ctgf inactivation on the postnatal skeleton are not known. To study the function of CTGF, we generated Ctgf+/LacZ heterozygous null mice and tissue-specific null Ctgf mice by mating Ctgf conditional mice, where

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5

WAHAB, Nadia Abdel, Natalia YEVDOKIMOVA, Benjamin S. WESTON, et al. "Role of connective tissue growth factor in the pathogenesis of diabetic nephropathy." Biochemical Journal 359, no. 1 (2001): 77–87. http://dx.doi.org/10.1042/bj3590077.

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We characterized a rabbit polyclonal antibody raised against human recombinant connective tissue growth factor (CTGF). The antibody recognised a higher molecular mass form (approx. 56kDa) of CTGF in mesangial cell lysates as well as the monomeric (36–38kDa) and lower molecular mass forms (< 30kDa) reported previously. Immunohistochemistry detected CTGF protein in glomeruli of kidneys of non-obese diabetic mice 14 days after the onset of diabetes, and this was prominent by 70 days. CTGF protein is also present in glomeruli of human patients with diabetic nephropathy. No CTGF was detected in

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6

Trampuž, Sara Redenšek, Sander van Riet, Åsa Nordling, and Magnus Ingelman-Sundberg. "The Role of CTGF in Liver Fibrosis Induced in 3D Human Liver Spheroids." Cells 12, no. 2 (2023): 302. http://dx.doi.org/10.3390/cells12020302.

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Connective tissue growth factor (CTGF) is involved in the regulation of extracellular matrix (ECM) production. Elevated levels of CTGF can be found in plasma from patients with liver fibrosis and in experimental animal models of liver fibrosis, but the exact role of CTGF in, e.g., diet-induced human liver fibrosis is not entirely known. To address this question, we utilized a 3D human liver co-culture spheroid model composed of hepatocytes and non-parenchymal cells, in which fibrosis is induced by TGF-β1, CTGF or free fatty acids (FFA). Treatment of the spheroids with TGF-β1 or FFA increased C

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7

Ball, DK, AW Rachfal, SA Kemper, and DR Brigstock. "The heparin-binding 10 kDa fragment of connective tissue growth factor (CTGF) containing module 4 alone stimulates cell adhesion." Journal of Endocrinology 176, no. 2 (2003): R1—R7. http://dx.doi.org/10.1677/joe.0.176r001.

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Connective tissue growth factor (CTGF) is a 349-residue mosaic protein that contains four structural modules implicated in protein-protein interactions. To address the functionality of residues 247-349 (containing module 4 alone), this region of CTGF was produced as a maltose binding protein (MBP) fusion protein in E. coli. After removal of MBP, recombinant CTGF commenced at Glu(247), was of M(r) 10 000, was immunoreactive with anti-CTGF[247-260], bound strongly to heparin, and promoted dose-dependent adhesion of fibroblasts, myofibroblasts, endothelial cells, and epithelial cells. An 8 kDa pr

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8

RISER, BRUCE L., MARK DENICHILO, PEDRO CORTES, et al. "Regulation of Connective Tissue Growth Factor Activity in Cultured Rat Mesangial Cells and Its Expression in Experimental Diabetic Glomerulosclerosis." Journal of the American Society of Nephrology 11, no. 1 (2000): 25–38. http://dx.doi.org/10.1681/asn.v11125.

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Abstract. Connective tissue growth factor (CTGF) is a peptide secreted by cultured endothelial cells and fibroblasts when stimulated by transforming growth factor-β (TGF-β), and is overexpressed during fibrotic processes in coronary arteries and in skin. To determine whether CTGF is implicated in the pathogenesis of diabetic glomerulosclerosis, cultured rat mesangial cells (MC) as well as kidney cortex and microdissected glomeruli were examined from obese, diabetic db/db mice and their normal counterparts. Exposure of MC to recombinant human CTGF significantly increased fibronectin and collage

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9

Tawk, Bouchra, Christian Schwager, Karim Zaoui, et al. "Connective tissue growth factor (CTGF) methylation status is associated with prognosis of patients with head and neck squamous cell carcinoma (HNSCC) treated with radiochemotherapy (RCHT): A multicenter study of the German Cancer Consortium Radiation Oncology Group (DKTK-ROG)." Journal of Clinical Oncology 37, no. 15_suppl (2019): 6050. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.6050.

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6050 Background: CTGF plays a central role in tissue remodeling and has emerged as an attractive novel therapeutic target. We sought to investigate the impact of CTGF methylation status (CTGF-M) in predicting outcome of HNSCC patients undergoing RCHT. Methods: CTGF-M was discovered by applying Illumina 450K/850K arrays to DNA extracted from FFPE material of patients homogeneously treated with surgery followed by adjuvant cisplatin-based RCHT in frame of the DKTK-ROG multicenter retrospective trial (n = 194, training cohort). Methylation probes correlating with overall survival (OS) and progres

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10

Battula, Venkata Lokesh, Maria da Graca Cabreira, Zhiqiang Wang, et al. "Connective Tissue Growth Factor (CTGF) Is Essential for Self Renewal and Proliferation of Mesenchymal Stromal Cells (MSCs) and Affects Leukemia-Stromal Interactions." Blood 116, no. 21 (2010): 3845. http://dx.doi.org/10.1182/blood.v116.21.3845.3845.

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Abstract Abstract 3845 Connective tissue growth factor (CTGF) is a member of the CCN family of growth factors that are critical regulators of vertebrate development. CTGF is a secreted protein that promotes extracellular matrix production, chemotaxis, cell proliferation and integrin expression. Since CTGF is highly expressed in acute lymphoblastic leukemia (ALL) and CTGF expression levels are related to ALL patient survival (Olga ST et al., Blood, 2007), we hypothesized that CTGF plays a role in regulating stromal cell proliferation and leukemia-stroma interaction. Our first goal was to charac

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11

Leask, Andrew, and David J. Abraham. "The role of connective tissue growth factor, a multifunctional matricellular protein, in fibroblast biology." Biochemistry and Cell Biology 81, no. 6 (2003): 355–63. http://dx.doi.org/10.1139/o03-069.

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Connective tissue growth factor (CTGF, CCN2), a member of the CCN family of proteins, is a cysteine-rich proadhesive matricellular protein that plays an essential role in the formation of blood vessels, bone, and connective tissue. As expression of this protein is potently induced by transforming growth factor-β (TGFβ), it has been hypothesized that CTGF mediates several of the downstream actions of TGFβ. In particular, CTGF is profibrotic, as CTGF is overexpressed in fibrotic disease and synergizes with TGFβ to promote sustained fibrosis in vivo. Over the last several years, key data regardin

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12

Muehlich, Susanne, Iwona Cicha, Christoph D. Garlichs, Bettina Krueger, Guido Posern, and Margarete Goppelt-Struebe. "Actin-dependent regulation of connective tissue growth factor." American Journal of Physiology-Cell Physiology 292, no. 5 (2007): C1732—C1738. http://dx.doi.org/10.1152/ajpcell.00552.2006.

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Expression of connective tissue growth factor (CTGF) in endothelial cells is modulated by shear stress affecting the organization of the cytoskeleton. The molecular connection between alterations of actin and CTGF expression was investigated in human umbilical vein endothelial cells (HUVEC) and a microvascular endothelial cell line. Overexpression of nonpolymerizable monomeric actin R62D interfered with stress fiber formation in HUVEC and concomitantly reduced immunoreactive CTGF. In microvascular endothelial cells, flow-dependent upregulation of CTGF was prevented by this actin mutant. In con

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13

Cicha, Iwona, Christoph Garlichs, Werner Daniel, and Margarete Goppelt-Struebe. "Activated human platelets release connective tissue growth factor." Thrombosis and Haemostasis 91, no. 04 (2004): 755–60. http://dx.doi.org/10.1160/th03-09-0602.

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SummaryConnective tissue growth factor (CTGF) is overexpressed in wound healing, fibrosis and advanced atherosclerotic lesions. Platelets adhere to CTGF, suggesting that this protein may be involved in the formation of platelet-rich thrombi at the sites of tissue injury or atherosclerotic plaque rupture. Since platelets contain a wide array of biologically active proteins, we investigated the presence, localization and release of CTGF from these cells. For this purpose, human platelets from healthy donors were washed and stimulated with thrombin or ADP. Following incubation, proteins from unst

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14

Harlow, Christopher R., Angela C. Bradshaw, Michael T. Rae, Kirsty D. Shearer, and Stephen G. Hillier. "Oestrogen formation and connective tissue growth factor expression in rat granulosa cells." Journal of Endocrinology 192, no. 1 (2007): 41–52. http://dx.doi.org/10.1677/joe.1.06689.

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Ovarian follicular development involves continual remodelling of the extracellular matrix (ECM) forming the basement membrane and intercellular framework that support granulosa cell (GC) growth and differentiation. Insight into the molecular regulation of ovarian ECM remodelling is potentially translatable to tissue remodelling elsewhere in the body. We therefore studied the link between a gene marker of ECM remodelling (connective tissue growth factor (CTGF)) and oestrogen biosynthesis (cytochrome P450aromatase (P450arom)) in rat granulosa cells. To determine if a cause–effect interaction exi

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15

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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16

Ricupero, Dennis A., David C. Rishikof, Ping-Ping Kuang, Christine F. Poliks, and Ronald H. Goldstein. "Regulation of connective tissue growth factor expression by prostaglandin E2." American Journal of Physiology-Lung Cellular and Molecular Physiology 277, no. 6 (1999): L1165—L1171. http://dx.doi.org/10.1152/ajplung.1999.277.6.l1165.

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Transforming growth factor-β (TGF-β) stimulates α1(I) collagen mRNA synthesis in human lung fibroblasts through a mechanism that is partially sensitive to cycloheximide and that may involve synthesis of connective tissue growth factor (CTGF). Northern blot analyses indicate that TGF-β stimulates time- and dose-dependent increases in CTGF mRNA. In TGF-β-stimulated fibroblasts, maximal levels of CTGF mRNA (3.7-fold above baseline) occur at 6 h. The TGF-β-stimulated increase in CTGF mRNA was not blocked by cycloheximide. Nuclear run-on analysis indicates that TGF-β increases the CTGF transcriptio

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17

Gerritsen, Karin G. F., Jan Willem Leeuwis, Maarten P. Koeners, et al. "Elevated Urinary Connective Tissue Growth Factor in Diabetic Nephropathy Is Caused by Local Production and Tubular Dysfunction." Journal of Diabetes Research 2015 (2015): 1–11. http://dx.doi.org/10.1155/2015/539787.

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Connective tissue growth factor (CTGF; CCN2) plays a role in the development of diabetic nephropathy (DN). Urinary CTGF (uCTGF) is elevated in DN patients and has been proposed as a biomarker for disease progression, but it is unknown which pathophysiological factors contribute to elevated uCTGF. We studied renal handling of CTGF by infusion of recombinant CTGF in diabetic mice. In addition, uCTGF was measured in type 1 DN patients and compared with glomerular and tubular dysfunction and damage markers. In diabetic mice, uCTGF was increased and fractional excretion (FE) of recombinant CTGF was

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18

Bogatkevich, Galina S., Anna Ludwicka-Bradley, C. Beth Singleton, Jennifer R. Bethard, and Richard M. Silver. "Proteomic analysis of CTGF-activated lung fibroblasts: identification of IQGAP1 as a key player in lung fibroblast migration." American Journal of Physiology-Lung Cellular and Molecular Physiology 295, no. 4 (2008): L603—L611. http://dx.doi.org/10.1152/ajplung.00530.2007.

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Connective tissue growth factor (CTGF, CCN2) is overexpressed in lung fibroblasts isolated from patients with interstitial lung disease (ILD) and systemic sclerosis (SSc, scleroderma) and is considered to be a molecular marker of fibrosis. To understand the significance of elevated CTGF, we investigated the changes in lung fibroblast proteome in response to CTGF overexpression. Using 2-dimensional gel electrophoresis followed by in-gel proteolytic digestion and mass spectrometric analysis, we identified 13 proteins affected by CTGF. Several of the CTGF-induced proteins, such as pro-α (I) colla

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19

den Hoedt, Claire H., Maaike K. van Gelder, Muriel P. Grooteman, et al. "Connective Tissue Growth Factor Is Related to All-cause Mortality in Hemodialysis Patients and Is Lowered by On-line Hemodiafiltration: Results from the Convective Transport Study." Toxins 11, no. 5 (2019): 268. http://dx.doi.org/10.3390/toxins11050268.

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Connective tissue growth factor (CTGF) plays a key role in the pathogenesis of tissue fibrosis. The aminoterminal fragment of CTGF is a middle molecule that accumulates in chronic kidney disease. The aims of this study are to explore determinants of plasma CTGF in hemodialysis (HD) patients, investigate whether CTGF relates to all-cause mortality in HD patients, and investigate whether online-hemodiafiltration (HDF) lowers CTGF. Data from 404 patients participating in the CONvective TRAnsport STudy (CONTRAST) were analyzed. Patients were randomized to low-flux HD or HDF. Pre-dialysis CTGF was

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20

Munemasa, Shoso, Akira Sakai, Yoshiaki Kuroda, et al. "Connective Tissue Growth Factor (CTGF) Is an Indicator of Bone Involvement in Multiple Myeloma." Blood 108, no. 11 (2006): 5025. http://dx.doi.org/10.1182/blood.v108.11.5025.5025.

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Abstract Bone disease in multiple myeloma (MM) is due to not only the activation of osteoclasts but also the impairment of osteoblast differentiation. Recent studies showed the overexpression of the Wnt signaling antagonists FRZB (secreted Frizzled-related protein 3, sFRP-3) and dickkopf1 (DKK1) is important in MM-related bone disease. Bone morphogenetic proteins (BMPs) and connective tissue growth factor (CTGF) are known to play essential roles in promoting the proliferation of early osteoprogenitor cells, specifically, differentiation from mesenchymal stem cells (MSC) to committed osteoproge

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21

Kroening, Sven, Emily Neubauer, Bernd Wullich, Jan Aten, and Margarete Goppelt-Struebe. "Characterization of connective tissue growth factor expression in primary cultures of human tubular epithelial cells: modulation by hypoxia." American Journal of Physiology-Renal Physiology 298, no. 3 (2010): F796—F806. http://dx.doi.org/10.1152/ajprenal.00528.2009.

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Tubular epithelial cells secrete connective tissue growth factor (CTGF, CCN2), which contributes to tubulointerstitial fibrosis. However, the molecular regulation of CTGF in human primary tubular epithelial cells (hPTECs) is not well defined. Therefore, CTGF expression was characterized in hPTECs isolated from healthy parts of tumor nephrectomies, with special emphasis on the regulation by transforming growth factor-β (TGF-β) and hypoxia, essential factors in the development of fibrosis. CTGF synthesis was strongly dependent on cell density. High CTGF levels were detected in sparse cells, wher

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22

Yan, Shuyun, Meng Zhang, Guimei Yang, Yumei Sun, and Dongmei Ai. "CTGF Promotes the Osteoblast Differentiation of Human Periodontal Ligament Stem Cells by Positively Regulating BMP2/Smad Signal Transduction." BioMed Research International 2022 (September 15, 2022): 1–10. http://dx.doi.org/10.1155/2022/2938015.

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Objective. This work is aimed at revealing the role and the molecular mechanism of connective tissue growth factor 2 (CTGF) in the osteoblast differentiation of periodontal ligament stem cells (PDLSCs). Methods. The osteogenic differentiation of PDLSCs was induced by osteogenic induction medium (OM), and the expression level of osteogenic related proteins ALP, RUNX2, OCN, and CTGF was estimated using quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting analysis. We constructed cell lines with CTGF overexpression or knockdown to verify the role of CTGF in the osteobla

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23

Chi, Hongjie, Haijun Feng, Xiangyu Shang, et al. "Circulating Connective Tissue Growth Factor Is Associated with Diastolic Dysfunction in Patients with Diastolic Heart Failure." Cardiology 143, no. 3-4 (2019): 77–84. http://dx.doi.org/10.1159/000499179.

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Background: Connective tissue growth factor (CTGF) and transforming growth factor β1 (TGF-β1) are emerging biomarkers for tissue fibrosis. The aim of this study was to investigate the association between circulating CTGF, TGF-β1 levels and cardiac diastolic dysfunction in patients with diastolic heart failure (DHF). Methods: Admitted subjects were screened for heart failure and those with left ventricular (LV) ejection fraction <45% were excluded. Diastolic dysfunction was defined as functional abnormalities that exist during LV relaxation and filling by echocardiographic criteria. Totally

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Jing, Jiaona, Ping Li, Tiejun Li, Yuncheng Sun та Huaijin Guan. "RNA Interference Targeting Connective Tissue Growth Factor Inhibits the Transforming Growth Factor-β2Induced Proliferation in Human Tenon Capsule Fibroblasts". Journal of Ophthalmology 2013 (2013): 1–9. http://dx.doi.org/10.1155/2013/354798.

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Purpose. This study was to determine the effect of CTGF-small interfering RNA (siRNA) on TGF-β2-induced proliferation in human Tenon capsule fibroblasts (HTFs).Methods. HTFs were transfected with four of CTGF-siRNAs separately for screening of gene silencing efficacy that was determined by transcript level measured by quantitative real-time PCR (qRT-PCR). Recombinant TGF-β2was added into the culture to stimulate the proliferation of HTFs. The gene silencing efficacy of the siRNAs was evaluated by qRT-PCR and immunofluorescence of CTGF transcript and protein levels. The viability of HTFs was de

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25

Kasaragod, Arvind B., M. Scott Lucia, Gary Cabirac, Gary R. Grotendorst, and Kurt R. Stenmark. "Connective Tissue Growth Factor Expression in Pediatric Myofibroblastic Tumors." Pediatric and Developmental Pathology 4, no. 1 (2001): 37–45. http://dx.doi.org/10.1007/s100240010123.

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Human connective tissue growth factor (CTGF) is a secreted cysteine-rich peptide and a member of the peptide family that includes serum-induced immediate gene products such as a v-src-induced peptide and a putative proto-oncogene, c-src. CTGF is secreted by endothelial cells, fibroblasts, smooth muscle cells, and myofibroblasts. Its expression is increased in various human and animal fibrotic diseases. We hypothesized that tumors with significant fibrous and vascular components would exhibit increased expression of CTGF. We examined the expression of CTGF mRNA by in situ hybridization in 12 pe

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26

ITO, YASUHIKO, ROEL GOLDSCHMEDING, RICHARD J. BENDE, et al. "Kinetics of Connective Tissue Growth Factor Expression during Experimental Proliferative Glomerulonephritis." Journal of the American Society of Nephrology 12, no. 3 (2001): 472–84. http://dx.doi.org/10.1681/asn.v123472.

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Abstract. Connective tissue growth factor (CTGF) is a member of the CCN family of immediate early genes, which are involved in cell proliferation, migration, and matrix production. Recently, CTGF was observed to be strongly upregulated in human proliferative and fibrogenic renal disease. By in situ hybridization and reverse transcriptase-PCR, the expression of CTGF was investigated in experimental proliferative glomerulonephritis induced by injection of anti—Thy-1.1 antibody in the rat. CTGF expression in cultured rat mesangial cells and glomerular visceral epithelial cells (GVEC) was studied

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27

Qi, Weier, Xinming Chen, Tania S. Polhill та ін. "TGF-β1 induces IL-8 and MCP-1 through a connective tissue growth factor-independent pathway". American Journal of Physiology-Renal Physiology 290, № 3 (2006): F703—F709. http://dx.doi.org/10.1152/ajprenal.00254.2005.

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Transforming growth factor-β1 (TGF-β1) functions as an important immunomodulatory cytokine in human kidney. Evidence suggests that connective tissue growth factor (CTGF) is an important downstream mediator of the profibrotic effects of TGF-β1. However, the role of CTGF in TGF-β1-induced chemokine production remains unknown. This study was undertaken to determine whether CTGF is involved in mediating TGF-β1-induced chemokine production in renal proximal tubular (HK-2) cells. Interleukin-8 (IL-8) and macrophage chemoattractant protein-1 (MCP-1) were measured. TGF-β1 induced an increase in IL-8 a

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Ahmed, M. Shakil, Jørgen Gravning, Vladimir N. Martinov, et al. "Mechanisms of novel cardioprotective functions of CCN2/CTGF in myocardial ischemia-reperfusion injury." American Journal of Physiology-Heart and Circulatory Physiology 300, no. 4 (2011): H1291—H1302. http://dx.doi.org/10.1152/ajpheart.00604.2010.

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CCN2/connective tissue growth factor (CTGF), a CCN family matricellular protein repressed in healthy hearts after birth, is induced in heart failure of various etiologies. Multiple cellular and biological functions have been assigned to CCN2/CTGF depending on cellular context. However, the functions and mechanisms of action of CCN2/CTGF in the heart as well as its roles in cardiac physiology and pathophysiology remain unknown. Transgenic mice with cardiac-restricted overexpression of CTGF (Tg-CTGF) were generated and compared with nontransgenic littermate control (NLC) mice. Tg-CTGF mice displ

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29

Tikellis, Christos, Mark E. Cooper, Stephen M. Twigg, Wendy C. Burns, and Mary Tolcos. "Connective Tissue Growth Factor Is Up-Regulated in the Diabetic Retina: Amelioration by Angiotensin-Converting Enzyme Inhibition." Endocrinology 145, no. 2 (2004): 860–66. http://dx.doi.org/10.1210/en.2003-0967.

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Abstract Connective tissue growth factor (CTGF) has been postulated to have prosclerotic and angiogenic properties. The aim of this present study was to characterize retinal CTGF expression in the absence and presence of diabetes and in the context of treatment with the angiotensin-converting enzyme (ACE) inhibitor, perindopril. Retinas were obtained from control, diabetic, and diabetic plus perindopril-treated (3 mg/d) rats. CTGF gene expression was quantitated by RT-PCR and localized by in situ hybridization. CTGF protein expression was analyzed by Western blotting and localized by immunohis

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30

Vial, Cecilia, Jaime Gutiérrez, Cristian Santander, Daniel Cabrera, and Enrique Brandan. "Decorin Interacts with Connective Tissue Growth Factor (CTGF)/CCN2 by LRR12 Inhibiting Its Biological Activity." Journal of Biological Chemistry 286, no. 27 (2011): 24242–52. http://dx.doi.org/10.1074/jbc.m110.189365.

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Fibrotic disorders are the end point of many chronic diseases in different tissues, where an accumulation of the extracellular matrix occurs, mainly because of the action of the connective tissue growth factor (CTGF/CCN2). Little is known about how this growth factor activity is regulated. We found that decorin null myoblasts are more sensitive to CTGF than wild type myoblasts, as evaluated by the accumulation of fibronectin or collagen III. Decorin added exogenously negatively regulated CTGF pro-fibrotic activity and the induction of actin stress fibers. Using co-immunoprecipitation and in vi

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Jaffa, Ayad A., William R. Usinger, M. Brent McHenry, et al. "Connective Tissue Growth Factor and Susceptibility to Renal and Vascular Disease Risk in Type 1 Diabetes." Journal of Clinical Endocrinology & Metabolism 93, no. 5 (2008): 1893–900. http://dx.doi.org/10.1210/jc.2007-2544.

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Abstract Objective: We explored the relevance and significance of connective tissue growth factor (CTGF) as a determinant of renal and vascular complications among type 1 diabetic patients. Methods and Results: We measured the circulating and urinary levels of CTGF and CTGF N fragment in 1050 subjects with type 1 diabetes from the Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications (DCCT/EDIC) Study cohort. We found that hypertensive diabetic subjects have significantly higher levels of plasma log CTGF N fragment relative to normotensive subjects (

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O'Donovan, Helen C., Fionnuala Hickey, Derek P. Brazil та ін. "Connective tissue growth factor antagonizes transforming growth factor-β1/Smad signalling in renal mesangial cells". Biochemical Journal 441, № 1 (2011): 499–510. http://dx.doi.org/10.1042/bj20110910.

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The critical involvement of TGF-β1 (transforming growth factor-β1) in DN (diabetic nephropathy) is well established. However, the role of CTGF (connective tissue growth factor) in regulating the complex interplay of TGF-β1 signalling networks is poorly understood. The purpose of the present study was to investigate co-operative signalling between CTGF and TGF-β1 and its physiological significance. CTGF was determined to bind directly to the TβRIII (TGF-β type III receptor) and antagonize TGF-β1-induced Smad phosphorylation and transcriptional responses via its N-terminal half. Furthermore, TGF

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Lasky, Joseph A., Luis A. Ortiz, Boihoang Tonthat, et al. "Connective tissue growth factor mRNA expression is upregulated in bleomycin-induced lung fibrosis." American Journal of Physiology-Lung Cellular and Molecular Physiology 275, no. 2 (1998): L365—L371. http://dx.doi.org/10.1152/ajplung.1998.275.2.l365.

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Connective tissue growth factor (CTGF) is a newly described 38-kDa peptide mitogen for fibroblasts and a promoter of connective tissue deposition in the skin. The CTGF gene promotor contains a transforming growth factor-β1 (TGF-β1) response element. Because TGF-β1 expression is upregulated in several models of fibroproliferative lung disease, we asked whether CTGF is also upregulated in a murine lung fibrosis model and whether CTGF could mediate some of the fibrogenic effects associated with TGF-β1. A portion of the rat CTGF gene was cloned and used to show that primary isolates of both murine

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Mizutani, Makoto, Yasuhiko Ito, Masashi Mizuno, et al. "Connective tissue growth factor (CTGF/CCN2) is increased in peritoneal dialysis patients with high peritoneal solute transport rate." American Journal of Physiology-Renal Physiology 298, no. 3 (2010): F721—F733. http://dx.doi.org/10.1152/ajprenal.00368.2009.

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Peritoneal fibrosis (PF) is an important complication of peritoneal dialysis (PD) therapy that often occurs in association with peritoneal high transport rate and ultrafiltration failure (UFF). To study the possible pathogenic role of connective tissue growth factor (CTGF) in the relationship of PF and UFF, dialysate CTGF contents ( n = 178) and tissue CTGF expression ( n = 61) were investigated by ELISA, real-time PCR, immunohistochemistry, and in situ hybridization. CTGF production with and without TGF-β1stimulation in human peritoneal mesothelial cells (HPMC) from the spent patients' perito

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Yu, Zhiyuan, Qun Kong, and Bruce C. Kone. "CREB trans-activation of disruptor of telomeric silencing-1 mediates forskolin inhibition of CTGF transcription in mesangial cells." American Journal of Physiology-Renal Physiology 298, no. 3 (2010): F617—F624. http://dx.doi.org/10.1152/ajprenal.00636.2009.

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Connective tissue growth factor (CTGF) participates in diverse fibrotic processes including glomerulosclerosis. The adenylyl cyclase agonist forskolin inhibits CTGF expression in mesangial cells by unclear mechanisms. We recently reported that the histone H3K79 methyltransferase disruptor of telomeric silencing-1 (Dot1) suppresses CTGF gene expression in collecting duct cells ( J Clin Invest 117: 773–783, 2007) and HEK 293 cells ( J Biol Chem In press). In the present study, we characterized the involvement of Dot1 in mediating the inhibitory effect of forskolin on CTGF transcription in mouse

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HEUSINGER-RIBEIRO, JULIANE, MICHAEL EBERLEIN, NADIA ABDEL WAHAB, and MARGARETE GOPPELT-STRUEBE. "Expression of Connective Tissue Growth Factor in Human Renal Fibroblasts: Regulatory Roles of RhoA and cAMP." Journal of the American Society of Nephrology 12, no. 9 (2001): 1853–61. http://dx.doi.org/10.1681/asn.v1291853.

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Abstract. The induction of connective tissue growth factor (CTGF) was investigated in a human renal fibroblast cell line that exhibited many characteristics of primary human renal fibroblasts. Induction of CTGF mRNA was observed after treatment of the cells with transforming growth factor-β (TGF-β) or, even more prominently, lysophosphatidic acid (LPA). LPA induced a rapid transient increase in CTGF mRNA expression, with maximal levels being observed after 1 to 2 h. This increase was accompanied by CTGF protein synthesis. Induction of CTGF was insensitive to pertussis toxin and was not depende

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Topolyanskaya, Svetlana V., Tatyana A. Eliseeva, Olga I. Turna, and Olga N. Vakulenko. "Connective Tissue Growth Factor in Patients with Coronary Heart Disease: a Pilot Study." Bulletin of Rehabilitation Medicine 21, no. 6 (2022): 42–51. http://dx.doi.org/10.38025/2078-1962-2022-21-6-42-51.

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AIM. To determine the concentration of connective tissue growth factor and assess the relationship of this index with a number of pathological conditions in elderly patients with CHD. MATERIAL AND METHODS. The study enrolled 50 patients older than 75 years with a diagnosis of coronary heart disease (CAD); most of them (71%) were women. The patients ranged in age from 75 to 96 years (mean age -87.8 years). The concentration of connective tissue growth factor (CTGF) in blood was determined by enzyme immunoassay. RESULTS AND DISCUSSION. In the group of CHD patients, the average CTGF concentration

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Smerdel-Ramoya, Anna, Stefano Zanotti, Lisa Stadmeyer, Deena Durant, and Ernesto Canalis. "Skeletal Overexpression of Connective Tissue Growth Factor Impairs Bone Formation and Causes Osteopenia." Endocrinology 149, no. 9 (2008): 4374–81. http://dx.doi.org/10.1210/en.2008-0254.

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Connective tissue growth factor (CTGF), a member of the CCN family of proteins, is expressed in skeletal cells, and the ctgf null mutation leads to neonatal lethality due to defects in skeletal development. To define the function of CTGF in the postnatal skeleton, we created transgenic mice overexpressing CTGF under the control of the human osteocalcin promoter. CTGF transgenic female and male mice exhibited a significant decrease in bone mineral density, compared with wild-type littermate controls. Bone histomorphometry revealed that CTGF overexpression caused decreased trabecular bone volume

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Henshaw, F. R., P. Boughton, L. Lo, S. V. McLennan, and S. M. Twigg. "Topically Applied Connective Tissue Growth Factor/CCN2 Improves Diabetic Preclinical Cutaneous Wound Healing: Potential Role for CTGF in Human Diabetic Foot Ulcer Healing." Journal of Diabetes Research 2015 (2015): 1–10. http://dx.doi.org/10.1155/2015/236238.

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Aims/Hypothesis. Topical application of CTGF/CCN2 to rodent diabetic and control wounds was examined. In parallel research, correlation of CTGF wound fluid levels with healing rate in human diabetic foot ulcers was undertaken.Methods. Full thickness cutaneous wounds in diabetic and nondiabetic control rats were treated topically with 1 μg rhCTGF or vehicle alone, on 2 consecutive days. Wound healing rate was observed on day 14 and wound sites were examined for breaking strength and granulation tissue. In the human study across 32 subjects, serial CTGF regulation was analyzed longitudinally in

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Yokoi, Hideki, Masashi Mukoyama, Akira Sugawara, et al. "Role of connective tissue growth factor in fibronectin expression and tubulointerstitial fibrosis." American Journal of Physiology-Renal Physiology 282, no. 5 (2002): F933—F942. http://dx.doi.org/10.1152/ajprenal.00122.2001.

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Connective tissue growth factor (CTGF) is one of the candidate factors mediating downstream events of transforming growth factor-β (TGF-β), but its role in fibrogenic properties of TGF-β and in tubulointerstitial fibrosis has not yet been clarified. Using unilateral ureteral obstruction (UUO) in rats, we analyzed gene expression of TGF-β1, CTGF, and fibronectin. We further investigated the effect of blockade of endogenous CTGF on TGF-β-induced fibronectin expression in cultured rat renal fibroblasts by antisense oligodeoxynucleotide (ODN) treatment. After UUO, CTGF mRNA expression in the obstr

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Lee, Jeong Hee, Jongsu Kim, Hong Sook Kim, and Young Jin Kang. "Unraveling Connective Tissue Growth Factor as a Therapeutic Target and Assessing Kahweol as a Potential Drug Candidate in Triple-Negative Breast Cancer Treatment." International Journal of Molecular Sciences 24, no. 22 (2023): 16307. http://dx.doi.org/10.3390/ijms242216307.

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Triple-negative breast cancer (TNBC) is characterized by aggressive behavior and limited treatment options, necessitating the identification of novel therapeutic targets. In this study, we investigated the clinical significance of connective tissue growth factor (CTGF) as a prognostic marker and explored the potential therapeutic effects of kahweol, a coffee diterpene molecule, in TNBC treatment. Initially, through a survival analysis on breast cancer patients from The Cancer Genome Atlas (TCGA) database, we found that CTGF exhibited significant prognostic effects exclusively in TNBC patients.

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Wang, Xiaoyu, Susan V. McLennan, Terri J. Allen, Tatiana Tsoutsman, Christopher Semsarian, and Stephen M. Twigg. "Adverse effects of high glucose and free fatty acid on cardiomyocytes are mediated by connective tissue growth factor." American Journal of Physiology-Cell Physiology 297, no. 6 (2009): C1490—C1500. http://dx.doi.org/10.1152/ajpcell.00049.2009.

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Diabetic cardiomyopathy is characterized by interstitial fibrosis and cardiomyocyte hypertrophy and apoptosis. Also known as CCN2, connective tissue growth factor (CTGF) is implicated in the fibrosis; however, whether it contributes to cardiomyocytes changes and adverse effects of high glucose and lipids on these cells remains unknown. Hearts from streptozotocin-induced diabetic rats had elevated CTGF and changes of pathological myocardial hypertrophy, fibrosis, and cardiomyocyte apoptosis. Rat H9c2 cardiomyocytes were then treated with recombinant human (rh)CTGF, high glucose, or the saturate

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Lu, Hongbo, Venkata Lokesh Battula, Borys Korchin, et al. "Targeting Connective Tissue Growth Factor (CTGF) In Acute Lymphoblastic Leukemia Pre-Clinical Models: Anti-CTGF Monoclonal Antibody Attenuates Tumor Growth In Mouse Models of ALL." Blood 116, no. 21 (2010): 3257. http://dx.doi.org/10.1182/blood.v116.21.3257.3257.

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Abstract Abstract 3257 Connective tissue growth factor (CTGF/CCN2) is a member of the CCN family of proteins involved in extracellular matrix production, tumor cell proliferation, adhesion, migration, and metastasis. In pancreatic cancer, CTGF derived from tumor cells is a critical regulator of tumor growth, and CTGF-specific antibody attenuates tumor growth and metastases in vivo (Cancer Res., 2006; 66(11):5816-27). Elevated CTGF levels have been detected in a number of malignancies, including in lymphoblasts from patients with acute lymphoblastic leukaemia (ALL), while no expression of CTGF

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Zhuang, Hua, Jing Wu, Wei Xu, et al. "Transfection of CTGF siRNA inhibits transdifferentiation in human lens epithelium cell line B3 in vitro." International Eye Research 1, no. 1 (2020): 17–23. http://dx.doi.org/10.18240/ier.2020.01.04.

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AIM: To investigate the expression of connective tissue growth factor (CTGF) and α-smooth muscle actin (α-SMA) in human lens epithelium cell (HLEC) line B3 after transfection by liposome-coated small interfering RNA (siRNA) targeting CTGF. METHODS: HLECs were transfected with siRNA targeting CTGF, labeled with 5’-fluorescein isothiocyanate (5’-FITC) and coated with lipofectamine. The transfection ratio was evaluated via fluorescence intensity. Cell counting kit-8 (CCK-8) assay was performed to assess cytoviability of both non-transfected and transfected HLECs. Quantitative reverse transcriptio

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Kogiso, Tomomi, Kayo Takayanagi, Tsutomu Ishizuka, et al. "Serum level of full-length connective tissue growth factor reflects liver fibrosis stage in patients with Fontan-associated liver disease." PLOS ONE 19, no. 1 (2024): e0296375. http://dx.doi.org/10.1371/journal.pone.0296375.

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Background Chronic liver disease leads to liver fibrosis, and an accurate diagnosis of the fibrosis stage is crucial for medical management. Connective tissue growth factor (CTGF) is produced by endothelial cells and platelets and plays a central role in inducing fibrosis in various organs. In the present study, we tested the validity of measuring the serum levels of two types of CTGF to estimate the biopsy-confirmed liver fibrosis stage. Methods We used two detection antibodies targeting the N- and C-terminal of CTGF to measure the serum levels of two forms of CTGF consisting of its full leng

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Ito, Yasuhiko, Roel Goldschmeding, Hirotake Kasuga та ін. "Expression patterns of connective tissue growth factor and of TGF-β isoforms during glomerular injury recapitulate glomerulogenesis". American Journal of Physiology-Renal Physiology 299, № 3 (2010): F545—F558. http://dx.doi.org/10.1152/ajprenal.00120.2009.

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Transforming growth factor (TGF)-β1, -β2, and -β3 are involved in control of wound repair and development of fibrosis. Connective tissue growth factor (CTGF) expression is stimulated by all TGF-β isoforms and is abundant in glomerulosclerosis and other fibrotic disorders. CTGF is hypothesized to mediate profibrotic effects of TGF-β1 or to facilitate interaction of TGF-β1 with its receptor, but its interactions with TGF-β isoforms in nonpathological conditions are unexplored so far. Tissue repair and remodeling may recapitulate gene transcription at play in organogenesis. To further delineate t

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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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Wong, Chloe Kok Sum, Alec Falkenham, Tanya Myers та Jean-Francois Légaré. "Connective tissue growth factor expression after angiotensin II exposure is dependent on transforming growth factor-β signaling via the canonical Smad-dependent pathway in hypertensive induced myocardial fibrosis". Journal of the Renin-Angiotensin-Aldosterone System 19, № 1 (2018): 147032031875935. http://dx.doi.org/10.1177/1470320318759358.

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Introduction: Transforming growth factor-β (TGF-β) and connective tissue growth factor (CTGF) are often described as the initial pro-fibrotic mediators upregulated early in fibrosis models dependent on angiotensin II (Ang-II). In the present study, we explore the mechanistic link between TGF-β and CTGF expression by using a novel TGF-β trap. Materials and methods: NIH/3T3 fibroblasts were subjected to TGF-β with or without TGF-β trap or 1D11 antibody, CTGF or CTGF plus TGF-β for six or 24 hours, and then used for quantitative real-time polymerase chain reaction (qRT-PCR) or immunocytochemistry

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Aoyama, Eriko, Takako Hattori, Mitsuhiro Hoshijima, et al. "N-terminal domains of CCN family 2/connective tissue growth factor bind to aggrecan." Biochemical Journal 420, no. 3 (2009): 413–20. http://dx.doi.org/10.1042/bj20081991.

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CCN2/CTGF (CCN family 2/connective tissue growth factor) is a multi-cellular protein with a broad range of activities. It modulates many cellular functions, including proliferation, migration, adhesion and extracellular matrix production, and it is thus involved in many biological and pathological processes. In particular, CCN2/CTGF is essential for normal skeletal development. To identify CCN2/CTGF-interactive proteins capable of modulating its action in cartilage, we carried out a yeast two-hybrid screening using CCN2/CTGF peptide as a bait and a cDNA library from a chondrocytic cell line, H

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Sohn, Mimi, Yan Tan, Bing Wang, Richard L. Klein, Maria Trojanowska, and Ayad A. Jaffa. "Mechanisms of low-density lipoprotein-induced expression of connective tissue growth factor in human aortic endothelial cells." American Journal of Physiology-Heart and Circulatory Physiology 290, no. 4 (2006): H1624—H1634. http://dx.doi.org/10.1152/ajpheart.01233.2004.

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Hyperlipidemia is a recognized risk factor for atherosclerotic vascular disease. The underlying mechanisms that link lipoproteins and vascular disease are undefined. Connective tissue growth factor (CTGF) is emerging as a key determinant of progressive fibrotic diseases, and its expression is upregulated by diabetes. To define the mechanisms through which low-density lipoproteins (LDL) promote vascular injury, we evaluated whether LDL can modulate the expression of CTGF and collagen IV in human aortic endothelial cells (HAECs). Treatment of HAECs with LDL (50 μg/ml) for 24 h produced a signifi

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