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Article ; Online: Vitamin D

Zheng, Meifang / Li, Hongyan / Gao, Yanhang / Brigstock, David R / Gao, Runping

2023 Volume 957, Page(s) 176000

Abstract: Objective: To evaluate the inhibitory effect of vitamin D: Material and methods: Double ...

Abstract	Objective: To evaluate the inhibitory effect of vitamin D Material and methods: Double-labeling immunofluorescence was used for the identification of VDR Results: Enhanced expression of VDR was detected in RP-2 cells stimulated with alcohol (ALC) plus Cal versus Cal alone and in PSCs in the pancreas of ACP versus HC. The increased VDR Conclusion: This study suggests that Cal administration may be a potential antifibrotic strategy via inhibiting TGF-β1-mediated PSC action during the development of ACP.
MeSH term(s)	Humans ; Cholecalciferol/pharmacology ; Transforming Growth Factor beta1 ; Chromatography, Liquid ; Pancreatic Stellate Cells ; Proteomics ; Tandem Mass Spectrometry ; Transforming Growth Factors
Chemical Substances	calcipotriene (143NQ3779B) ; Cholecalciferol (1C6V77QF41) ; Transforming Growth Factor beta1 ; Transforming Growth Factors (76057-06-2)
Language	English
Publishing date	2023-08-19
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	80121-5
ISSN	1879-0712 ; 0014-2999
ISSN (online)	1879-0712
ISSN	0014-2999
DOI	10.1016/j.ejphar.2023.176000
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Article: The CCN family: a new stimulus package.

Brigstock, D R

The Journal of endocrinology

2003 Volume 178, Issue 2, Page(s) 169–175

Abstract: The CCN family comprises cysteine-rich 61 (CYR61/CCN1), connective tIssue growth factor (CTGF/CCN2), nephroblastoma overexpressed (NOV/CCN3), and Wnt-induced secreted proteins-1 (WISP-1/CCN4), -2 (WISP-2/CCN5) and -3 (WISP-3/CCN6). These proteins ... ...

Abstract	The CCN family comprises cysteine-rich 61 (CYR61/CCN1), connective tIssue growth factor (CTGF/CCN2), nephroblastoma overexpressed (NOV/CCN3), and Wnt-induced secreted proteins-1 (WISP-1/CCN4), -2 (WISP-2/CCN5) and -3 (WISP-3/CCN6). These proteins stimulate mitosis, adhesion, apoptosis, extracellular matrix production, growth arrest and migration of multiple cell types. Many of these activities probably occur through the ability of CCN proteins to bind and activate cell surface integrins. Accumulating evidence supports a role for these factors in endocrine pathways and endocrine-related processes. To illustrate the broad role played by the CCN family in basic and clinical endocrinology, this Article highlights the relationship between CCN proteins and hormone action, skeletal growth, placental angiogenesis, IGF-binding proteins and diabetes-induced fibrosis.
MeSH term(s)	Bone and Bones/metabolism ; Breast Neoplasms/metabolism ; CCN Intercellular Signaling Proteins ; Connective Tissue Growth Factor ; Cysteine-Rich Protein 61 ; Diabetes Mellitus, Type 1/metabolism ; Estrogens/metabolism ; Female ; Fibrosis ; Growth Substances/metabolism ; Humans ; Immediate-Early Proteins/metabolism ; Insulin-Like Growth Factor Binding Proteins ; Integrins/metabolism ; Intercellular Signaling Peptides and Proteins/metabolism ; Intracellular Signaling Peptides and Proteins ; Neoplasm Proteins/metabolism ; Neovascularization, Physiologic ; Nephroblastoma Overexpressed Protein ; Oncogene Proteins/metabolism ; Osteogenesis/physiology ; Placental Circulation ; Pregnancy ; Protein Binding ; Proto-Oncogene Proteins ; Repressor Proteins ; Somatomedins/metabolism ; Transcription Factors/metabolism ; Uterine Neoplasms/metabolism
Chemical Substances	CCN Intercellular Signaling Proteins ; CCN1 protein, human ; CCN2 protein, human ; CCN3 protein, human ; CCN4 protein, human ; CCN5 protein, human ; CCN6 protein, human ; Cysteine-Rich Protein 61 ; Estrogens ; Growth Substances ; Immediate-Early Proteins ; Insulin-Like Growth Factor Binding Proteins ; Integrins ; Intercellular Signaling Peptides and Proteins ; Intracellular Signaling Peptides and Proteins ; Neoplasm Proteins ; Nephroblastoma Overexpressed Protein ; Oncogene Proteins ; Proto-Oncogene Proteins ; Repressor Proteins ; Somatomedins ; Transcription Factors ; Connective Tissue Growth Factor (139568-91-5)
Language	English
Publishing date	2003-07-29
Publishing country	England
Document type	Journal Article ; Research Support, U.S. Gov't, P.H.S. ; Review
ZDB-ID	3028-4
ISSN	1479-6805 ; 0022-0795
ISSN (online)	1479-6805
ISSN	0022-0795
DOI	10.1677/joe.0.1780169
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Article: Report on the 9th international workshop on the CCN family of genes, November 2-7, 2017, Saint-Malo, France.

Yeger, Herman / Brigstock, David / Fisher, Gary / Lau, Lester / Leask, Andrew / Perbal, Bernard

Journal of cell communication and signaling

2018 Volume 12, Issue 3, Page(s) 505–511

Language	English
Publishing date	2018-06-20
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2299380-0
ISSN	1873-961X ; 1873-9601
ISSN (online)	1873-961X
ISSN	1873-9601
DOI	10.1007/s12079-018-0472-4
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Article ; Online: Elevation of circulating microRNA levels in obese children compared to healthy controls.

Thompson, M D / Cismowski, M J / Serpico, M / Pusateri, A / Brigstock, D R

Clinical obesity

2017 Volume 7, Issue 4, Page(s) 216–221

Abstract: As childhood obesity increases, it is becoming important to understand the complications of obesity in children and develop novel biomarkers. Evidence indicates that microRNAs (miRNA) are dys-regulated in obesity and may serve as sensitive and specific ... ...

Abstract	As childhood obesity increases, it is becoming important to understand the complications of obesity in children and develop novel biomarkers. Evidence indicates that microRNAs (miRNA) are dys-regulated in obesity and may serve as sensitive and specific circulating biomarkers. Non-alcoholic fatty liver disease (NAFLD) is a complication of obesity that ultimately requires a liver biopsy to determine disease severity. While studies have been conducted in adults, no study to date has examined circulating miRNAs in children with obesity and NAFLD. The goal of this study was to evaluate a panel of selected circulating miRNAs in obese children compared to healthy controls. We present here an analysis of a pre-selected panel of 20 candidate miRNAs in obese children compared to healthy controls. The miRNAs were chosen based on having been previously reported to be involved in NAFLD. We found that 16 out of 20 miRNAs tested were elevated at least twofold in children with obesity compared to controls. miR-122 and miR-199a showed the greatest increase in children with obesity versus controls. Both also had a high area under the curve when receiver-operator curves were plotted. Several circulating miRNAs correlated with body mass index (BMI) or serum transaminases. This study provides initial evidence that circulating miRNAs can be measured in the paediatric population and provides several diagnostic candidates increased in children with obesity that may be relevant to NAFLD.
Language	English
Publishing date	2017-08
Publishing country	England
Document type	Journal Article
ZDB-ID	2625816-X
ISSN	1758-8111 ; 1758-8103
ISSN (online)	1758-8111
ISSN	1758-8103
DOI	10.1111/cob.12192
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Article ; Online: Human Breast Milk-Derived Extracellular Vesicles in the Protection Against Experimental Necrotizing Enterocolitis.

Pisano, Courtney / Galley, Jeffrey / Elbahrawy, Mostafa / Wang, Yijie / Farrell, Aidan / Brigstock, David / Besner, Gail E

Journal of pediatric surgery

2019 Volume 55, Issue 1, Page(s) 54–58

Abstract: Purpose: Necrotizing enterocolitis (NEC) is a leading cause of death in premature infants. Breast feeding decreases the incidence of NEC but, even with aggressive promotion of nursing in Neonatal Intensive Care Units, morbidity and mortality remain high. ...

Abstract	Purpose: Necrotizing enterocolitis (NEC) is a leading cause of death in premature infants. Breast feeding decreases the incidence of NEC but, even with aggressive promotion of nursing in Neonatal Intensive Care Units, morbidity and mortality remain high. Previous studies from our laboratory have demonstrated that extracellular vesicles (EVs) purified from mouse and rat stem cells can protect the intestines from NEC. The aim of this study was to determine whether human breast milk (BM)-derived EVs could prevent NEC. Methods: EVs were purified from human donor breast milk. NEC was induced in premature rat pups by exposure to asphyxia/hypothermia/hypercaloric feeds. Pups were randomized to: (1) breast fed, no injury, (2) NEC, (3) NEC + BM-derived EVs once intraperitoneally (IP), (4) NEC + BM-derived EVs enterally (PO) with each feed. Intestinal tracts were examined for histologic damage. Additionally, the effect of BM-derived EVs on intestinal epithelial cells (IEC) subjected to hypoxia/reoxygenation injury in vitro was examined. Results: NEC incidence was 0% in breast-fed pups and 62% in pups subjected to NEC. IP administration of BM-derived EVs decreased NEC incidence to 29% and enteral administration further decreased NEC incidence to 11.9%. (p < 0.05). BM-derived EVs significantly increased cell proliferation and decreased apoptosis in IEC in vitro. Conclusion: Breast milk-derived EVs delivered either IP or enterally significantly decrease the incidence and severity of experimental NEC, protect IEC from injury in vitro, and may represent an innovative therapeutic option for NEC in the future. Type of study: Basic science study. Level of evidence: N/A.
MeSH term(s)	Administration, Oral ; Animals ; Animals, Newborn ; Biological Products/administration & dosage ; Biological Products/pharmacology ; Disease Models, Animal ; Enterocolitis, Necrotizing ; Extracellular Vesicles ; Female ; Humans ; Infusions, Parenteral ; Intestines/cytology ; Intestines/drug effects ; Milk, Human/cytology ; Protective Agents/administration & dosage ; Protective Agents/pharmacology ; Rats
Chemical Substances	Biological Products ; Protective Agents
Language	English
Publishing date	2019-10-25
Publishing country	United States
Document type	Journal Article
ZDB-ID	80165-3
ISSN	1531-5037 ; 0022-3468
ISSN (online)	1531-5037
ISSN	0022-3468
DOI	10.1016/j.jpedsurg.2019.09.052
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Article: The connective tissue growth factor/cysteine-rich 61/nephroblastoma overexpressed (CCN) family.

Brigstock, D R

Endocrine reviews

1999 Volume 20, Issue 2, Page(s) 189–206

MeSH term(s)	Amino Acid Sequence ; CCN Intercellular Signaling Proteins ; Connective Tissue Growth Factor ; Gene Expression ; Growth Substances/chemistry ; Growth Substances/genetics ; Heparin/pharmacology ; Humans ; Immediate-Early Proteins ; Intercellular Signaling Peptides and Proteins ; Intracellular Signaling Peptides and Proteins ; Molecular Sequence Data ; Oncogene Proteins ; Proto-Oncogene Proteins ; RNA, Messenger/biosynthesis ; Sequence Alignment ; Wilms Tumor/genetics
Chemical Substances	CCN Intercellular Signaling Proteins ; CCN2 protein, human ; CCN4 protein, human ; Growth Substances ; Immediate-Early Proteins ; Intercellular Signaling Peptides and Proteins ; Intracellular Signaling Peptides and Proteins ; Oncogene Proteins ; Proto-Oncogene Proteins ; RNA, Messenger ; Connective Tissue Growth Factor (139568-91-5) ; Heparin (9005-49-6)
Language	English
Publishing date	1999-04
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, U.S. Gov't, P.H.S. ; Review
ZDB-ID	603096-8
ISSN	1945-7189 ; 0163-769X
ISSN (online)	1945-7189
ISSN	0163-769X
DOI	10.1210/edrv.20.2.0360
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Article: Report on the 7(th) international workshop on the CCN family of genes : October 16-19, 2013-Nice, France.

Perbal, B / Trackman, P / Castellot, J / Brigstock, D / Takigawa, M / Lau, L / Leask, A

Journal of cell communication and signaling

2014 Volume 8, Issue 1, Page(s) 71–76

Abstract: In this report, chairs of the 7th International Workshop on the CCN family of Genes, review the progress made in understanding the biological functions of CCN proteins (CCN1, CCN2, CCN3, CCN4, CCN5 and CCN6) with a particular focus on their implications ... ...

Abstract	In this report, chairs of the 7th International Workshop on the CCN family of Genes, review the progress made in understanding the biological functions of CCN proteins (CCN1, CCN2, CCN3, CCN4, CCN5 and CCN6) with a particular focus on their implications in various pathological conditions, including cancer, fibrosis, diabetes, and cardiovascular diseases.
Language	English
Publishing date	2014-02-20
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2299380-0
ISSN	1873-961X ; 1873-9601
ISSN (online)	1873-961X
ISSN	1873-9601
DOI	10.1007/s12079-014-0227-9
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Article: A novel integrin alpha5beta1 binding domain in module 4 of connective tissue growth factor (CCN2/CTGF) promotes adhesion and migration of activated pancreatic stellate cells.

Gao, R / Brigstock, D R

Gut

2005 Volume 55, Issue 6, Page(s) 856–862

Abstract: Background: Connective tissue growth factor (CCN2) is upregulated in pancreatic fibrosis and desmoplastic pancreatic tumours. CCN2 interacts with integrin alpha5beta1 on pancreatic stellate cells (PSC) in which it stimulates fibrogenesis, adhesion, ... ...

Abstract	Background: Connective tissue growth factor (CCN2) is upregulated in pancreatic fibrosis and desmoplastic pancreatic tumours. CCN2 interacts with integrin alpha5beta1 on pancreatic stellate cells (PSC) in which it stimulates fibrogenesis, adhesion, migration, and proliferation. Aim: To determine the structural domain(s) in CCN2 that interact with integrin alpha5beta1 to regulation PSC functions. Methods: Primary activated rat PSC were tested for their adherence to isoforms of CCN2 comprising modules 1-4 (CCN2(1-4)), modules 3-4 (CCN2(3-4)), module 3 alone (CCN2(3)), or module 4 alone (CCN2(4)). Adhesion studies were performed in the presence of EDTA, divalent cations, anti-integrin alpha5beta1 antibodies, CCN2 synthetic peptides, or heparin, or after pretreatment of the cells with heparinase, chondroitinase, or sodium chlorate. CCN2 integrin alpha5beta1 binding was analysed in cell free systems. The ability of CCN2(1-4), CCN2(3-4), or CCN2(4) to stimulate PSC migration was evaluated in the presence of anti-integrin alpha5beta1 or heparin. Results: PSC adhesion was stimulated by CCN2(1-4), CCN2(3-4), or CCN2(4) and supported by Mg2+ but not Ca2+. CCN2(4) supported PSC adhesion or migration were blocked by anti-integrin alpha5beta1 antibodies or by treatment of cells with heparinase or sodium chlorate. A direct interaction between CCN2(4) and integrin alpha5beta1 was demonstrated in cell free assays. The sequence GVCTDGR in module 4 mediated the binding between CCN2(4) and integrin alpha5beta1 as well as CCN2(4) mediated PSC adhesion and migration. Conclusions: A GVCTDGR sequence in module 4 of CCN2 is a novel integrin alpha5beta1 binding site that is essential for CCN2 stimulated functions in PSC and which represents a new therapeutic target in PSC mediated fibrogenesis.
MeSH term(s)	Animals ; Binding Sites ; Cell Adhesion/drug effects ; Cell Adhesion/physiology ; Cell Movement/physiology ; Cell-Free System ; Cells, Cultured ; Connective Tissue Growth Factor ; Culture Media, Conditioned ; Dose-Response Relationship, Drug ; Immediate-Early Proteins/chemistry ; Immediate-Early Proteins/pharmacology ; Immediate-Early Proteins/physiology ; Integrin alpha5beta1/metabolism ; Intercellular Signaling Peptides and Proteins/chemistry ; Intercellular Signaling Peptides and Proteins/pharmacology ; Intercellular Signaling Peptides and Proteins/physiology ; Male ; Pancreas/cytology ; Pancreas/drug effects ; Pancreas/physiology ; Rats ; Rats, Sprague-Dawley ; Structure-Activity Relationship
Chemical Substances	CCN2 protein, rat ; Culture Media, Conditioned ; Immediate-Early Proteins ; Integrin alpha5beta1 ; Intercellular Signaling Peptides and Proteins ; Connective Tissue Growth Factor (139568-91-5)
Language	English
Publishing date	2005-12-16
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	80128-8
ISSN	1468-3288 ; 0017-5749
ISSN (online)	1468-3288
ISSN	0017-5749
DOI	10.1136/gut.2005.079178
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Article ; Online: Role of Gut-Derived Endotoxin on Type I Collagen Production in the Rat Pancreas After Chronic Alcohol Exposure.

Li, Hongyan / Xiu, Ming / Wang, Shuhua / Brigstock, David R / Sun, Li / Qu, Limei / Gao, Runping

Alcoholism, clinical and experimental research

2017 Volume 42, Issue 2, Page(s) 306–314

Abstract: ... control (CON) liquid diet or ethanol (EtOH) (15 g/kg/d) liquid diet. Eleven CON or EtOH rats were ...

Abstract	Background: Pancreatic fibrosis is a key pathological feature of alcoholic chronic pancreatitis (ACP). Bacterial endotoxin lipopolysaccharide (LPS) is considered as an important cofactor in the fibrogenesis of ACP. However, there are limitations in the use of exogenous LPS for evaluating the role of endotoxin in ACP pathogenesis. In this study, we determined the relationship between the concentration of LPS in the portal vein and pancreatic type I collagen (Col1) content in chronic alcohol-fed rats. Methods: Male Sprague Dawley rats were divided into 2 groups and fed with Lieber-DeCarli isocaloric control (CON) liquid diet or ethanol (EtOH) (15 g/kg/d) liquid diet. Eleven CON or EtOH rats were euthanized at the end of week 8, 9, or 10. The plasma LPS from portal vein was determined. Pancreatic inflammatory injury and fibrosis were assessed. Pancreatic stellate cells (PSCs) and macrophages were identified; pancreatic type I collagen alpha 1 (Col1A1) and Toll-like receptor (TLR4) mRNA and protein were examined; pancreatic chemokines and transforming growth factor-beta1 (TGF-β1) were determined. Results: Pancreatic inflammatory scores were increased in 10-week EtOH rats compared with CON rats, but there was no significant difference in collagen deposition between 2 groups. The levels of portal vein LPS and pancreatic TLR4 and Col1A1 mRNA and protein were increased in a time-dependent fashion in EtOH rats, with the highest levels occurring at 10 weeks. Additionally, by 8 weeks, pancreatic TLR4 and Col1A1 mRNA in EtOH rats were statistically increased as compared to CON rats, whereas portal vein LPS remained unchanged. The number of PSCs and macrophages and expression of chemokines (MCP-1, MIP-1α, and RANTES), TGF-β1, or Col1A1 were significantly increased, each of which was positively correlated with the level of portal vein LPS in 10-week EtOH rats. Conclusions: These results suggest that LPS is associated with alcohol-induced fibrosis in pancreatitis and targeting of bacterial endotoxin may be a promising therapeutic strategy for ACP.
MeSH term(s)	Animals ; Central Nervous System Depressants/pharmacology ; Chemokines/drug effects ; Chemokines/metabolism ; Collagen Type I/biosynthesis ; Collagen Type I/drug effects ; Ethanol/pharmacology ; Fibrosis ; Lipopolysaccharides/pharmacology ; Macrophages/drug effects ; Male ; Pancreas/drug effects ; Pancreas/metabolism ; Pancreas/pathology ; Pancreatic Stellate Cells/drug effects ; Pancreatitis, Alcoholic/metabolism ; Pancreatitis, Alcoholic/pathology ; Portal Vein ; RNA, Messenger/drug effects ; RNA, Messenger/metabolism ; Rats ; Rats, Sprague-Dawley ; Toll-Like Receptor 4/drug effects ; Toll-Like Receptor 4/genetics ; Toll-Like Receptor 4/metabolism ; Transforming Growth Factor beta1/drug effects ; Transforming Growth Factor beta1/metabolism
Chemical Substances	Central Nervous System Depressants ; Chemokines ; Collagen Type I ; Lipopolysaccharides ; RNA, Messenger ; Tgfb1 protein, rat ; Tlr4 protein, rat ; Toll-Like Receptor 4 ; Transforming Growth Factor beta1 ; collagen type I, alpha 1 chain ; Ethanol (3K9958V90M)
Language	English
Publishing date	2017-12-18
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	428999-7
ISSN	1530-0277 ; 0145-6008
ISSN (online)	1530-0277
ISSN	0145-6008
DOI	10.1111/acer.13550
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Article: Enhanced Steatosis and Fibrosis in Liver of Adult Offspring Exposed to Maternal High-Fat Diet.

Thompson, Michael D / Cismowski, Mary J / Trask, Aaron J / Lallier, Scott W / Graf, Amanda E / Rogers, Lynette K / Lucchesi, Pamela A / Brigstock, David R

Gene expression

2016 Volume 17, Issue 1, Page(s) 47–59

Abstract: Early life exposures can increase the risk of developing chronic diseases including nonalcoholic fatty liver disease. Maternal high-fat diet increases susceptibility to development of steatosis in the offspring. We determined the effect of maternal high- ... ...

Abstract	Early life exposures can increase the risk of developing chronic diseases including nonalcoholic fatty liver disease. Maternal high-fat diet increases susceptibility to development of steatosis in the offspring. We determined the effect of maternal high-fat diet exposure in utero and during lactation on offspring liver histopathology, particularly fibrosis. Female C57Bl/6J mice were fed a control or high-fat diet (HFD) for 8 weeks and bred with lean males. Nursing dams were continued on the same diet with offspring sacrificed during the perinatal period or maintained on either control or high-fat diet for 12 weeks. Increased hepatocyte proliferation and stellate cell activation were observed in the liver of HFD-exposed pups. Offspring exposed to perinatal high-fat diet and high-fat diet postweaning showed extensive hepatosteatosis compared to offspring on high-fat diet after perinatal control diet. Offspring exposed to perinatal high-fat diet and then placed on control diet for 12 weeks developed steatosis and pericellular fibrosis. Importantly, we found that exposure to perinatal high-fat diet unexpectedly promotes more rapid disease progression of nonalcoholic fatty liver disease, with a sustained fibrotic phenotype, only in adult offspring fed a postweaning control diet.
MeSH term(s)	Animals ; Cell Proliferation/physiology ; Diet, High-Fat/adverse effects ; Disease Progression ; Fatty Liver/etiology ; Fatty Liver/pathology ; Female ; Fibrosis/etiology ; Fibrosis/pathology ; Hepatocytes/pathology ; Lactation/physiology ; Liver/pathology ; Male ; Maternal Exposure ; Maternal Nutritional Physiological Phenomena/physiology ; Mice ; Mice, Inbred C57BL ; Non-alcoholic Fatty Liver Disease/etiology ; Non-alcoholic Fatty Liver Disease/pathology ; Pregnancy ; Prenatal Exposure Delayed Effects/etiology ; Prenatal Exposure Delayed Effects/pathology
Language	English
Publishing date	2016
Publishing country	United States
Document type	Journal Article
ZDB-ID	1151108-4
ISSN	1052-2166 ; 1052-2116
ISSN	1052-2166 ; 1052-2116
DOI	10.3727/105221616X692135
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