NDLI: BAPX-1/NKX-3.2 acts as a chondrocyte hypertrophy molecular switch in osteoarthritis.

Please wait, while we are loading the content...

Year: 2017 Volume: 69

Year: 2016 Volume: 68

Year: 2015 Volume: 67

Year: 2015 Volume: 67 Issue: 12

Year: 2015 Volume: 67 Issue: 11

Perspectives from masters in rheumatology and autoimmunity: perspectives on the conventional wisdom.

Release of neutrophil extracellular traps by neutrophils stimulated with antiphospholipid antibodies: a newly identified mechanism of thrombosis in the antiphospholipid syndrome.

Differences in sedentary time and physical activity between female patients with fibromyalgia and healthy controls: the al-Ándalus project.

Safety and efficacy of atacicept in combination with rituximab for reducing the signs and symptoms of rheumatoid arthritis: a phase II, randomized, double-blind, placebo-controlled pilot trial.

Brief report: intraarticular sprifermin not only increases cartilage thickness, but also reduces cartilage loss: location-independent post hoc analysis using magnetic resonance imaging.

Risk factors for the rapid increase in risk of acute coronary events in patients with new-onset rheumatoid arthritis: a nested case-control study.

Association of variants in CCR6 with susceptibility to lupus nephritis in Chinese.

Low-grade inflammation in symptomatic knee osteoarthritis: prognostic value of inflammatory plasma lipids and peripheral blood leukocyte biomarkers.

Association of systemic lupus erythematosus with decreased immunosuppressive potential of the IgG glycome.

Hypertrophic osteoarthropathy presenting as inflammatory arthritis.

Gene-based meta-analysis of genome-wide association study data identifies independent single-nucleotide polymorphisms in ANXA6 as being associated with systemic lupus erythematosus in Asian populations.

Correlation of the osteoarthritis susceptibility variants that map to chromosome 20q13 with an expression quantitative trait locus operating on NCOA3 and with functional variation at the polymorphism rs116855380.

Exacerbation of collagen antibody-induced arthritis in transgenic mice overexpressing peroxiredoxin 6.

Monocarboxylate transporter 4, associated with the acidification of synovial fluid, is a novel therapeutic target for inflammatory arthritis.

Brief report: enhancement of patient recruitment in rheumatoid arthritis clinical trials using a multi-biomarker disease activity score as an inclusion criterion.

Erosion or vascular channel?

Performance on the adult rheumatology in-training examination and relationship to outcomes on the rheumatology certification examination.

Review: animal models as a tool to dissect pivotal pathways driving spondyloarthritis.

Lubricin restoration in a mouse model of congenital deficiency.

Local Joint Inflammation and Histone Citrullination in a Murine Model of the Transition From Preclinical Autoimmunity to Inflammatory Arthritis

Three-dimensional appearance of apophyseal joint ankylosis.

Study on the protective effect of the KIR3DL1 gene in ankylosing spondylitis.

Dissecting the heterogeneity of skin gene expression patterns in systemic sclerosis.

Editorial: genomic advances in systemic sclerosis: it is time for precision.

A longitudinal biomarker for the extent of skin disease in patients with diffuse cutaneous systemic sclerosis.

Reply: To PMID 25581113.

Reply: To PMID 25545846.

Damage-associated molecular patterns generated in osteoarthritis directly excite murine nociceptive neurons through Toll-like receptor 4.

Musculoskeletal symptoms in patients with cryopyrin-associated periodic syndromes: a large database study.

BAPX-1/NKX-3.2 acts as a chondrocyte hypertrophy molecular switch in osteoarthritis.

Autoantibodies in prediction of the development of rheumatoid arthritis among healthy relatives of patients with the disease.

Autoimmune disease-associated haplotypes of BLK exhibit lowered thresholds for B cell activation and expansion of Ig class-switched B cells.

Brief report: lack of replication of an association between anti-citrullinated fibrinogen and subclinical atherosclerosis in patients with rheumatoid arthritis.

Is it time to leave the family? Comment on the editorial by Gladman.

Editorial: inflammatory activity in symptomatic knee osteoarthritis: not all inflammation is local.

Assessment of the characteristics of circulating follicular helper T-like cells in systemic lupus erythematosus: comment on the article by Choi et al.

Inhibition of natural killer cell cytotoxicity by interleukin-6: implications for the pathogenesis of macrophage activation syndrome.

Symptom assessment in knee osteoarthritis needs to account for physical activity level.

In memoriam: Ephraim P. Engleman, MD, 1911-2015.

Amended 95% confidence intervals in tables in the article by Jani et al (Arthritis Rheumatol, August 2015).

Year: 2015 Volume: 67 Issue: 10

Year: 2015 Volume: 67 Issue: Supplementary 10

Year: 2015 Volume: 67 Issue: 9

Year: 2015 Volume: 67 Issue: 8

Year: 2015 Volume: 67 Issue: 7

Year: 2015 Volume: 67 Issue: 6

Year: 2015 Volume: 67 Issue: 5

Year: 2015 Volume: 67 Issue: 4

Year: 2015 Volume: 67 Issue: 3

Year: 2015 Volume: 67 Issue: 2

Year: 2015 Volume: 67 Issue: 1

Year: 2014 Volume: 66

BAPX-1/NKX-3.2 acts as a chondrocyte hypertrophy molecular switch in osteoarthritis.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Caron, Marjolein M. J. Emans, Pieter J. Surtel, Don A. M. Van Der Kraan, Peter M. Van Rhijn, Lodewijk W. Welting, Tim J. M.
Description	Country affiliation: Netherlands Author Affiliation: Caron MM ( Maastricht University Medical Centre, Maastricht, The Netherlands.); Emans PJ ( Maastricht University Medical Centre, Maastricht, The Netherlands.); Surtel DA ( Maastricht University Medical Centre, Maastricht, The Netherlands.); van der Kraan PM ( Radboud University Medical Centre, Nijmegen, The Netherlands.); van Rhijn LW ( Maastricht University Medical Centre, Maastricht, The Netherlands.); Welting TJ ( Maastricht University Medical Centre, Maastricht, The Netherlands.)
Abstract	OBJECTIVE: Osteoarthritis (OA) development involves a shift of the articular chondrocyte phenotype toward hypertrophic differentiation via still poorly characterized mechanisms. The purpose of this study was to test our hypothesis that the function of BAPX-1/NKX-3.2 is impaired in OA chondrocytes and leads directly to loss of hypertrophic protection of the articular chondrocyte, which is central in the changing chondrocyte phenotype that drives OA. METHODS: Human articular chondrocytes (HACs; from healthy and OA donors) and SW-1353 chondrocytic cells were exposed to bone morphogenetic protein 7 (BMP-7), interleukin-1ß (IL-1ß), tumor necrosis factor, or OA synovial fluid (SF; 20% [volume/volume]). Loss-of-function and gain-of-function experiments for BAPX-1/NKX-3.2 were performed. Mouse experimental models of OA were used, and (immuno)histochemistry of tissue sections was performed. Gene and protein expression of BAPX-1/NKX-3.2 and chondrogenic, hypertrophic, and OA-related mediators were determined by real-time quantitative polymerase chain reaction analysis and immunoblotting. In addition, alkaline phosphatase (AP) activity and prostaglandin E2 levels were measured. RESULTS: BAPX-1/NKX-3.2 expression correlated negatively with expression of chondrocyte hypertrophic markers (RUNX-2, COL10A1, AP), cartilage-degrading enzymes (matrix metalloproteinase 13, ADAMTS-5), and mediators of inflammation (cyclooxygenase 2, IL-6) in healthy and OA chondrocytes, as well as in OA induced chondrocytes. BAPX-1/NKX-3.2 positivity was diminished in articular chondrocytes in the knee joints of mice with experimental OA. Knockdown of BAPX-1/NKX-3.2 in HACs did not influence the expression of SOX9, COL2A1, or aggrecan, but led to an acute hypertrophic shift in the HAC phenotype. Overexpression of BAPX-1/NKX-3.2 decreased hypertrophic gene expression in HACs. Furthermore, the hypertrophic OA chondrocyte phenotype could be counteracted by overexpression of BAPX-1/NKX-3.2 and by BMP-7 in a BAPX-1/NKX-3.2 dependent manner. CONCLUSION: Our findings indicate that BAPX-1/NKX-3.2 is a molecular switch that is involved in controlling the hypertrophic phenotype of the postdevelopmental (OA) articular chondrocyte.
File Format	HTM / HTML
ISSN	23265191
Issue Number	11
Volume Number	67
e-ISSN	23265205
Journal	Arthritis & Rheumatology
Language	English
Publisher	Wiley
Publisher Date	2015-11-01
Publisher Place	United States
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Discipline Rheumatology Arthritis, Experimental Metabolism Cartilage, Articular Chondrocytes Homeodomain Proteins Osteoarthritis Transcription Factors Animals Pathology Bone Morphogenetic Protein 7 Pharmacology Drug Effects Cell Differentiation Cell Enlargement Humans Interleukin-1beta Mice Tumor Necrosis Factor-alpha Journal Article Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology Rheumatology

Central Library (ISO-9001:2015 Certified)
Indian Institute of Technology Kharagpur
Kharagpur, West Bengal, India | PIN - 721302

See location in the Map
03222 282435
Mail: support@ndl.gov.in

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in