24R,25-Dihydroxyvitamin D3 Protects against Articular Cartilage Damage following Anterior Cruciate Ligament Transection in Male Rats

Autor: Qingfen Pan, Richard D. Coutts, Barbara D. Boyan, Sharon L. Hyzy, Zvi Schwartz, Kayla M. Scott, Robert M. Healey
Jazyk: angličtina
Rok vydání: 2016
Předmět:
0301 basic medicine
Cartilage
Articular

Male
Pathology
Cell signaling
24
25-Dihydroxyvitamin D 3

Physiology
Knees
Interleukin-1beta
lcsh:Medicine
Osteoarthritis
Knee Joints
Signal transduction
Pathology and Laboratory Medicine
Injections
Intra-Articular

0302 clinical medicine
Animal Cells
Synovial Fluid
Medicine and Health Sciences
lcsh:Science
Musculoskeletal System
Immune Response
Cells
Cultured

Connective Tissue Cells
Multidisciplinary
Chemistry
Signaling cascades
Vitamins
Osteoarthritis
Knee

Body Fluids
Dose–response relationship
medicine.anatomical_structure
Connective Tissue
Legs
Anatomy
Cellular Types
Research Article
medicine.medical_specialty
Anterior cruciate ligament
Immunology
Chondrocyte
Transforming Growth Factor beta1
03 medical and health sciences
Chondrocytes
Signs and Symptoms
Rheumatology
In vivo
Diagnostic Medicine
Internal medicine
medicine
Animals
Humans
030203 arthritis & rheumatology
Inflammation
Dose-Response Relationship
Drug

Cartilage
Arthritis
Anterior Cruciate Ligament Injuries
lcsh:R
Limbs (Anatomy)
Biology and Life Sciences
Cell Biology
Articular cartilage damage
medicine.disease
Rats
Joints (Anatomy)
Disease Models
Animal

030104 developmental biology
Endocrinology
Biological Tissue
TGF-beta signaling cascade
Gene Expression Regulation
Apoptosis
lcsh:Q
Articular Cartilage
Zdroj: PLoS ONE
PLoS ONE, Vol 11, Iss 8, p e0161782 (2016)
ISSN: 1932-6203
Popis: Osteoarthritis (OA) in humans is associated with low circulating 25-hydroxyvitamin D3 [25(OH)D3]. In vitamin D replete rats, radiolabeled 24R,25-dihydroxyvitamin D3 [24R,25(OH)2D3] accumulates in articular cartilage following injection of [3H]-25(OH)D3. Previously, we showed that 24R,25(OH)2D3 blocks chondrocyte apoptosis via phospholipase D and p53, suggesting a role for 24R,25(OH)2D3 in maintaining cartilage health. We examined the ability of 24R,25(OH)2D3 to prevent degenerative changes in articular cartilage in an OA-like environment and the potential mechanisms involved. In vitro, rat articular chondrocytes were treated with IL-1β with and without 24R,25(OH)2D3 or 1α,25(OH)2D3. 24R,25(OH)2D3 but not 1α,25(OH)2D3 blocked the effects of IL-1β in a dose-dependent manner, and its effect was partially mediated through the TGF-β1 signaling pathway. In vivo, unilateral anterior cruciate ligament transections were performed in immunocompetent rats followed by intra-articular injections of 24R,25(OH)2D3 or vehicle (t = 0, 7, 14, 21 days). Tissues were harvested on day 28. Joints treated with vehicle had changes typical of OA whereas joints treated with 24R,25(OH)2D3 had less articular cartilage damage and levels of inflammatory mediators. These results indicate that 24R,25(OH)2D3 protects against OA, and suggest that it may be a therapeutic approach for preventing trauma-induced osteoarthritis.
Databáze: OpenAIRE
načítá se...