Functional characterization of an orphan nuclear receptor, Rev-ErbAalpha, in chondrocytes and its potential role in osteoarthritis

Arthritis Rheum. 2006 Nov;54(11):3513-22. doi: 10.1002/art.22170.

Abstract

Objective: To evaluate the expression and function of the orphan nuclear receptor Rev-ErbAalpha in articular cartilage and to investigate its role in osteoarthritis (OA).

Methods: Expression of Rev-ErbAalpha was analyzed at both the messenger RNA and protein levels in human and bovine articular cartilage and chondrocytes by real-time polymerase chain reaction (TaqMan) and immunocytochemical techniques. The effects of cartilage catabolic and anabolic agents on the expression of Rev-ErbAalpha were evaluated by TaqMan analysis. Overexpression was achieved by either adenoviral transduction or treatment with a peroxisome proliferator-activated receptor alpha agonist, whereas expression was suppressed by antisense oligonucleotides.

Results: Among the 48 known nuclear receptors, Rev-ErbAalpha was found to be the most highly expressed in OA cartilage. It is known to function as a transcription repressor. Treatment of articular chondrocytes with known catabolic agents resulted in the induction of Rev-ErbAalpha, whereas stimulation with anabolic agents led to a decrease in expression. Overexpression of the nuclear receptor was associated with an increase in the expression of matrix-degrading enzymes such as matrix metalloproteinase 13 and aggrecanase. In contrast, a decrease in Rev-ErbAalpha expression led to a concomitant reduction in the activity of matrix-degrading enzymes.

Conclusion: This study is the first to demonstrate that Rev-ErbAalpha is highly expressed in OA articular chondrocytes and that its expression is modulated by known cartilage catabolic and anabolic stimuli. We also demonstrated that modulation of Rev-ErbAalpha expression in chondrocytes may be a novel means of regulating the expression and production of multiple matrix-degrading enzymes. These observations suggest that Rev-ErbAalpha may be a novel therapeutic target for OA.

MeSH terms

  • ADAM Proteins / genetics
  • ADAM Proteins / metabolism
  • ADAMTS5 Protein
  • Animals
  • Antineoplastic Agents / pharmacology
  • Cartilage / cytology
  • Cartilage / physiology
  • Cattle
  • Cells, Cultured
  • Chondrocytes / drug effects
  • Chondrocytes / physiology*
  • DNA-Binding Proteins / genetics*
  • DNA-Binding Proteins / metabolism
  • Down-Regulation / drug effects
  • Extracellular Matrix Proteins / genetics
  • Extracellular Matrix Proteins / metabolism
  • Gene Expression / drug effects
  • Humans
  • Insulin-Like Growth Factor I / pharmacology
  • Interleukin-1 / pharmacology
  • Matrix Metalloproteinase 13 / genetics
  • Matrix Metalloproteinase 13 / metabolism
  • Nuclear Receptor Subfamily 1, Group D, Member 1
  • Oligonucleotides, Antisense
  • Osteoarthritis / metabolism
  • Osteoarthritis / physiopathology*
  • RNA, Messenger / metabolism
  • Receptors, Cytoplasmic and Nuclear / genetics*
  • Receptors, Cytoplasmic and Nuclear / metabolism
  • Transforming Growth Factor beta / pharmacology
  • Tretinoin / pharmacology
  • Tumor Necrosis Factor-alpha / pharmacology
  • Up-Regulation / drug effects

Substances

  • Antineoplastic Agents
  • DNA-Binding Proteins
  • Extracellular Matrix Proteins
  • Interleukin-1
  • NR1D1 protein, human
  • Nuclear Receptor Subfamily 1, Group D, Member 1
  • Oligonucleotides, Antisense
  • RNA, Messenger
  • Receptors, Cytoplasmic and Nuclear
  • Transforming Growth Factor beta
  • Tumor Necrosis Factor-alpha
  • Tretinoin
  • Insulin-Like Growth Factor I
  • ADAM Proteins
  • ADAMTS5 Protein
  • ADAMTS5 protein, human
  • Matrix Metalloproteinase 13