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Expanding the adipokine network in cartilage: identification and regulation of novel factors in human and murine chondrocytes
  1. Javier Conde1,
  2. Rodolfo Gomez1,
  3. Giuseppe Bianco1,
  4. Morena Scotece1,
  5. Pamela Lear2,
  6. Carlos Dieguez3,
  7. Juan Gomez-Reino1,
  8. Francisca Lago2,
  9. Oreste Gualillo1
  1. 1NEIRID LAB: Neuroendocrine Interactions in Rheumatology and Inflammatory Disease, Research Laboratory 9, Institute of Medical Research (IDIS), Santiago University Clinical Hospital, Santiago de Compostela, Spain
  2. 2Molecular and Cellular Cardiology, Research Laboratory 7, Institute of Medical Research (IDIS), Santiago University Clinical Hospital, Santiago de Compostela, Spain
  3. 3Department of Physiology, School of Medicine, University of Santiago de Compostela, Santiago de Compostela, Spain; and Carlos III Health Institute Network Centre for Biomedical Research on Obesity and Nutrition, University Clinical Hospital, Santiago de Compostela, Spain
  1. Correspondence to Dr Oreste Gualillo, Santiago University Clinical Hospital, Research Laboratory 9 (NEIRID LAB, Laboratory of Neuro Endocrine Interactions in Rheumatology and Inflammatory Diseases). Building C, Level 2, Calle Choupana s/n, 15706, Santiago de Compostela, Spain; oreste.gualillo{at}; or oreste.gualillo{at}


Background Obesity is a major risk factor for a plethora of diseases including joint disorders associated with cartilage destruction. Recently, it has been demonstrated that adipose tissue might contribute to degenerative joint diseases via the secretion of potent bioactive molecules termed adipokines.

Objective To study expression of the novel adipokines chemerin, lipocalin 2 (LCN2) and serum amyloid A3 (SAA3) in murine and human chondrocytes, under basal conditions, in response to a range of biological and pharmacological treatments, and during chondrocyte differentiation.

Methods Chemerin, LCN2 and SAA3 mRNA and protein expression were evaluated by quantitative real-time reverse transcription PCR and western blot analysis, respectively, in the ATDC-5 murine chondrocyte cell line, a human immortalised chondrocyte cell line (T/C-28a2) and primary cultured human chondrocytes.

Results Human and murine chondrocytes expressed chemerin, LCN2 and SAA3 mRNA; interleukin (IL)-1β was a potent inducer of these novel adipokines. Moreover, dexamethasone, lipopolysaccharides (LPS) and other relevant adipokines such as leptin and adiponectin were able to modulate chemerin, LCN2 and SAA3 mRNA expression alone and when coadministered. Intracellular signal transducers involved in the IL-1β-mediated upregulation of LCN2 and SAA3 included Janus kinase (JAK) 2, phosphatidylinositol 3-kinase (PI3K) and mitogen-activated protein (MAP) kinases. Finally, expression of chemerin, LCN2 and SAA3 mRNA expression were modulated throughout chondrocyte differentiation.

Conclusion Chemerin, LCN2 and SAA3 are implicated in chondrocyte pathophysiology, and regulated by other relevant factors that drive inflammatory process such as IL-1β, LPS and adipokines including leptin and adiponectin. It seems likely that JAK2, PI3K and MAP kinases are involved in mediating these responses.

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  • Patient consent Obtained.

  • Provenance and peer review Not commissioned; externally peer reviewed.

  • Competing interests None.