eCM (Eur Cell Mater / e Cells & Materials) eCM Open Access Scientific Journal
 ISSN:1473-2262         NLM:100973416 (link)         DOI:10.22203/eCM

2015   Volume No 30 – pages 303-314

Title: The infrapatellar fat pad from diseased joints inhibits chondrogenesis of mesenchymal stem cells

Authors: W Wei, R Rudjito, N Fahy, JAN Verhaar, S Clockaerts, YM Bastiaansen-Jenniskens, GJVM van Osch

Address: Department of Orthopaedics and Otorhinolaryngology, Ee1655, Erasmus MC University Medical Centre, Wytemaweg 80, 3015 CN, Rotterdam, The Netherlands

E-mail: g.vanosch at erasmusmc.nl

Key Words: Cartilage repair, mesenchymal stem cells, infrapatellar fat pad, osteoarthritis, inflammation, obesity.

Publication date: December 2nd 2015

Abstract: Cartilage repair by bone marrow derived mesenchymal stem cells (MSCs) can be influenced by inflammation in the knee. Next to synovium, the infrapatellar fat pad (IPFP) has been described as a source for inflammatory factors. Here, we investigated whether factors secreted by the IPFP affect chondrogenesis of MSCs and whether this is influenced by different joint pathologies or obesity. Furthermore, we examined the role of IPFP resident macrophages. First, we made conditioned medium from IPFP obtained from osteoarthritic joints, IPFP from traumatically injured joints during anterior cruciate ligament reconstruction, and subcutaneous adipose tissue. Additionally, we made conditioned medium of macrophages isolated from osteoarthritic IPFP and of polarised monocytes from peripheral blood. We evaluated the effect of different types of conditioned medium on MSC chondrogenesis. Conditioned medium from IPFP decreased collagen 2 and aggrecan gene expression as well as thionin and collagen type 2 staining. This anti-chondrogenic effect was the same for conditioned medium from IPFP of osteoarthritic and traumatically injured joints. Furthermore, IPFP from obese (Body Mass Index >30) donors did not inhibit chondrogenesis more than that of lean (Body Mass Index <25) donors. Finally, conditioned medium from macrophages isolated from IPFP decreased the expression of hyaline cartilage genes, as did peripheral blood monocytes stimulated with pro-inflammatory cytokines. The IPFP and the resident pro-inflammatory macrophages could therefore be targets for therapies to improve MSC-based cartilage repair.

Article download: Pages 303-314 (PDF file)
DOI: 10.22203/eCM.v030a21