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Consequences of chondrocyte hypertrophy on osteoarthritic cartilage: potential effect on angiogenesis.
Osteoarthritis Cartilage. 2013 Dec; 21(12):1913-23.OC

Abstract

OBJECTIVE

The aim of this study was to investigate the link between the hypertrophic phenotype of chondrocytes and angiogenesis in osteoarthritis (OA) and more particularly to demonstrate that OA hypertrophic chondrocytes potentially express a phenotype promoting angiogenesis through the expression of factors controlling endothelial cells migration, invasion and adhesion.

METHOD

Human OA chondrocytes were cultivated in alginate beads in medium supplemented with 10% fetal bovine serum (FBS) to induce chondrocyte hypertrophy. The hypertrophic phenotype was characterized throughout 28 days of culture by measuring the expression of specific genes and by a microscopic observation of cellular morphology. The effect of media conditioned by OA hypertrophic chondrocyte on endothelial cells migration, invasion and adhesion was evaluated in functional assays. Moreover, hypertrophic OA chondrocytes were tested for the expression of angiogenic factors by real-time RT-PCR.

RESULTS

Specific markers of hypertrophy and observation of cellular morphology attested of the hypertrophic phenotype of chondrocytes in our culture model. Functional angiogenesis assays showed that factors produced by hypertrophic chondrocytes stimulated migration, invasion and adhesion of endothelial cells. Among the evaluated angiogenic factors, bone sialoprotein (BSP) was the most highly upregulated in hypertrophic chondrocytes. The inhibition of endothelial cell adhesion by a GRGDS peptide confirmed the implication of RGD domain proteins, like BSP, in hypertrophic chondrocyte-induced adhesion of endothelial cells.

CONCLUSION

Hypertrophic differentiation of chondrocyte may promote angiogenesis. Our findings established the relation of BSP with OA chondrocyte hypertrophy and suggested that this factor could constitute a potential target to control cartilage neovascularisation in OA.

Authors+Show Affiliations

Bone and Cartilage Research Unit, University of Liège, Liège, Belgium. Electronic address: l.pesesse@ulg.ac.be.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

23973427

Citation

Pesesse, L, et al. "Consequences of Chondrocyte Hypertrophy On Osteoarthritic Cartilage: Potential Effect On Angiogenesis." Osteoarthritis and Cartilage, vol. 21, no. 12, 2013, pp. 1913-23.
Pesesse L, Sanchez C, Delcour JP, et al. Consequences of chondrocyte hypertrophy on osteoarthritic cartilage: potential effect on angiogenesis. Osteoarthritis Cartilage. 2013;21(12):1913-23.
Pesesse, L., Sanchez, C., Delcour, J. P., Bellahcène, A., Baudouin, C., Msika, P., & Henrotin, Y. (2013). Consequences of chondrocyte hypertrophy on osteoarthritic cartilage: potential effect on angiogenesis. Osteoarthritis and Cartilage, 21(12), 1913-23. https://doi.org/10.1016/j.joca.2013.08.018
Pesesse L, et al. Consequences of Chondrocyte Hypertrophy On Osteoarthritic Cartilage: Potential Effect On Angiogenesis. Osteoarthritis Cartilage. 2013;21(12):1913-23. PubMed PMID: 23973427.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Consequences of chondrocyte hypertrophy on osteoarthritic cartilage: potential effect on angiogenesis. AU - Pesesse,L, AU - Sanchez,C, AU - Delcour,J-P, AU - Bellahcène,A, AU - Baudouin,C, AU - Msika,P, AU - Henrotin,Y, Y1 - 2013/08/22/ PY - 2013/04/08/received PY - 2013/08/09/revised PY - 2013/08/14/accepted PY - 2013/8/27/entrez PY - 2013/8/27/pubmed PY - 2014/7/31/medline KW - Angiogenesis KW - Bone sialoprotein KW - Chondrocyte hypertrophy KW - Osteoarthritis SP - 1913 EP - 23 JF - Osteoarthritis and cartilage JO - Osteoarthritis Cartilage VL - 21 IS - 12 N2 - OBJECTIVE: The aim of this study was to investigate the link between the hypertrophic phenotype of chondrocytes and angiogenesis in osteoarthritis (OA) and more particularly to demonstrate that OA hypertrophic chondrocytes potentially express a phenotype promoting angiogenesis through the expression of factors controlling endothelial cells migration, invasion and adhesion. METHOD: Human OA chondrocytes were cultivated in alginate beads in medium supplemented with 10% fetal bovine serum (FBS) to induce chondrocyte hypertrophy. The hypertrophic phenotype was characterized throughout 28 days of culture by measuring the expression of specific genes and by a microscopic observation of cellular morphology. The effect of media conditioned by OA hypertrophic chondrocyte on endothelial cells migration, invasion and adhesion was evaluated in functional assays. Moreover, hypertrophic OA chondrocytes were tested for the expression of angiogenic factors by real-time RT-PCR. RESULTS: Specific markers of hypertrophy and observation of cellular morphology attested of the hypertrophic phenotype of chondrocytes in our culture model. Functional angiogenesis assays showed that factors produced by hypertrophic chondrocytes stimulated migration, invasion and adhesion of endothelial cells. Among the evaluated angiogenic factors, bone sialoprotein (BSP) was the most highly upregulated in hypertrophic chondrocytes. The inhibition of endothelial cell adhesion by a GRGDS peptide confirmed the implication of RGD domain proteins, like BSP, in hypertrophic chondrocyte-induced adhesion of endothelial cells. CONCLUSION: Hypertrophic differentiation of chondrocyte may promote angiogenesis. Our findings established the relation of BSP with OA chondrocyte hypertrophy and suggested that this factor could constitute a potential target to control cartilage neovascularisation in OA. SN - 1522-9653 UR - https://www.unboundmedicine.com/medline/citation/23973427/Consequences_of_chondrocyte_hypertrophy_on_osteoarthritic_cartilage:_potential_effect_on_angiogenesis_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1063-4584(13)00925-4 DB - PRIME DP - Unbound Medicine ER -