Recombinant human bone morphogenetic protein-2 maintains the articular chondrocyte phenotype in long-term culture.

Recombinant human bone morphogenetic protein-2 maintains the articular chondrocyte phenotype in long-term culture. Research Abstract Details 

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Recombinant human bone morphogenetic protein-2 maintains the articular chondrocyte phenotype in long-term culture. Abstract Text:

L Z Sailor,R M Hewick,E A Morris,

Bone morphogenetic proteins have been shown to increase matrix synthesis by articular chondrocytes in short-term cultures. Members of this family of proteins have also been shown to induce endochondral ossification in vivo. The present study was performed to determine if the addition of human recombinant bone morphogenetic protein-2 to a long-term monolayer articular chondrocyte cell culture system affected the ability of the chondrocytes to divide in vitro, whether the cytokine altered expression of the articular chondrocyte phenotype and synthesis of matrix proteoglycans, and whether the cytokine was capable of inducing differentiation to a hypertrophic chondrocyte. Human recombinant bone morphogenetic protein-2 did not alter cell proliferation. It caused 3.5-6.2 times more proteoglycan synthesis by articular chondrocytes during each of the time points tested after 4 days in culture. Total proteoglycan accumulation in the extracellular matrix after 28 days in culture was 6.7 times as great in the treated cultures as in the control. Treatment with human recombinant bone morphogenetic protein-2 maintained the articular chondrocyte phenotype of cells in culture as demonstrated by Northern blot analysis: the expression of type-I collagen genes was increased and that of type-II collagen and aggrecan mRNA was lost in untreated chondrocyte cultures after 14-21 days in culture. In contrast, exposure to 100 ng/ml human recombinant bone morphogenetic protein-2 maintained expression of type-II collagen and increased expression of aggrecan compared with controls during the 28-day culture period. Northern blot analysis of the expression of type-X collagen and osteocalcin by chondrocytes treated with human recombinant bone morphogenetic protein-2 showed a lack of expression of these genes, indicating no alteration in phenotype. These experiments demonstrated the ability of human recombinant bone morphogenetic protein-2 to promote the articular chondrocyte phenotype and matrix synthesis in long-term culture. Characteristics of cell growth were not affected, and the cytokine did not induce differentiation to a hypertrophic chondrocyte.

Recombinant human bone morphogenetic protein-2 maintains the articular chondrocyte phenotype in long-term culture. Publishing Authors By Initials

LZ Sailor,RM Hewick,EA Morris,

For similar peptides: intercellular signaling peptides and proteins: cytokines: transforming growth factor beta research abstracts see: peptides: intercellular signaling peptides and proteins: cytokines: transforming growth factor beta research

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Recombinant human bone morphogenetic protein-2 maintains the articular chondrocyte phenotype in long-term culture. Journal Published:

PUBLICATION TYPE: Journal Article

Journal: Journal of orthopaedic research : official publica

VOLUME: 14

Page Numbers: 937-45

Journal Abbreviation: J. Orthop. Res.

ISSN: 0736-0266

DAY: 19

MONTH: Nov

YEAR: 1996

Recombinant human bone morphogenetic protein-2 maintains the articular chondrocyte phenotype in long-term culture. Information

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LANGUAGE: eng

NlmUniqueID: 8404726

Recombinant human bone morphogenetic protein-2 maintains the articular chondrocyte phenotype in long-term culture. Keywords Mesh Terms:

KEYWORDS: Transforming Growth Factor beta

MESH TERMS: genetics

Chemical & Substance for Abstract: Recombinant human bone morphogenetic protein-2 maintains the articular chondrocyte phenotype in long-term culture. Information

Substance Name: Collagen

Registry Number: 9007-34-5

Grant and Affiliation Information for Recombinant human bone morphogenetic protein-2 maintains the articular chondrocyte phenotype in long-term culture.

AFFILIATION: Genetics Institute, Cambridge, MA 02140, USA.

Country: UNITED STATES

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MEDLINETA: J Orthop Res

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