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Biological effects of adeno-associated virus vectors of human transforming growth factor ?_1 and ?_3 for reversion of rabbit intervertebral disc degeneration / 中华骨科杂志
Chinese Journal of Orthopaedics ; (12)1999.
Artigo em Chinês | WPRIM | ID: wpr-542866
ABSTRACT
Objective To study the biological effects of pSNAV2-hTGF?1 and pSNAV2-hTGF?3 on the reversion of rabbit disc degeneration. Methods Rabbit nucleus pulpous and annulus fibrosus cells were isolated and cultured. The fluorescence labled pSNAV2 were used to detect the transfect rates of rabbit disc cells at first. Then, the pSNAV2-hTGF?1 and pSNAV2-hTGF?3 were transfected into the degenerated rabbit disc cells respectively. The biological effects of hTGF?1 and hTGF?3 on degenerated rabbit disc cells were detected with Western-bloting and 35S detection to analyze and compare the matrix synthesis of the tranfected cells. Results pSNAV2 could transfect degenerated disc cells effectively in the early stages. Both the pSNAV2-hTGF?1 and pSNAV2-hTGF?3 could stimulate the synthesis of collagen Ⅱ and proteoglycan of the rabbit disc cells. For the early stage of degenerated disc cells, the synthesis of collagen Ⅱ and proteoglycan were greater transfected with pSNAV2-hTGF?1 than transfected with pSNAV2-hTGF?3. The pSNAV2-hTGF?1 could promote the degenerated rabbit annulus fibrosus cells to synthesize collagen Ⅰ and pSNAV2-hTGF?3 could promote the degenerated nucleus pulpous cells of later stage to synthesize the collagen Ⅱ. Conclusion Both pSNAV2-hTGF?1 and pSNAV2-hTGF?3 can promote the degenerated rabbit disc cells of early stage to synthesize the matrix. pSNAV2-hTGF?3 can efficently promote the seriously degenerated nucleus pulpous cells to synthesize the collagen Ⅱ.

Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Idioma: Chinês Revista: Chinese Journal of Orthopaedics Ano de publicação: 1999 Tipo de documento: Artigo

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Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Idioma: Chinês Revista: Chinese Journal of Orthopaedics Ano de publicação: 1999 Tipo de documento: Artigo