Cotransfected human chondrocytes: over-expression of IGF-I and SOX9 enhances the synthesis of cartilage matrix components collagen-II and glycosaminoglycans
Damage to cartilage causes a loss of type II collagen (Col-II) and glycosaminoglycans (GAG). To restore the original cartilage architecture, cell factors that stimulate Col-II and GAG production are needed. Insulin-like growth factor I (IGF-I) and transcription factor SOX9 are essential for the synt...
| Main Authors: | , , , , , , |
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| Format: | Article |
| Language: | English |
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Asociación Brasileña de Divulgación Científica
2015
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| Online Access: | http://eprints.uanl.mx/29808/1/29808.pdf |
| _version_ | 1838551023743926272 |
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| author | Simental Mendía, M. Lara Arias, J. Álvarez Lozano, E. Said Fernández, S. Soto Domínguez, A. Padilla Rivas, G. R. Martínez Rodríguez, H. G. |
| author_facet | Simental Mendía, M. Lara Arias, J. Álvarez Lozano, E. Said Fernández, S. Soto Domínguez, A. Padilla Rivas, G. R. Martínez Rodríguez, H. G. |
| author_sort | Simental Mendía, M. |
| collection | Repositorio Institucional |
| description | Damage to cartilage causes a loss of type II collagen (Col-II) and glycosaminoglycans (GAG). To restore the original cartilage architecture, cell factors that stimulate Col-II and GAG production are needed. Insulin-like growth factor I (IGF-I) and transcription factor SOX9 are essential for the synthesis of cartilage matrix, chondrocyte proliferation, and phenotype maintenance. We evaluated the combined effect of IGF-I and SOX9 transgene expression on Col-II and GAG production by cultured human articular chondrocytes. Transient transfection and cotransfection were performed using two mammalian expression plasmids (pCMV-SPORT6), one for each transgene. At day 9 post-transfection, the chondrocytes that were overexpressing IGF-I/SOX9 showed 2-fold increased mRNA expression of the Col-II gene, as well as a 57% increase in Col-II protein, whereas type I collagen expression (Col-I) was decreased by 59.3% compared with controls. The production of GAG by these cells increased significantly compared with the controls at day 9 (3.3- vs 1.8-times, an increase of almost 83%). Thus, IGF-I/SOX9 cotransfected chondrocytes may be useful for cell-based articular cartilage therapies. |
| format | Article |
| id | eprints-29808 |
| institution | UANL |
| language | English |
| publishDate | 2015 |
| publisher | Asociación Brasileña de Divulgación Científica |
| record_format | eprints |
| spelling | eprints-298082025-07-09T17:19:43Z http://eprints.uanl.mx/29808/ Cotransfected human chondrocytes: over-expression of IGF-I and SOX9 enhances the synthesis of cartilage matrix components collagen-II and glycosaminoglycans Simental Mendía, M. Lara Arias, J. Álvarez Lozano, E. Said Fernández, S. Soto Domínguez, A. Padilla Rivas, G. R. Martínez Rodríguez, H. G. Damage to cartilage causes a loss of type II collagen (Col-II) and glycosaminoglycans (GAG). To restore the original cartilage architecture, cell factors that stimulate Col-II and GAG production are needed. Insulin-like growth factor I (IGF-I) and transcription factor SOX9 are essential for the synthesis of cartilage matrix, chondrocyte proliferation, and phenotype maintenance. We evaluated the combined effect of IGF-I and SOX9 transgene expression on Col-II and GAG production by cultured human articular chondrocytes. Transient transfection and cotransfection were performed using two mammalian expression plasmids (pCMV-SPORT6), one for each transgene. At day 9 post-transfection, the chondrocytes that were overexpressing IGF-I/SOX9 showed 2-fold increased mRNA expression of the Col-II gene, as well as a 57% increase in Col-II protein, whereas type I collagen expression (Col-I) was decreased by 59.3% compared with controls. The production of GAG by these cells increased significantly compared with the controls at day 9 (3.3- vs 1.8-times, an increase of almost 83%). Thus, IGF-I/SOX9 cotransfected chondrocytes may be useful for cell-based articular cartilage therapies. Asociación Brasileña de Divulgación Científica 2015 Article PeerReviewed text en cc_by_nc_nd http://eprints.uanl.mx/29808/1/29808.pdf http://eprints.uanl.mx/29808/1.haspreviewThumbnailVersion/29808.pdf Simental Mendía, M. y Lara Arias, J. y Álvarez Lozano, E. y Said Fernández, S. y Soto Domínguez, A. y Padilla Rivas, G. R. y Martínez Rodríguez, H. G. (2015) Cotransfected human chondrocytes: over-expression of IGF-I and SOX9 enhances the synthesis of cartilage matrix components collagen-II and glycosaminoglycans. Brazilian Journal of Medical and Biological Research, 48 (12). pp. 1063-1070. ISSN 1414-431X doi:10.1590/1414-431X20154732 |
| spellingShingle | Simental Mendía, M. Lara Arias, J. Álvarez Lozano, E. Said Fernández, S. Soto Domínguez, A. Padilla Rivas, G. R. Martínez Rodríguez, H. G. Cotransfected human chondrocytes: over-expression of IGF-I and SOX9 enhances the synthesis of cartilage matrix components collagen-II and glycosaminoglycans |
| thumbnail | https://rediab.uanl.mx/themes/sandal5/images/online.png |
| title | Cotransfected human chondrocytes: over-expression of IGF-I and SOX9 enhances the synthesis of cartilage matrix components collagen-II and glycosaminoglycans |
| title_full | Cotransfected human chondrocytes: over-expression of IGF-I and SOX9 enhances the synthesis of cartilage matrix components collagen-II and glycosaminoglycans |
| title_fullStr | Cotransfected human chondrocytes: over-expression of IGF-I and SOX9 enhances the synthesis of cartilage matrix components collagen-II and glycosaminoglycans |
| title_full_unstemmed | Cotransfected human chondrocytes: over-expression of IGF-I and SOX9 enhances the synthesis of cartilage matrix components collagen-II and glycosaminoglycans |
| title_short | Cotransfected human chondrocytes: over-expression of IGF-I and SOX9 enhances the synthesis of cartilage matrix components collagen-II and glycosaminoglycans |
| title_sort | cotransfected human chondrocytes over expression of igf i and sox9 enhances the synthesis of cartilage matrix components collagen ii and glycosaminoglycans |
| url | http://eprints.uanl.mx/29808/1/29808.pdf |
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