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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Articular chondrocytes from aging rats respond poorly to insulin-like growth factor-1: an altered signaling pathway.

This study investigates the effect of insulin-like growth factor-1 (IGF-1) and phorbol 12-myrystate 13-acetate (PMA) on 3H-thymidine, 35SO(4) and 3H -glycine incorporations, adenosine 3':5'-cyclic monophosphate (cAMP) production and protein kinase C ( PKC) activation in cultured rat articular chondrocyte monolayers (RACM) derived from animals of different ages. It was found that IGF-1 stimulates all these cellular functions in cultures derived from all age groups in a concentration dependent manner, although the cells from 14-month old animals responded poorly. IGF-1 also induces in cells from 1-month old rats an increase in the expression of mRNAs specific for aggrecan and type II collagen molecules as shown with RT-PCR. These effects are mediated via IGF-1 interaction with specific receptors because the monoclonal antibody against the receptor protein suppresses more than 60% of the ligand-induced DNA synthesis. PMA, a direct PKC activator, potentiated IGF-1-induced effects in all cells but much more strongly in cells from young than in cells from 14-month old animals. The age-related failure of RACM to respond adequately to IGF-1 was correlated with a decrease in IGF-1-induced cAMP production, and IGF-1- induced and PMA- induced PKC activations. These results show that IGF-1 regulates the synthesis of DNA, proteoglycans (PG) and collagen II at the level of transcription and suggest that the reduced response of cell monolayers derived from 14-month old rats to IGF-1 is probably due to a failure of old cells to adequately transduce IGF-1 receptor-generated downstream signaling.[1]


  1. Articular chondrocytes from aging rats respond poorly to insulin-like growth factor-1: an altered signaling pathway. Messai, H., Duchossoy, Y., Khatib, A.M., Panasyuk, A., Mitrovic, D.R. Mech. Ageing Dev. (2000) [Pubmed]
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