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KMID : 0578319910010040475
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Molecules and Cells
1991 Volume.1 No. 4 p.475 ~ p.481
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A Possible Role of Protein Kinase C In the Chondrogenesis of Chick Limb Bud Mesenchyme Cells
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Kang, Shin-Sung
Jun, Chang-Duk/Jung, Chang Jung/Chung, Hun-Taeg/Park, Tae Kyu
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Abstract
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To investigate the involvement of protein kinase C (PKC) in the regulation of chondrogenesis of chick limb bud mesenchymal cells, we examined the effect of phorbol 12-myristate 13-acetate (PMA) (a potent activator of PKC) and staurosporine (a potent inhibitor of PKC) on chick chondroblast of Hamburger-Hamilton stage of 23/24 in vitro. PMA inhibited the chondrogenesis and cellular proliferation, whereas staurosporine promoted the chondrogenesis without any effect on proliferation in a dose dependent manner. The inihibitory effect of treatment with 100 nM of PMA for 24 h on chondrogenesis was overcomed by following continuous treatment with 5 nM of staurosporine. However, prolonged incubation for 48 h of chondroblast with PMA (day 1-2), abolished the stimulatory effect of staurosporine on chondrognesis. Moreover, PMA exerted no effect on chondrogenic inhibition in prolonged pretreatment with staurosporine. The inhibitory effect of PMA is appreciably reversed in the presence of Caz+ and/or Caz+ ionophore A23187. Moreover, the PMA induced a rapid increase of intracellular Ca 21 concentration and reached to maxi-mum within 180 s, while staurosporine and H-7 decreased the intracellular Cat+ concentration immediately. Thus, it can be concluded that the chondrogenic event might be settled at the early step in in vitro chondrogenesis and PKC acts as a negative modulator. And this negative effect of PKC on chondrogenesis may be related to stimulating Caz+ efflux, whose stimulation may be associated with a PKC-catalyzed phosphorylation of cell membrane Ca 21 channels and/or other intracellular Ca´-+-dependent signal transduction pathway.
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