Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.7.11.26 (GSK)
 6,788 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to study the role of protein kinase in the proliferation of lung fibroblasts induced by crocidolite. An in vitro model was established by rabbit alveolar macrophage (AM) and human embryonic pulmonary fibroblasts (HEPF). Using MTT color response method to measure HEPF proliferation, the influence of the inhibitor or activator of protein kinase (PKA, PKC and TPK) on the proliferation of crocidolite-induced HEPF were investigated. TiO2 was taken as negative control and SiO2 positive control. The results showed that the inhibitors of PKA, PKC and TPK could all inhibit the proliferation of HEPF induced by crocidolite, their activators could also promote the proliferation of HEPF. There all existed significant dose-effect relationships (P < 0.01), and the intensity in crocidolite group was inhibited or activated more than that in the controls. Through acting intensity analysis, the intensity was found as follows: TPK > PKC > PKA. It was suggested that TPK, PKC and PKA signal pathways were all involved in the process of the proliferation of crocidolite-induced HEPF, but TPK maybe played a key role in this process. This study provide leads for further research on identifying the bioactive factors of proliferation of crocidolite-induce HEPF.
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PMID:[Role of protein kinase in the proliferation of human embryonic pulmonary fibrolasts stimulated by the supernatants of crocidolite-exposed alveolar macrophages]. 1125 51