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on bovine vascular smooth muscle cell (VSMC) proliferation and signal transduction mechanism involved were investigated. The levels of PKC-alpha protein and mRNA were determined by cell-based ELISA, RT-PCR, Western blotting and immunocytochemical methods. Meanwhile, mRNA levels of c-jun, c-myc and c-fos were assayed by RT-PCR method. The results showed that HDO inhibited newborn calf serum (NCS)-induced expression of PKC-alpha and proto-oncogenes, which may be one of the mechanisms for the inhibition of VSMC proliferation by HDO. Flow cytometry analysis indicated that HDO blocked NCS-induced cell cycle progression by arresting cells at G0/G1 phase. The results imply that HDO inhibits VSMC proliferation by moderating the gene level of PKC-alpha, eventually inhibiting proto-oncogene mRNA expression and blocking G1/S transition.", "digital" : null, "printed" : null, "sourceYear" : 2013, "packet" : "(Bíró Tamás (Élettan); 2013.09.19. 10:07:48)", "foreignEdition" : false, "foreignLanguage" : true, "fullPublication" : true, "conferencePublication" : false, "nationalOrigin" : false, "missingAuthor" : false, "oaType" : "NONE", "oaCheckDate" : "2024-02-05", "oaFree" : false, "citationCount" : 0, "citationCountUnpublished" : 0, "citationCountWoOther" : 0, "independentCitCountWoOther" : 0, "doiCitationCount" : 0, "wosCitationCount" : 0, "scopusCitationCount" : 0, "independentCitationCount" : 0, "unhandledCitationCount" : 0, "citingPubCount" : 0, "independentCitingPubCount" : 0, "unhandledCitingPubCount" : 0, "citedPubCount" : 2, "citedCount" : 2, "ratings" : [ { "otype" : "SjrRating", "mtid" : 5673466, "link" : "/api/sjrrating/5673466", "label" : "sjr:Q2 (2012) Scopus - Pharmacology, Toxicology and Pharmaceutics (miscellaneous) ACTA PHARMACEUTICA SINICA 0513-4870", "listPos" : 35, "rankValue" : 0.49, "type" : "journal", "ratingType" : { "otype" : "RatingType", "mtid" : 10002, "link" : "/api/ratingtype/10002", "label" : "sjr", "code" : "sjr", "published" : true, "snippet" : true }, "subject" : { "otype" : "ClassificationExternal", "mtid" : 3001, "link" : "/api/classificationexternal/3001", "label" : "Scopus - Pharmacology, Toxicology and Pharmaceutics (miscellaneous)", "published" : true, "oldId" : 3001, "snippet" : true }, "ranking" : "Q2", "calculation" : "DIRECT", "published" : true, "oldId" : 5673466, "snippet" : true } ], "ratingsForSort" : "Q2", "referenceList" : "Ross, R., The pathogenes is of atherosclerosis: A perspective for the 1990s (1993) Nature, 362, pp. 801-809. , J; \n\nLittle, P.J., Ivey, M.E., Osman, N., Endothelin-1 actions on vascular smooth muscle cell functions as a target for the prevention of atherosclerosis (2008) Curr Vasc Pharmacol, 6, pp. 195-203. , J; \n\nYun, M.R., Lee, J.Y., Park, H.S., Heo, H.J., Park, J.Y., Bae, S.S., Hong, K.W., Kim, C.D., Oleic acid enhances vascular smooth muscle cell proliferation via phosphatidylinositol 3-kinase/Akt signaling pathway (2006) Pharmacological Research, 54 (2), pp. 97-102. , DOI 10.1049/el:20063971, PII S1043661806000387; \n\nMukundan, L., Milhorn, D.M., Matta, B., Suttles, J., CD40-mediated activation of vascular smooth muscle cell chemokine production through a Src-initiated, MAPK-dependent pathway (2004) Cellular Signalling, 16 (3), pp. 375-384. , DOI 10.1016/j.cellsig.2003.08.008; \n\nYang, J., Han, Y., Sun, H., (-)-Epigallocatechin gallate suppresses proliferation of vascular smooth muscle cells induced by high glucose by inhibition of PKC and ERK1/2 signalings (2011) J Agric Food Chem, 59, pp. 11483-11490. , J; \n\nBarnett, M.E., Madgwick, D.K., Takemoto, D.J., Protein kinase C as a stress sensor (2007) Cellular Signalling, 19 (9), pp. 1820-1829. , DOI 10.1016/j.cellsig.2007.05.014, PII S0898656807001556; \n\nDempsey, E.C., Cool, C.D., Littler, C.M., Lung disease and PKCs (2007) Pharmacological Research, 55 (6), pp. 545-559. , DOI 10.1016/j.phrs.2007.04.010, PII S1043661807000916; \n\nMackay, H.J., Twelves, C.J., Targeting the protein kinase C family: Are we there yet? 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