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Effects of extracellular nucleotides in the thyroid: P2Y2 receptor-mediated ERK1/2 activation and c-Fos induction in PC Cl3 cells.
Cell Signal. 2005 Jun; 17(6):739-49.CS

Abstract

Aim of the present paper was to investigate the signaling pathways of P2Y2 in rat thyroid PC Cl3 cell line and its effects on proliferation. This study demonstrates that P2Y2 activation provoked: (a) a cytosol-to-membrane translocation of PKC-alpha, -betaI and -epsilon; (b) the phosphorylation of the extra cellular signal-regulated kinases 1 and 2 (ERK1/2); (c) the expression of c-Fos protein; (d) no effects on the G1/S progression and overall cell proliferation. The P2Y2-stimulated ERK1/2 phosphorylation was: (a) completely blocked by PD098059, a mitogen-activated protein kinase (MEK) inhibitor or by W-7, a Ca2+-calmodulin (CaM) antagonist; (b) reduced by GF109203X, inhibitor of PKCs, or AG1478, inhibitor of EGFR tyrosine kinase, or LY294002/wortmannin, inhibitors of phosphoinositide 3-kinases, or cytochalasin D, inhibitor of actin microfilament bundles polymerization. The c-Fos induction was greatly diminished by Go6976 or PD098059, and completely abolished when combined. In conclusion, data indicate that the P2Y2-induced phosphorylation of ERK1/2 and the induction of c-Fos are due to the operation of CaM, with PKC, PI3K, EGFR and receptor endocytosis mechanisms endorsing the signalling. On the other hand, no mitogenic effects of P2Y2 are whatsoever noticed in PC Cl3 cells.

Authors+Show Affiliations

Laboratorio di Fisiologia Cellulare, Dipartimento di Scienze e Tecnologie Biologiche e Ambientali, Universita' di Lecce, Ecotekne, Via Prov. le per Monteroni, 73100 Lecce, Italy.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

15722198

Citation

Elia, Maria Giovanna, et al. "Effects of Extracellular Nucleotides in the Thyroid: P2Y2 Receptor-mediated ERK1/2 Activation and c-Fos Induction in PC Cl3 Cells." Cellular Signalling, vol. 17, no. 6, 2005, pp. 739-49.
Elia MG, Muscella A, Romano S, et al. Effects of extracellular nucleotides in the thyroid: P2Y2 receptor-mediated ERK1/2 activation and c-Fos induction in PC Cl3 cells. Cell Signal. 2005;17(6):739-49.
Elia, M. G., Muscella, A., Romano, S., Greco, S., Di Jeso, B., Verri, T., Storelli, C., & Marsigliante, S. (2005). Effects of extracellular nucleotides in the thyroid: P2Y2 receptor-mediated ERK1/2 activation and c-Fos induction in PC Cl3 cells. Cellular Signalling, 17(6), 739-49.
Elia MG, et al. Effects of Extracellular Nucleotides in the Thyroid: P2Y2 Receptor-mediated ERK1/2 Activation and c-Fos Induction in PC Cl3 Cells. Cell Signal. 2005;17(6):739-49. PubMed PMID: 15722198.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Effects of extracellular nucleotides in the thyroid: P2Y2 receptor-mediated ERK1/2 activation and c-Fos induction in PC Cl3 cells. AU - Elia,Maria Giovanna, AU - Muscella,Antonella, AU - Romano,Simona, AU - Greco,Simona, AU - Di Jeso,Bruno, AU - Verri,Tiziano, AU - Storelli,Carlo, AU - Marsigliante,Santo, Y1 - 2004/11/23/ PY - 2004/09/21/received PY - 2004/10/22/revised PY - 2004/10/26/accepted PY - 2005/2/22/pubmed PY - 2005/6/21/medline PY - 2005/2/22/entrez SP - 739 EP - 49 JF - Cellular signalling JO - Cell. Signal. VL - 17 IS - 6 N2 - Aim of the present paper was to investigate the signaling pathways of P2Y2 in rat thyroid PC Cl3 cell line and its effects on proliferation. This study demonstrates that P2Y2 activation provoked: (a) a cytosol-to-membrane translocation of PKC-alpha, -betaI and -epsilon; (b) the phosphorylation of the extra cellular signal-regulated kinases 1 and 2 (ERK1/2); (c) the expression of c-Fos protein; (d) no effects on the G1/S progression and overall cell proliferation. The P2Y2-stimulated ERK1/2 phosphorylation was: (a) completely blocked by PD098059, a mitogen-activated protein kinase (MEK) inhibitor or by W-7, a Ca2+-calmodulin (CaM) antagonist; (b) reduced by GF109203X, inhibitor of PKCs, or AG1478, inhibitor of EGFR tyrosine kinase, or LY294002/wortmannin, inhibitors of phosphoinositide 3-kinases, or cytochalasin D, inhibitor of actin microfilament bundles polymerization. The c-Fos induction was greatly diminished by Go6976 or PD098059, and completely abolished when combined. In conclusion, data indicate that the P2Y2-induced phosphorylation of ERK1/2 and the induction of c-Fos are due to the operation of CaM, with PKC, PI3K, EGFR and receptor endocytosis mechanisms endorsing the signalling. On the other hand, no mitogenic effects of P2Y2 are whatsoever noticed in PC Cl3 cells. SN - 0898-6568 UR - https://www.unboundmedicine.com/medline/citation/15722198/Effects_of_extracellular_nucleotides_in_the_thyroid:_P2Y2_receptor_mediated_ERK1/2_activation_and_c_Fos_induction_in_PC_Cl3_cells_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0898-6568(04)00235-9 DB - PRIME DP - Unbound Medicine ER -