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Regulation of neurite outgrowth through protein kinase C and protease nexin-1 in neuroblastoma cell.
Kobe J Med Sci. 1992 Jun; 38(3):147-59.KJ

Abstract

Accumulating evidence has demonstrated that protein kinase C (PKC) and protease nexin-1 (PN-1) may be involved in neuronal differentiation including migration, neurite outgrowth, target recognition, and synaptogenesis. We investigated the potential roles of PKC and PN-1 in neurite outgrowth of human neuroblastoma cell line, GOTO. Upon withdrawal of serum GOTO cells extended neurite processes within 3 h and formed fine network of neurites after 24 h. This morphological change was completely inhibited by thrombin and phorbol-12-myristate-13-acetate (PMA). Withdrawal of serum increased the neurofilament (NF)-L and -M mRNA levels and thrombin did not inhibit the effect of withdrawal of serum. A potent PKC inhibitor, H-7 induced neurite outgrowth in the presence of serum, however, it did not increase the NF mRNA levels. Actinomycin D and cycloheximide did not inhibit the initial neurite outgrowth induced by withdrawal of serum, while these inhibited the increase in the NF mRNA levels. Thrombin retracted the serum depletion-induced neurites but did not retract the neurites induced by H-7. The specific activity and subcellular localization of PKC did not differ between GOTO cells cultured in serum-containing and -free media for 12 h. The serine protease inhibitory activity was undetectable in the serum-free conditioned medium of GOTO cells but the PN-1 mRNA was clearly detected by Northern blot analysis to a less extent than glial cells. Withdrawal of serum or treatment with H-7 did not increase the PN-1 mRNA level in GOTO cells, but thrombin increased its level about 7 folds in serum-free condition. These results indicate that the initial neurite outgrowth requires neither new RNA nor protein synthesis, and that PKC negatively regulates neurite outgrowth and thrombin blocks neurite outgrowth through PKC-dependent pathways.

Authors+Show Affiliations

Department of Pediatrics, Kobe University School of Medicine.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

1453685

Citation

Tsuneishi, S. "Regulation of Neurite Outgrowth Through Protein Kinase C and Protease Nexin-1 in Neuroblastoma Cell." The Kobe Journal of Medical Sciences, vol. 38, no. 3, 1992, pp. 147-59.
Tsuneishi S. Regulation of neurite outgrowth through protein kinase C and protease nexin-1 in neuroblastoma cell. Kobe J Med Sci. 1992;38(3):147-59.
Tsuneishi, S. (1992). Regulation of neurite outgrowth through protein kinase C and protease nexin-1 in neuroblastoma cell. The Kobe Journal of Medical Sciences, 38(3), 147-59.
Tsuneishi S. Regulation of Neurite Outgrowth Through Protein Kinase C and Protease Nexin-1 in Neuroblastoma Cell. Kobe J Med Sci. 1992;38(3):147-59. PubMed PMID: 1453685.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Regulation of neurite outgrowth through protein kinase C and protease nexin-1 in neuroblastoma cell. A1 - Tsuneishi,S, PY - 1992/6/1/pubmed PY - 1992/6/1/medline PY - 1992/6/1/entrez SP - 147 EP - 59 JF - The Kobe journal of medical sciences JO - Kobe J Med Sci VL - 38 IS - 3 N2 - Accumulating evidence has demonstrated that protein kinase C (PKC) and protease nexin-1 (PN-1) may be involved in neuronal differentiation including migration, neurite outgrowth, target recognition, and synaptogenesis. We investigated the potential roles of PKC and PN-1 in neurite outgrowth of human neuroblastoma cell line, GOTO. Upon withdrawal of serum GOTO cells extended neurite processes within 3 h and formed fine network of neurites after 24 h. This morphological change was completely inhibited by thrombin and phorbol-12-myristate-13-acetate (PMA). Withdrawal of serum increased the neurofilament (NF)-L and -M mRNA levels and thrombin did not inhibit the effect of withdrawal of serum. A potent PKC inhibitor, H-7 induced neurite outgrowth in the presence of serum, however, it did not increase the NF mRNA levels. Actinomycin D and cycloheximide did not inhibit the initial neurite outgrowth induced by withdrawal of serum, while these inhibited the increase in the NF mRNA levels. Thrombin retracted the serum depletion-induced neurites but did not retract the neurites induced by H-7. The specific activity and subcellular localization of PKC did not differ between GOTO cells cultured in serum-containing and -free media for 12 h. The serine protease inhibitory activity was undetectable in the serum-free conditioned medium of GOTO cells but the PN-1 mRNA was clearly detected by Northern blot analysis to a less extent than glial cells. Withdrawal of serum or treatment with H-7 did not increase the PN-1 mRNA level in GOTO cells, but thrombin increased its level about 7 folds in serum-free condition. These results indicate that the initial neurite outgrowth requires neither new RNA nor protein synthesis, and that PKC negatively regulates neurite outgrowth and thrombin blocks neurite outgrowth through PKC-dependent pathways. SN - 0023-2513 UR - https://www.unboundmedicine.com/medline/citation/1453685/Regulation_of_neurite_outgrowth_through_protein_kinase_C_and_protease_nexin_1_in_neuroblastoma_cell_ L2 - http://www.diseaseinfosearch.org/result/8994 DB - PRIME DP - Unbound Medicine ER -