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Opposing influences of protein kinase activities on neurite outgrowth in human neuroblastoma cells: initiation by kinase A and restriction by kinase C.
J Neurosci Res. 1992 Nov; 33(3):398-407.JN

Abstract

The respective roles of cAMP-dependent protein kinase (protein kinase A [PKA]) and protein kinase C (PKC) in the early stages of neurite outgrowth were examined in SH-SY-5Y human neuroblastoma cells. Forskolin or dbcAMP, agents that increase intracellular cAMP levels, and intracellular delivery of PKA catalytic subunit induced neurite outgrowth. The PKA inhibitor, N-(2-guanidinoethyl)-5-isoquinolinesulfonamide (HA 1004), prevented the increases, and decreased further the percentage of cells possessing short, filopodia-like neurites in the absence of inducers. In contrast to effects on PKA activation, PKC activation by 12-0-tetradecanoylphorbol-13-acetate (TPA) reduced the percentage of filopodia-like neurites elaborated by otherwise untreated cells, and prevented neurite outgrowth induced by PKA activators. PKC inhibitors 1-(5-isoquinolinesulfonyl)-2-methylpiperazine dihydrochloride (H7), staurosporine, and sphingosine induced neurite outgrowth. Neurites induced by PKA activation contained higher levels of tubulin immunoreactivity than those induced by PKC inhibition. Furthermore, PKA-induced neurites rapidly retracted in the presence of colchicine, while those elaborated following PKC inhibition were more resistant. These data suggest that neurites elaborated in response to PKA activation are dependent upon microtubule polymerization, and that neurite induction following PKC inhibition is mediated by a different mechanism. PKA activators and PKC inhibitors exerted additive effects on neurite outgrowth, suggesting that the distinct pathways regulated by these two kinases function cooperatively during neuritogenesis.

Authors+Show Affiliations

Laboratories for Molecular Neuroscience, Mailman Research Center, McLean Hospital, Belmont, MA 02178.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.

Language

eng

PubMed ID

1335089

Citation

Shea, T B., et al. "Opposing Influences of Protein Kinase Activities On Neurite Outgrowth in Human Neuroblastoma Cells: Initiation By Kinase a and Restriction By Kinase C." Journal of Neuroscience Research, vol. 33, no. 3, 1992, pp. 398-407.
Shea TB, Beermann ML, Leli U, et al. Opposing influences of protein kinase activities on neurite outgrowth in human neuroblastoma cells: initiation by kinase A and restriction by kinase C. J Neurosci Res. 1992;33(3):398-407.
Shea, T. B., Beermann, M. L., Leli, U., & Nixon, R. A. (1992). Opposing influences of protein kinase activities on neurite outgrowth in human neuroblastoma cells: initiation by kinase A and restriction by kinase C. Journal of Neuroscience Research, 33(3), 398-407.
Shea TB, et al. Opposing Influences of Protein Kinase Activities On Neurite Outgrowth in Human Neuroblastoma Cells: Initiation By Kinase a and Restriction By Kinase C. J Neurosci Res. 1992;33(3):398-407. PubMed PMID: 1335089.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Opposing influences of protein kinase activities on neurite outgrowth in human neuroblastoma cells: initiation by kinase A and restriction by kinase C. AU - Shea,T B, AU - Beermann,M L, AU - Leli,U, AU - Nixon,R A, PY - 1992/11/1/pubmed PY - 1992/11/1/medline PY - 1992/11/1/entrez SP - 398 EP - 407 JF - Journal of neuroscience research JO - J Neurosci Res VL - 33 IS - 3 N2 - The respective roles of cAMP-dependent protein kinase (protein kinase A [PKA]) and protein kinase C (PKC) in the early stages of neurite outgrowth were examined in SH-SY-5Y human neuroblastoma cells. Forskolin or dbcAMP, agents that increase intracellular cAMP levels, and intracellular delivery of PKA catalytic subunit induced neurite outgrowth. The PKA inhibitor, N-(2-guanidinoethyl)-5-isoquinolinesulfonamide (HA 1004), prevented the increases, and decreased further the percentage of cells possessing short, filopodia-like neurites in the absence of inducers. In contrast to effects on PKA activation, PKC activation by 12-0-tetradecanoylphorbol-13-acetate (TPA) reduced the percentage of filopodia-like neurites elaborated by otherwise untreated cells, and prevented neurite outgrowth induced by PKA activators. PKC inhibitors 1-(5-isoquinolinesulfonyl)-2-methylpiperazine dihydrochloride (H7), staurosporine, and sphingosine induced neurite outgrowth. Neurites induced by PKA activation contained higher levels of tubulin immunoreactivity than those induced by PKC inhibition. Furthermore, PKA-induced neurites rapidly retracted in the presence of colchicine, while those elaborated following PKC inhibition were more resistant. These data suggest that neurites elaborated in response to PKA activation are dependent upon microtubule polymerization, and that neurite induction following PKC inhibition is mediated by a different mechanism. PKA activators and PKC inhibitors exerted additive effects on neurite outgrowth, suggesting that the distinct pathways regulated by these two kinases function cooperatively during neuritogenesis. SN - 0360-4012 UR - https://www.unboundmedicine.com/medline/citation/1335089/Opposing_influences_of_protein_kinase_activities_on_neurite_outgrowth_in_human_neuroblastoma_cells:_initiation_by_kinase_A_and_restriction_by_kinase_C_ L2 - https://doi.org/10.1002/jnr.490330306 DB - PRIME DP - Unbound Medicine ER -