Distinct roles of PKC isoforms in NCAM-mediated neurite outgrowth
(2005) In Journal of Neurochemistry 92(4). p.886-894- Abstract
- The role of protein kinase C (PKC) isoforms in the neural cell adhesion molecule (NCAM)-mediated neurite outgrowth was tested using a co-culture system consisting of fibroblasts with or without NCAM expression upon which either primary cerebellar granular neurones (CGN) or pheochromocytoma (PC12-E2) cells were grown. The latter transiently expressed various PKC isoforms and domains derived from selected PKCs. PKC inhibitors of various specificity inhibited NCAM-stimulated neuritogenesis from CGN, indicating that PKC is involved in this process. Moreover, stimulation by the NCAM-mimetic peptide, C3d, elicited phosphorylation of PKC in CGN. Expression of kinase-deficient forms of PKCalpha, betaI and betaII blocked NCAM-mediated neurite... (More)
- The role of protein kinase C (PKC) isoforms in the neural cell adhesion molecule (NCAM)-mediated neurite outgrowth was tested using a co-culture system consisting of fibroblasts with or without NCAM expression upon which either primary cerebellar granular neurones (CGN) or pheochromocytoma (PC12-E2) cells were grown. The latter transiently expressed various PKC isoforms and domains derived from selected PKCs. PKC inhibitors of various specificity inhibited NCAM-stimulated neuritogenesis from CGN, indicating that PKC is involved in this process. Moreover, stimulation by the NCAM-mimetic peptide, C3d, elicited phosphorylation of PKC in CGN. Expression of kinase-deficient forms of PKCalpha, betaI and betaII blocked NCAM-mediated neurite extension, but had no effect on nerve growth factor (NGF)-mediated neurite outgrowth. Expression of two PKCepsilon constructs: (i) a fragment from PKCepsilon encompassing the pseudosubstrate, the C1a domain (including the actin-binding site, ABS), and parts of the V3 region, or (ii) the PKCepsilon-specific ABS blocked NCAM-mediated neurite extension in both cases. These two constructs also partially inhibited NGF-stimulated neuritogenesis indicating that PKCepsilon is a positive regulator of both NCAM- and NGF-mediated differentiation. We suggest that PKCepsilon is a common downstream mediator for several neuritogenic factors, whereas one or more conventional PKCs are specifically involved in NCAM-stimulated neurite outgrowth. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/254312
- author
- Kolkova, K ; Stensman, Helena LU ; Berezin, V ; Bock, E and Larsson, Christer LU
- organization
- publishing date
- 2005
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- pheochromocytoma cells, outgrowth, neural cell adhesion molecule, neurite, cerebellar granular neurones, protein kinase C
- in
- Journal of Neurochemistry
- volume
- 92
- issue
- 4
- pages
- 886 - 894
- publisher
- Wiley-Blackwell
- external identifiers
-
- pmid:15686491
- wos:000226706600020
- scopus:13644266768
- pmid:15686491
- ISSN
- 1471-4159
- DOI
- 10.1111/j.1471-4159.2004.02919.x
- language
- English
- LU publication?
- yes
- additional info
- The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Tumour Cell Biology (013017530)
- id
- cfb3d0d0-74a5-4e5f-9caa-974ce3c20ce3 (old id 254312)
- date added to LUP
- 2016-04-01 16:19:13
- date last changed
- 2022-01-28 18:50:29
@article{cfb3d0d0-74a5-4e5f-9caa-974ce3c20ce3,
abstract = {{The role of protein kinase C (PKC) isoforms in the neural cell adhesion molecule (NCAM)-mediated neurite outgrowth was tested using a co-culture system consisting of fibroblasts with or without NCAM expression upon which either primary cerebellar granular neurones (CGN) or pheochromocytoma (PC12-E2) cells were grown. The latter transiently expressed various PKC isoforms and domains derived from selected PKCs. PKC inhibitors of various specificity inhibited NCAM-stimulated neuritogenesis from CGN, indicating that PKC is involved in this process. Moreover, stimulation by the NCAM-mimetic peptide, C3d, elicited phosphorylation of PKC in CGN. Expression of kinase-deficient forms of PKCalpha, betaI and betaII blocked NCAM-mediated neurite extension, but had no effect on nerve growth factor (NGF)-mediated neurite outgrowth. Expression of two PKCepsilon constructs: (i) a fragment from PKCepsilon encompassing the pseudosubstrate, the C1a domain (including the actin-binding site, ABS), and parts of the V3 region, or (ii) the PKCepsilon-specific ABS blocked NCAM-mediated neurite extension in both cases. These two constructs also partially inhibited NGF-stimulated neuritogenesis indicating that PKCepsilon is a positive regulator of both NCAM- and NGF-mediated differentiation. We suggest that PKCepsilon is a common downstream mediator for several neuritogenic factors, whereas one or more conventional PKCs are specifically involved in NCAM-stimulated neurite outgrowth.}},
author = {{Kolkova, K and Stensman, Helena and Berezin, V and Bock, E and Larsson, Christer}},
issn = {{1471-4159}},
keywords = {{pheochromocytoma cells; outgrowth; neural cell adhesion molecule; neurite; cerebellar granular neurones; protein kinase C}},
language = {{eng}},
number = {{4}},
pages = {{886--894}},
publisher = {{Wiley-Blackwell}},
series = {{Journal of Neurochemistry}},
title = {{Distinct roles of PKC isoforms in NCAM-mediated neurite outgrowth}},
url = {{http://dx.doi.org/10.1111/j.1471-4159.2004.02919.x}},
doi = {{10.1111/j.1471-4159.2004.02919.x}},
volume = {{92}},
year = {{2005}},
}