J1-160 and J1-180 are oligodendrocyte-secreted nonpermissive substrates for cell adhesion
- PMID: 2477380
- PMCID: PMC2115782
- DOI: 10.1083/jcb.109.4.1765
J1-160 and J1-180 are oligodendrocyte-secreted nonpermissive substrates for cell adhesion
Abstract
The glia-derived J1 extracellular matrix glycoproteins have been referred to as J1-160/J1-180 (the developmentally late appearing lower molecular weight group) and J1-200/J1-220 (the developmentally early appearing higher molecular group immunochemically related to tenascin). Members of the two groups show distinct cross-reactivities. To characterize the structural and functional differences between these J1 glycoproteins, two monoclonal antibodies were generated which recognize only the members of the lower molecular weight group. The two antibodies detect immunochemical similarities among the members of the lower molecular weight group, but do not react with J1/tenascin. J1-160 and J1-180 are specifically expressed by differentiated oligodendrocytes in culture and by myelin of the central nervous system and have not been found in the peripheral nervous system nor in any other organ of the adult mice tested. Electron microscopic examination of rotary-shadowed J1-160 and J1-180 reveals, respectively, dimeric and trimeric (tribrachion) kink-armed rodlike structures, which are linked by disulfide bridges. J1-160/J1-180 are nonpermissive substrates for the attachment and spreading of early postnatal small cerebellar neurons, astrocytes, and fibroblasts. In a mixture with laminin, J1-160/J1-180 are nonpermissive substrates for neurons, but not for astrocytes or fibroblasts. The repulsive effect toward neurons can be neutralized by one of the monoclonal antibodies, but not by the other. These observations are discussed in the context of cell interactions during regeneration in the mammalian nervous system.
Similar articles
-
Oligodendrocyte-derived J1-160/180 extracellular matrix glycoproteins are adhesive or repulsive depending on the partner cell type and time of interaction.Exp Neurol. 1990 Jul;109(1):98-110. doi: 10.1016/s0014-4886(05)80012-3. Exp Neurol. 1990. PMID: 2192910
-
The high-molecular-weight J1 glycoproteins are immunochemically related to tenascin.Differentiation. 1988;37(2):104-14. doi: 10.1111/j.1432-0436.1988.tb00802.x. Differentiation. 1988. PMID: 2456237
-
J1/tenascin is a repulsive substrate for central nervous system neurons.Neuron. 1990 Nov;5(5):627-37. doi: 10.1016/0896-6273(90)90217-4. Neuron. 1990. PMID: 1699568
-
Tenascin/J1/cytotactin: the potential function of hexabrachion proteins in neural development.Dev Neurosci. 1989;11(4-5):266-75. doi: 10.1159/000111905. Dev Neurosci. 1989. PMID: 2477211 Review. No abstract available.
-
Tenascin glycoproteins in developing neural tissues: only decoration?Perspect Dev Neurobiol. 1994;2(1):53-66. Perspect Dev Neurobiol. 1994. PMID: 7530144 Review.
Cited by
-
Functional switch between motor tracts in the presence of the mAb IN-1 in the adult rat.Proc Natl Acad Sci U S A. 2001 Jun 5;98(12):6929-34. doi: 10.1073/pnas.111165498. Epub 2001 May 29. Proc Natl Acad Sci U S A. 2001. PMID: 11381120 Free PMC article.
-
Tenascin-R is antiadhesive for activated microglia that induce downregulation of the protein after peripheral nerve injury: a new role in neuronal protection.J Neurosci. 1998 Aug 15;18(16):6218-29. doi: 10.1523/JNEUROSCI.18-16-06218.1998. J Neurosci. 1998. PMID: 9698315 Free PMC article.
-
Inhibitors of myelination: ECM changes, CSPGs and PTPs.Exp Neurol. 2014 Jan;251:39-46. doi: 10.1016/j.expneurol.2013.10.017. Epub 2013 Nov 4. Exp Neurol. 2014. PMID: 24200549 Free PMC article.
-
Regulation of the E/I-balance by the neural matrisome.Front Mol Neurosci. 2023 Apr 18;16:1102334. doi: 10.3389/fnmol.2023.1102334. eCollection 2023. Front Mol Neurosci. 2023. PMID: 37143468 Free PMC article. Review.
-
Extracellular matrix regulation of inflammation in the healthy and injured spinal cord.Exp Neurol. 2014 Aug;258:24-34. doi: 10.1016/j.expneurol.2013.11.020. Exp Neurol. 2014. PMID: 25017885 Free PMC article. Review.
References
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Other Literature Sources
Molecular Biology Databases