Extracellular Matrix Molecules And Their Receptors: Functions In Neural Development

Reichardt, L.

doi:10.1146/annurev.neuro.14.1.531

Cited by 107 publications

(116 citation statements)

References 155 publications

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“…Indeed, morphological studies of dy mice show that Schwann cells of spinal roots remain in an immature state due to the lack of capacity for proliferation and ensheathing axons as well as myelin formation [3,4]. This is consistent with the results of the in vitro studies showing that laminin promotes Schwann cell proliferation, ensheathment and myelination [9,20,21,23,26]. In addition, these findings point to the presence of a Schwann cell laminin-2 receptor which mediates the biological effects of laminin-2.…”

Section: Introductionsupporting

confidence: 81%

Expression of dystroglycan and laminin-2 in peripheral nerve under axonal degeneration and regeneration

Masaki¹,

Matsumura

Saito

et al. 2000

Acta Neuropathol

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In Schwann cells, the transmembrane glycoprotein beta-dystroglycan composes the dystroglycan complex, together with the extracellular glycoprotein alpha-dystroglycan which binds laminin-2, a major component of the Schwann cell basal lamina. To provide clues to the biological functions of the interaction of the dystroglycan complex with laminin-2 in peripheral nerve, the expression of beta-dystroglycan and laminin-alpha2 chain was studied in rat sciatic nerves undergoing axonal degeneration and regeneration as well as in normal condition. In normal sciatic nerve, immunoreactivity for the cytoplasmic domain of beta-dystroglycan was consistently and selectively localized in the Schwann cell cytoplasm underlying the outer (abaxonal) membrane apposing the basal lamina. While beta-dystroglycan expression was gradually down-regulated in Schwann cells losing contact with axons during axonal degeneration, it was progressively up-regulated as the regenerating process of ensheathment and myelination proceeded during regeneration. Interestingly, beta-dystroglycan expression, when detectable, was always restricted to the Schwann cell cytoplasm beneath the outer membrane apposing the basal lamina during both axonal degeneration and regeneration. Furthermore, laminin-alpha2 immunoreactivity roughly paralleled that of beta-dystroglycan during both axonal degeneration and regeneration, indicating that the expression of beta-dystroglycan and laminin-alpha2 is induced and maintained by the Schwann cell contact with axons. Our results indicate that the dystroglycan complex is involved in the adhesion of the Schwann cell outer membrane with the basal lamina and suggest that the dystroglycan complex may play a role in the process of Schwann cell ensheathment and myelination through the interaction with laminin-2.

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Section: Introductionsupporting

confidence: 81%

Expression of dystroglycan and laminin-2 in peripheral nerve under axonal degeneration and regeneration

Masaki¹,

Matsumura

Saito

et al. 2000

Acta Neuropathol

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“…On the other hand, the FNIII domains present in anosmin-1 are common motifs widely distributed amongst a large variety of proteins like extracellular matrix proteins (tenascin), cell adhesion molecules (i.e. NCAM, L1, TAG-1 and F3/contactin), receptor-linked protein kinases and tyrosine phosphatases [67][68][69][70] Several of these molecules have been implicated in processes of neuronal migration and axonal targeting [71][72][73]. Interestingly, the FNIII repeats present in anosmin-1 are more similar to those found in the cellular adhesion molecules L1 [74], TAG-1 [75], and F3/contactin [69,76].…”

Section: The Kal1 Gene Encodes For Anosmin-1mentioning

confidence: 99%

Kallmann’s syndrome, a neuronal migration defect

Cariboni

Maggi

2006

Cell. Mol. Life Sci.

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Infertility and inability to smell are the phenotypical features of Kallmann's syndrome (KS), a genetic disease which affects 1 in 10,000 males and 1 in 50,000 females, the majority of the cases being sporadic. The molecular pathogenesis of KS is complex but mainly referable to the impairment of olfactory axon development and of the migration of gonadotropin-releasing hormone (GnRH) neurons. Only two different genes have been identified so far as responsible for the disease: KAL1 and KAL2, encoding anosmin-1 and fibroblast growth factor receptor 1 (FGFR1), respectively. In this review we focus our attention on insights evoked by recent studies, which propose a new direct role for anosmin-1 in the migration GnRH neurons, and a fascinating hypothesis of interactions between anosmin-1 and FGFR1 systems.

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“…Examination of these sequences reveals several groups having similar properties (Table III). One common structural motif occurs in peptide A-208, that contains the IKVAV sequence previously shown to be active in many cell types (Powell and Kleinman, 1987;reviewed in Sanes, 1989;Reichardt and Tomaselli, 1991). Other peptides that have a similar stretch of hydrophobic amino acids interrupted by a positively charged residue include B-187, A-167, B-30, and C-57.…”

Section: Discussionmentioning

confidence: 99%

“…Laminin-1 has many biological activities, including stimulation of tumor growth and metastasis, cell-matrix attachment, cell migration, wound repair, and neurite outgrowth. Laminin-1 is an extremely potent stimulator of neurite outgrowth for a variety of primary neuronal cells and neuronal cell lines, with activity in the nanomolar range (reviewed in Sanes, 1989;Kleinman et al, 1990;Reichardt and Tomaselli, 1991;Powell and Kleinman, 1997). Laminin occurs in at least eleven isoforms (Burgeson et al, 1994), some of which are expressed in developing axon tracts, suggesting that the laminins also function in neurite outgrowth in vivo (reviewed in Powell and Kleinman, 1997).…”

mentioning

confidence: 99%

Neural cell response to multiple novel sites on laminin-1

et al. 2000

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The basement membrane protein laminin‐1 is a potent stimulator of neurite outgrowth for a variety of neuronal cell types. Previous studies have identified neurite outgrowth activity in several distinct regions of the laminin‐1 molecule. In this study, 545 overlapping 12‐ to 14‐mer synthetic peptides, corresponding to most of the amino acid sequence of the α1, β1, and γ1 chains of laminin‐1, were screened for cell attachment and neurite outgrowth activity using primary cultures of mouse cerebellar granule neurons and two neuronal cell lines. We identified 48 peptides derived from novel regions of the laminin‐1 molecule that were positive for neural cell adhesion activity. Only the cerebellar cells were found to have true neurite outgrowth activity with certain of the peptides, whereas some peptides induced short spike‐like process with the cell lines. Although 23 of these peptides were active on all 3 cell types screened, 25 others showed cell‐type specificity in their activity. These studies show that (1) there are multiple and distinct sites on laminin‐1 for cell adhesion and neurite‐like outgrowth and (2) that there are neural cell‐type‐specific active domains. The multiple active sites found explains, in part, the potent activity of laminin‐1 on neurite outgrowth. J. Neurosci. Res. 61:302–312, 2000. Published 2000 Wiley‐Liss, Inc.

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Extracellular Matrix Molecules And Their Receptors: Functions In Neural Development

Cited by 107 publications

References 155 publications

Expression of dystroglycan and laminin-2 in peripheral nerve under axonal degeneration and regeneration

Expression of dystroglycan and laminin-2 in peripheral nerve under axonal degeneration and regeneration

Kallmann’s syndrome, a neuronal migration defect

Neural cell response to multiple novel sites on laminin-1

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