Distribution of laminin in the developing peripheral nervous system of the chick

Rogers, Sherry L.; Edson, K. J.; Letourneau, Paul C.; McLoon, Steven C.

doi:10.1016/0012-1606(86)90177-6

Cited by 203 publications

(90 citation statements)

References 24 publications

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“…Recent studies show that laminin is present transiently in developing CNS, including the optic stalk, at a time when neurites extend to their target sites (Adler et al, 1985;McLoon et al, 1986;Rogers et al, 1986). In the present experiments, SC without ECM expressed punctate laminin-like immunoreactivity similar to that described on cell surfaces in the developing CNS (Liesi, 1985;Rogers et al, 1986).…”

Section: Discussionsupporting

confidence: 67%

Schwann cell surfaces but not extracellular matrix organized by Schwann cells support neurite outgrowth from embryonic rat retina

et al. 1988

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Despite evidence that glial cell surfaces and components of the extracellular matrix (ECM) support neurite outgrowth in many culture systems, the relative contributions of these factors have rarely been compared directly. Specifically, it remains to be determined which components of peripheral nerve support growth of central nerve fibers. We have directly compared neurite outgrowth from embryonic day 15 rat retinal explants placed onto beds of (1) Schwann cells without ECM, (2) Schwann cells expressing ECM (including a basal lamina), (3) cell-free ECM prepared from neuron-Schwann cell cultures, (4) nonglial cells (fibroblasts), and (5) 2 isolated ECM components, laminin and type I collagen. From the first day in culture, retinal explants extended neurites when placed on Schwann cells without ECM. Outgrowth on Schwann cells expressing ECM was also extensive, but not obviously different form that on Schwann cells alone. Ultrastructural study revealed that 95% of retinal neurites in ECM-containing cultures contacted other neurites and Schwann cell surfaces exclusively. On cell-free ECM prepared from neuron-Schwann cell cultures, neurite extension was poor to nonexistent. No neurite outgrowth occurred on fibroblasts. Retinal explants also failed to extend neurites onto purified laminin and ammoniated type I collagen substrata; however, growth was rapid and extensive on air-dried type I collagen. In cultures containing islands of air-dried type I collagen on a laminin-coated coverslip, retinal explants attached and extended neurites on collagen, but these neurites did not extend off the island onto the laminin substratum. We conclude from these experiments that neurite extension from embryonic rat retina is supported by a factor found on the surface of Schwann cells and that neither organized nor isolated ECM components provide this neurite promotion. These findings are discussed in relation to possible species differences in growth requirements for retinal ganglion cell neurites and to the specificity of response of different CNS neurites to ECM substrata.

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Section: Discussionsupporting

confidence: 67%

Schwann cell surfaces but not extracellular matrix organized by Schwann cells support neurite outgrowth from embryonic rat retina

et al. 1988

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“…It has been proposed that LN facilitates all of these processes in several neural systems [51][52][53]. The spatio-temporally controlled expression of LN-1 in the developing peripheral nervous system, as well as the visual pathway and the cerebellum, suggests that LN plays a role in axon outgrowth and guidance [54][55][56]. The LN expression has been found to be essential for ventral turning of axons during development.…”

Section: Discussionmentioning

confidence: 99%

Differences between the effect of anisotropic and isotropic laminin and nerve growth factor presenting scaffolds on nerve regeneration across long peripheral nerve gaps

2008

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Anisotropic scaffolds of agarose hydrogels containing gradients of laminin-1 (LN-1) and nerve growth factor (NGF) molecules were used to promote sciatic nerve regeneration across a challenging 20 mm nerve gap in rats.Step and continuous gradient anisotropic scaffolds were fabricated and characterized and regeneration was compared to that in isotropic scaffolds with uniform concentrations of LN-1 and NGF and sciatic nerve grafts harvested from syngenic rats. Polysulfone tubular guidance channels were used to present the agarose based scaffolds to the nerve stumps. Fourmonths after implantation, regenerating axons were observed in animals implanted with anisotropic scaffolds with gradients of both LN-1 and NGF molecules and nerve grafts, but not in animals with isotropic scaffold implants. Also, the scaffolds with gradient of either LN-1 or NGF, with the other component being uniformly distributed in the scaffold, did not elicit axonal regeneration. The total number of myelinated axons was similar for the anisotropic scaffold and the nerve graft conditions, with the anisotropic scaffolds having a higher density of axons than the nerve grafts. Axonal diameter distribution was similar for the anisotropic scaffolds and the nerve grafts. The nerve grafts and anisotropic scaffolds resulted in better functional outcome compared to isotropic scaffolds as measured by the relative gastrocnemius muscle weight (RGMW). Additionally the state of neuromuscular junctions as assessed by pre-and post-synaptic staining revealed that both the anistropic scaffolds performed as well as nerve grafts.

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“…Although data on the precise location of the various LN isoforms in embryos are still sketchy, previous studies clearly established the widespread occurrence of LN in the vicinity of neural crest cells throughout their ontogeny (Duband and Thiery, 1987;Miner et al, 1998;Rogers et al, 1986;Tosney et al, 1994). Thus, the ␣1 chain, essentially characteristic of LN-1, has been found to be abundant along the migration routes in mouse (Miner et al, 1998).…”

Section: Journal Of Cell Science 119 (15)mentioning

confidence: 95%

α1β1-integrin engagement to distinct laminin-1 domains orchestrates spreading, migration and survival of neural crest cells through independent signaling pathways

Desban

Lissitzky

Rousselle

et al. 2006

Journal of Cell Science

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Integrin engagement regulates cell adhesion, shape, migration, growth, and differentiation, but molecular mechanisms coordinating these functions in cells remain unclear. Because of their migratory and differentiation potential, neural crest cells constitute a powerful paradigm to address this question. Here, we describe that laminin-1, a major component of their migration routes, promotes crest cell spreading, migration and survival through two distinct integrin-binding domains that are situated on both sides of its α1 subunit and can be separated in the LN-1 elastase proteolytic fragments E1' and E8. Interaction with either domain was mediated by the same integrin α1β1 but produced distinct, complementary responses through specific signaling cascades. FAK activation upon E8 binding induced spreading, formation of actin bundles and focal adhesions, stimulated oriented migration, but failed to support survival. Conversely, Erk activation upon E1' binding promoted long-term survival and random migration without actin reorganization. Consistent with this, interaction with laminin-5 or laminin-10/11, which do not harbor integrin-binding domains in the N-terminal side of their α chains, failed to support survival. Thus, the signaling activity and function of integrins might depend on binding domains in their ligands, thereby revealing ligand control of integrin function as a possible mechanism for the modulation and coordination of cell response to adhesive signals.

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Distribution of laminin in the developing peripheral nervous system of the chick

Cited by 203 publications

References 24 publications

Schwann cell surfaces but not extracellular matrix organized by Schwann cells support neurite outgrowth from embryonic rat retina

Schwann cell surfaces but not extracellular matrix organized by Schwann cells support neurite outgrowth from embryonic rat retina

Differences between the effect of anisotropic and isotropic laminin and nerve growth factor presenting scaffolds on nerve regeneration across long peripheral nerve gaps

α1β1-integrin engagement to distinct laminin-1 domains orchestrates spreading, migration and survival of neural crest cells through independent signaling pathways

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