A neuronal cell line (PC12) expresses two β1-class integrins—α1β1, and α3β1—that recognize different neurite outgrowth-promoting domains in laminin

Tomaselli, Kevin J.; Hall, Don; Flier, Leonard A.; Gehlsen, Kurt R.; Turner, David C.; Carbonetto, Salvatore; Reichardt, Louis F.

doi:10.1016/0896-6273(90)90219-6

Cited by 166 publications

(148 citation statements)

References 60 publications

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“…This behavior is reminiscent of what we observed previously in the rat neuronal cell line PC1 2 (Rossino etaL, 1990). In this system we have demonstrated that NGF induces a specific up-regulation of a laminin-binding integrin that is the rat equivalent of the human al/f1 complex (Tomaselli et al, 1990). As for RA-treated SY5Y cells, increased expression of the al /41 integrin in NGF-treated PC1 2 cells correlated to increased neurite response to laminin.…”

Section: Discussionmentioning

confidence: 71%

“…Integrin al /41 and a3/31 represent the major integrin complexes of the two human neuroblastoma cell lines SY5Y and IMR32 (this paper) and of the rat neuronal cell line PC1 2 (Rossino etal., 1990;Tomaselli etal., 1990 (Tomaselli et al, 1990). A complete inhibition of neurite extension requires a combination of al and a3 antibodies.…”

Section: Discussionmentioning

confidence: 99%

“…antibodies alone are ineffective, whereas antibodies to al partially inhibit neurite extension (Turner et al, 1989;Tomaselli et al, 1990).…”

Section: Discussionmentioning

confidence: 99%

“…Nerve cells recognize laminin via cell-surface receptors of the integrin family (Reichardt et al, 1989). Two major laminin-binding integrins, al /,l and a3/f31, have been identified in neuronal cells in culture and support neurite extension (Rossino et al, 1990;Tomaselli et al, 1990).…”

Section: Introductionmentioning

confidence: 99%

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Up-regulation of the integrin alpha 1/beta 1 in human neuroblastoma cells differentiated by retinoic acid: correlation with increased neurite outgrowth response to laminin.

et al. 1991

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Retinoic acid (RA) is known to induce differentiation of neuroblastoma cells in vitro. Here we show that treatment of two human neuroblastoma cell lines, SY5Y and IMR32, with RA resulted in a fivefold increase of the integrin alpha 1/beta 1 expression. The effect was selective because expression of the alpha 3/beta 1 integrin, also present in these cells, was not increased. The up-regulation of the alpha 1/beta 1 differentiated SY5Y cells correlated with increased neurite response to laminin. In fact, RA-treated SY5Y cells elongated neurites on laminin-coated substratum more efficiently compared with untreated cells or cells treated with nerve growth factor, insulin, or phorbol 12-myristate 13-acetate. These three agents induced partial morphological differentiation but did not increase alpha 1 integrin expression. Neurite extension in RA-treated cells was more efficient on laminin than on fibronectin or collagen type I and was inhibited with beta 1 integrin antibodies on all three substrates. Affinity chromatography experiments showed that alpha 1/beta 1 is the major laminin receptor in both untreated and RA-treated SY5Y cells. These data show that RA, a naturally occurring morphogen implicated in embryonic development, can selectively regulate the expression of integrin complexes in neuronal cells and suggest an important role of the alpha 1/beta 1 laminin receptor in the morphological differentiation of nerve cells.

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Section: Discussionmentioning

confidence: 71%

Section: Discussionmentioning

confidence: 99%

“…antibodies alone are ineffective, whereas antibodies to al partially inhibit neurite extension (Turner et al, 1989;Tomaselli et al, 1990).…”

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Up-regulation of the integrin alpha 1/beta 1 in human neuroblastoma cells differentiated by retinoic acid: correlation with increased neurite outgrowth response to laminin.

et al. 1991

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“…As a major component of basement membrane ECM, laminin has frequently been shown to influence neurite outgrowth both in vitro [42][43][44][45] and in vivo [44,[46][47][48][49] . Laminin forms a sheetlike polymer that is best known for its critical involvement in basal membrane formation.…”

Section: Polymersmentioning

confidence: 99%

Biomaterials for spinal cord repair

Haggerty

Oudega

2013

Neurosci. Bull.

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Spinal cord injury (SCi) results in permanent loss of function leading to often devastating personal, economic and social problems. A contributing factor to the permanence of SCi is that damaged axons do not regenerate, which prevents the re-establishment of axonal circuits involved in function. Many groups are working to develop treatments that address the lack of axon regeneration after SCi. The emergence of biomaterials for regeneration and increased collaboration between engineers, basic and translational scientists, and clinicians hold promise for the development of effective therapies for SCi. A plethora of biomaterials is available and has been tested in various models of SCi. Considering the clinical relevance of contusion injuries, we primarily focus on polymers that meet the specific criteria for addressing this type of injury. Biomaterials may provide structural support and/or serve as a delivery vehicle for factors to arrest growth inhibition and promote axonal growth. Designing materials to address the specific needs of the damaged central nervous system is crucial and possible with current technology. Here, we review the most prominent materials, their optimal characteristics, and their potential roles in repairing and regenerating damaged axons following SCi.Keywords: spinal cord injury; axon regeneration; biodegradable materials; extracellular matrix proteins; functional recovery; growth factor; guidance; injury and repair; spinal motor neuron IntroductionSpinal cord injury (SCi) causes loss of neurons and axons resulting in motor and sensory function impairments. There are thousands of new cases of SCi in the world annually [1,2] occurring often in young adults. The lack of endogenous repair and the significant costs to the individual, family and society [1] are important motivations behind the continuing efforts to develop effective therapies. Promoting axonal regeneration is considered a potential repair strategy because it could lead to recovery of axonal circuits involved in motor and/or sensory function [3] .The central nervous system (CNS) neurons are intrinsically capable of some regeneration of damaged axons [4] but their attempts after SCi are frustrated by structural and chemical obstructions in the damaged nervous tissue [5] . Spinal cord repair approaches typically lead to small functional gains. one feature that most of these approaches have in common is a poor axonal regeneration response, suggesting that promoting axonal regeneration, including synapse formation, is essential to achieve substantial functional repair after SCi. if so, it is rational to anticipate that effective spinal cord therapies will need to include interventions addressing the axon growth-inhibition that leads to the poor axonal growth responses. As introduced above, axonal regeneration is considered an important repair mechanism for the injured spinal cord. Therefore, this review focuses on materials that have shown most promise to elicit an axonal regeneration response to foster functional restoration after ...

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Integrin ?1 localization in murine central and peripheral nervous system

Murase

Hayashi

1998

J. Comp. Neurol.

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The distribution of neurons expressing integrin alpha1 subunit protein (INTalpha1) was examined in adult mouse tissues of not only the central nervous system, but also the sympathetic ganglia, and the adrenal gland by immunohistochemistry and immunoelectron microscopy. INTalpha1-positive neurons were observed in most tissues examined, and most of them were found to coexpress tyrosine hydroxylase (TH) except for Purkinje cells and hippocampal neurons. Expression of INTalpha1 was also observed in the malpositioned cortical neurons in reeler mutants, and appeared not to be affected by the aberrant cell migration of the reeler cortical neurons. In situ hybridization showed that the expression of INTalpha1 mRNA was correlated with synthesis of the INTalpha1 protein in each case, and this finding indicated that expression of the protein was controlled by transcriptional regulation of the INTalpha1 gene.

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A neuronal cell line (PC12) expresses two β1-class integrins—α1β1, and α3β1—that recognize different neurite outgrowth-promoting domains in laminin

Cited by 166 publications

References 60 publications

Up-regulation of the integrin alpha 1/beta 1 in human neuroblastoma cells differentiated by retinoic acid: correlation with increased neurite outgrowth response to laminin.

Up-regulation of the integrin alpha 1/beta 1 in human neuroblastoma cells differentiated by retinoic acid: correlation with increased neurite outgrowth response to laminin.

Biomaterials for spinal cord repair

Integrin ?1 localization in murine central and peripheral nervous system

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