Publications

Here is a selection of publications where different laminin isoforms are being used to create more authentic cell culture systems

  • Area of interest

  • α6β1 and α7β1 Integrins Are Required in Schwann Cells to Sort Axons

    Marta Pellegatta, Adèle De Arcangelis, Alessandra D'Urso, Alessandro Nodari, Desirée Zambroni, Monica Ghidinelli, Vittoria Matafora, Courtney Williamson, Elisabeth Georges-Labouesse, Jordan Kreidberg, Ulrike Mayer, Karen K. McKee, Peter D. Yurchenco, Angelo Quattrini, Lawrence Wrabetz and Maria Laura Feltri. JNeurosci, 2013

    In this article, the α subunits that form predominant laminin-binding β1 integrins were deleted in Schwann cells. The authors conclude that α6β1 and α7β1 are the laminin-binding integrins required for axonal sorting. The basal lamina of Schwann cells contains especially laminins 211, 411 and 511.

  • Laminin Alters Fyn Regulatory Mechanisms and Promotes Oligodendrocyte Development

    Jenne Relucio, Iva D. Tzvetanova, Wei Ao, Sabine Lindquist and Holly Colognato. JNeurosci, 2009

    The authors report that in laminin-deficient mice, oligodendrocyte progenitors accumulated inappropriately in adult brains. Laminin-211 was found to promote the transition of oligodendrocyte progenitors to newly formed oligodendrocytes. Laminin-enhanced differentiation was Src family kinase-dependent and resulted in the activation of the Src family kinase Fyn.

  • Astrocytic laminin regulates pericyte differentiation and maintains blood brain barrier integrity

    Yao Yao, Zu-Lin Chen, Erin H. Norris, Sidney Strickland. Nature Communications, 2014

    In this article, conditional knockout mice and an acute adenovirus-mediated knockdown model were used to show that lack of astrocytic laminin, a brain-specific BM component, induces BBB breakdown.

  • Properly formed but improperly localized synaptic specializations in the absence of laminin α4

    Bruce L. Patton, Jeanette M. Cunningham, Jill Thyboll, Jarkko Kortesmaa, Håkan Westerblad, Lars Edström, Karl Tryggvason & Joshua R. Sanes. Nature Neuroscience, 2001

    The authors show that the formation and localization of synaptic specializations are regulated separately, and α4β2γ1 (laminin-421) is critical in the latter process.

  • Integrin-laminin interactions controlling neurite outgrowth from adult DRG neurons in vitro

    Stefan Plantman, Manuel Patarroyo, Kaj Fried, Anna Domogatskaya, Karl Tryggvason, Henrik Hammarberg, Staffan Cullheim. Molecular and Cellular Neuroscience, 2008

    The authors examined neurite outgrowth from adult mouse DRG neurons on four laminin isoforms (laminin-1/LM-111, laminin-2/LM-211, laminin-8/LM-411 and laminin-10/LM-511) in vitro. The growth on LN111 and LN511 was trophic factor-independent and superior to the one on LN211 and LN411.

  • Laminins 2 (α2β1γ1, Lm-211) and 8 (α4β1γ1, Lm-411) are synthesized and secreted by tooth pulp fibroblasts and differentially promote neurite outgrowth from trigeminal ganglion sensory neurons

    Kaj Fried, Wondossen Sime, Christina Lillesaar, Ismo Virtanen, Karl Tryggvasson, Manuel Patarroyo. Experimental Cell Research, 2005

    The authors reported that LN-2 (LN211) and LN-8 (LN411) are synthesized by tooth pulp fibroblasts and differentially promote neurite outgrowth from TG neurons. They discuss that LN-8 may contribute to sensory innervation of teeth and other tissues during development and/or regeneration.

  • Impeded Interaction between Schwann Cells and Axons in the Absence of Laminin α4

    Wilhelm Wallquist, Stefan Plantman, Sebastian Thams, Jill Thyboll, Jarkko Kortesmaa, Jan Lännergren, Anna Domogatskaya, Sven Ove Ögren, Mårten Risling, Henrik Hammarberg, Karl Tryggvason and Staffan Cullheim. JNeurosci, 2005

    The Schwann cell basal lamina is is required for normal myelination. The authors show here that absence of the laminin α4 chain, which distinguishes laminin-411 from laminin-211, leads to a disturbance in radial sorting, impaired myelination, and signs of ataxia and proprioceptive disturbances. Laminin-211 and laminin-411 have different critical functions in peripheral nerves, mediated by different integrin receptors.

  • The hippocampal laminin matrix is dynamic and critical for neuronal survival

    Zu-Lin Chen, Justin A. Indyk, and Sidney Strickland Molecular Biology of the Cell, 2003

    In this article, the authors investigated how laminin is involved in neuronal viability by infusing laminin-1 (α1,β1,γ1) into the mouse hippocampus. The results demonstrate that the laminin matrix is a dynamic structure amenable to modification by exogenous molecules.

  • Laminins containing the β2 and γ3 chains regulate astrocyte migration and angiogenesis in the retina

    Gnanaguru G., Bachay G., Biswas S., Pinzón-Duarte G., Hunter D.D. Brunken W.J.Development, 2013

    Astrocytes regulate retinal vascular development. Generated extrinsically to the retina, astrocytes migrate into the retina through the optic nerve head. In this study, we show that astrocytes migrate within a laminin-containing basement membrane. Genetic deletion of the laminin β2 and γ3 chains affects astrocyte migration and spatial distribution. We show that laminins act as haptotactic factors in vitro in an isoform-specific manner, inducing astrocyte migration and promoting astrocyte differentiation. The addition of exogenous laminins to laminin-null retinal explants rescues astrocyte migration and spatial patterning. Furthermore, we show that the loss of laminins reduces β1 integrin expression in astrocytes which can be restored when astrocytes are cultured on Biolaminin 521 or Matrigel. Finally, they show that laminins containing β2 and γ3 chains regulate subsequent retinal blood vessel growth and maintain vascular integrity. These in vivo and in vitro studies demonstrate clearly that laminins containing β2 and γ3 chains are indispensable for migration and spatial organization of astrocytes and that they play a crucial role during retinal angiogenesis in vivo.

  • Astrocytic laminin regulates pericyte differentiation and maintains blood-brain barrier integrity

    Yao Y., Chen Z-L., Norris E.H., Strickland S.Nature comm, 2014

    Here they show that lack of astrocytic laminin, a brain-specific BM component, induces BBB breakdown. Use conditional knockout mice and an acute adenovirus-mediated knockdown model. Using functional blocking antibody and RNAi, we further demonstrate that astrocytic laminin, by binding to integrin a2 receptor, prevents pericyte differentiation from the BBB-stabilizing resting stage to the BBB-disrupting contractile stage, and thus maintains the integrity of BBB. Loss of astrocytic laminin also decreases aquaporin-4 (AQP4) and tight junction protein expression. These results indicate that astrocytic laminin maintains the integrity of BBB through, at least in part, regulation of pericyte differentiation.