Publications
Here is a selection of publications where different laminin isoforms were used to create more authentic cell culture systems.
YAP and TAZ control peripheral myelination and the expression of laminin receptors in Schwann cells
Poitelon Y., Lopez-Anido C., Catignas K., Berti C., Palmisano M., Williamson C., Ameroso D., Abiko K., Hwang Y., Gregorieff A., Wrana JL., Asmani M., Zhao R., Sim FJ., Wrabetz L., Svaren J., Feltri ML. Nature Neuroscience, 2016
A mechanistic article just published by Poitelon and colleagues in Nat Neurosci, adding further evidence for the importance of laminin-211 for radial sorting and proper axon myelination by Schwann cells. The authors show that laminin-211 in combination with mechanical stimuli activate and modulate Yap and Taz, which are downstream effectors in the Hippo pathway, required for radial sorting fo axons and subsequent myelination.
Laminin targeting of a peripheral nerve-highlighting peptide enables degenerated nerve visualization
Glasgow H.L., Whitney M.A., Gross L.A., Friedman B., Adams S.R., Crisp J.L., Hussain T., Frei A.P., Novy K., Wollscheid B., Nguyen Q.T., Tsien R.Y.PNAS, 2106
Here, the extracellular matrix proteins laminin-421 and -211 were identified as NP41 binding targets, and TRICEPS-based glycoprotein capture supported laminin-421 as the primary binding target. Fluorescently labeled nerve-binding peptide NP41 holds promise to reduce surgical nerve damage and facilitate nerve repair. Clinical translation hinges on the identification of binding targets to assess potential toxicity and understand the mechanism. For target identification, the authors developed a receptor capture method, enabling covalent tagging and identification of proteins within close proximity to a bound ligand. The results explain the ability of NP41 to highlight degenerated nerve “ghosts” months after transection that were invisible to the unaided eye but contain laminins. Targeting the extracellular matrix is advantageous for clinical imaging agents, likely reducing undesirable neurological effects.
The adhesion GPCR GPR126 has distinct, domain-dependent functions in Schwann cell development mediated by interaction with Laminin-211
Petersen SC. et al.
In the peripheral nervous system, Schwann cell (SC) myelination requires the adhesion G protein-coupled receptor GPR126, which undergoes autoproteolytic cleavage into an N-terminal fragment (NTF) and a seven-transmembrane-containing C-terminal fragment (CTF). The authors noticed biphasic roles of GPR126 which were governed by interactions with Laminin-211 - a novel ligand for GPR126 that modulates receptor signaling via a tethered agonist. The work suggests a model in which Laminin-211 mediates GPR126-induced cAMP levels to control early and late stages of SC development.
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.
Laminin and growth factor receptor activation stimulates differential growth responses in subpopulations of adult DRG neurons
Tucker B.A., Rahimtula M., Mearow K.M.European Journal of Neuroscience, 2006
Here they show laminin-induced neurite outgrowth and its relation to three known DRG neuronal types. They also show PI3K pathway is responsible. They also discuss this in the light of possible therapeutic targets. The study is limited in that that they only use invitrogen laminin (purified laminin-111) and isoform-specific effects cannot be seen, but they come to a number of highly interesting conclusions: 1) The current findings provide strong support for the use of the ECM molecule laminin in conjunction with NGF and GDNF in order to stimulate optimal levels of axon growth from all populations of regenerating sensory neurons. 2) identified intracellular signaling components that provide potential therapeutic targets when attempting to stimulate the regeneration of peripheral axons. Pharmacological alterations of the PI 3-K/Akt pathway resulting in activation of either PI 3-K or Akt could be beneficial. 3) Laminin-induced neurite growth occurs in the absence of added trophic factors only in heavy-chain neurofilament-positive and calcitonin gene-related peptide-positive DRG neurons [nerve growth factor (NGF)-responsive population]. In contrast, laminin alone is not sufficient to stimulate significant neurite growth from lectin Griffonia simplicifolia IB4-positive neurons (IB4+ve), although it is still required to elicit a growth response from these cells in the presence of glial-derived neurotrophic factor.