scholarly journals The Cell Adhesion Molecule L1 Is Developmentally Regulated in the Renal Epithelium and Is Involved in Kidney Branching Morphogenesis

1998 ◽  
Vol 143 (7) ◽  
pp. 2067-2079 ◽  
Author(s):  
Hanna Debiec ◽  
Erik Ilsø Christensen ◽  
Pierre Marie Ronco
Keyword(s):  
Cell Adhesion ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Collecting Duct ◽  
Neuronal Cell ◽  
Branching Morphogenesis ◽  
Immunoglobulin Superfamily ◽  
Glycosylation Pattern ◽  
Cell Adhesion Molecule L1

We immunopurified a surface antigen specific for the collecting duct (CD) epithelium. Microsequencing of three polypeptides identified the antigen as the neuronal cell adhesion molecule L1, a member of the immunoglobulin superfamily. The kidney isoform showed a deletion of exon 3. L1 was expressed in the mesonephric duct and the metanephros throughout CD development. In the adult CD examined by electron microscopy, L1 was not expressed on intercalated cells but was restricted to CD principal cells and to the papilla tall cells. By contrast, L1 appeared late in the distal portion of the elongating nephron in the mesenchymally derived epithelium and decreased during postnatal development. Immunoblot analysis showed that expression, proteolytic cleavage, and the glycosylation pattern of L1 protein were regulated during renal development. L1 was not detected in epithelia of other organs developing by branching morphogenesis. Addition of anti-L1 antibody to kidney or lung organotypic cultures induced dysmorphogenesis of the ureteric bud epithelium but not of the lung. These results suggest a functional role for L1 in CD development in vitro. We further postulate that L1 may be involved in the guidance of developing distal tubule and in generation and maintenance of specialized cell phenotypes in CD.

scholarly journals Elevated phenylalanine levels interfere with neurite outgrowth stimulated by the neuronal cell adhesion molecule L1 in vitro

FEBS Letters ◽  
2006 ◽  
Vol 580 (14) ◽  
pp. 3489-3492 ◽  
Author(s):  
Christine Hartwig ◽  
Andreas Gal ◽  
Rene Santer ◽  
Kurt Ullrich ◽  
Ulrich Finckh ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Neurite Outgrowth ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Neuronal Cell ◽  
Neuronal Cell Adhesion Molecule ◽  
Cell Adhesion Molecule L1

Axonal cell-adhesion molecule L1 in CNS myelination

2004 ◽  
Vol 1 (1) ◽  
pp. 65-72 ◽  
Author(s):  
G. BARBIN ◽  
M.S. AIGROT ◽  
P. CHARLES ◽  
A. FOUCHER ◽  
M. GRUMET ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Culture Medium ◽  
Immunoglobulin Superfamily ◽  
Map Kinase Pathway ◽  
Cell Adhesion Molecule L1 ◽  
Cns Myelination ◽  
Kinase Pathway

Of the axonal signals influencing myelination, adhesion molecules expressed at the axonal surface are strong candidates to mediate interactions between myelinating cells and axons. The recognition cell-adhesion molecule L1, a member of the immunoglobulin superfamily has been shown to play important roles in neuronal migration and survival, and in PNS myelination. We have investigated the role of axonally expressed L1 in CNS myelination. In co-cultures of myelinating oligodendrocytes and neurons derived from murine brain, we demonstrate that, before myelination, L1 immunoreactivity is confined to neurites. After myelination commences, L1 expression is downregulated on myelinated axons and adjacent, but not yet myelinated, internodes. Interfering with L1 before the onset of myelination, by adding either anti-L1 antibody or L1-Fc fusion proteins to the culture medium, inhibits myelination. In addition, in purified cultures of oligodendrocytes, L1-Fc fusion protein prevents lysophosphatidic acid-induced activation of the mitogen-activated kinase (MAP)-kinase pathway. Together, our data indicate that L1 is involved in the initiation of CNS myelination, and that this effect might involve the dephosphorylation of oligodendroglial phosphoproteins.

Heterophilic interactions between cell adhesion molecule L1 and ?v ?3-integrin induce HUVEC process extension in vitro and angiogenesis in vivo

Angiogenesis ◽  
2004 ◽  
Vol 7 (3) ◽  
pp. 213-223 ◽  
Author(s):  
Heike Hall ◽  
Valentin Djonov ◽  
Martin Ehrbar ◽  
Matthias Hoechli ◽  
Jeffrey A. Hubbell
Keyword(s):  
Cell Adhesion ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Cell Adhesion Molecule L1

scholarly journals Tacrine alleviates neuropathic pain in mice by mimicking the cell adhesion molecule L1

2021 ◽  
Keyword(s):  
Nervous System ◽  
Neuropathic Pain ◽  
Cell Adhesion ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Thermal Hyperalgesia ◽  
Modern Medicine ◽  
Stat3 Signaling Pathway ◽  
Cell Adhesion Molecule L1

Neuropathic pain, which is caused by nervous system damage or dysfunctions, remains one of the most intractable challenges in modern medicine due to the lack of effective drugs. Tacrine, which is a small organic compound, is known to mimic the beneficial characteristics of the neural cell adhesion molecule L1 (L1CAM, L1) in vitro. Although previous studies indicated that L1 constitutes a viable strategy for promoting regeneration after nervous system injury, it is not clear whether L1 has a definite role in peripheral nerve injury. In this study, we observed that tacrine eased thermal hyperalgesia and mechanical allodynia after sciatic nerve chronic construction injury and restored functional morphological damage. Furthermore, tacrine suppressed the proliferation and activation of glia and reduced the level of IL-1β, IL-6 and TNF-α. Tacrine also inhibited the JAK2/STAT3 signaling pathway, which is involved in neuroinflammation. These observations indicated that tacrine is a promising candidate for an analgesic agent for neuropathic pain.

scholarly journals Initial appearance and regional distribution of the neuron-glia cell adhesion molecule in the chick embryo.

1985 ◽  
Vol 100 (2) ◽  
pp. 442-456 ◽  
Author(s):  
J P Thiery ◽  
A Delouvée ◽  
M Grumet ◽  
G M Edelman
Keyword(s):  
Nervous System ◽  
Cell Adhesion ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Neural Cell Adhesion Molecule ◽  
Regional Distribution ◽  
Neuronal Cell ◽  
Glia Cell ◽  
Neural Cell Adhesion

This study represents a global survey of the times of the first appearance of the neuron-glia cell adhesion molecule (Ng-CAM) in various regions and on particular cells of the chick embryonic nervous system. Ng-CAM, originally characterized by means of an in vitro binding assay between glial cells and brain membrane vesicles, first appears in development at the surface of early postmitotic neurons. By 3 d in the chick embryo, the first neurons detected by antibodies to Ng-CAM are located in the ventral neural tube; these precursors of motor neurons emit well-stained fibers to the periphery. To identify locations of appearance of Ng-CAM in the peripheral nervous system (PNS), we used a monoclonal antibody called NC-1 that is specific for neural crest cells in early embryos to show the presence of numerous crest cells in the neuritic outgrowth from the neural tube; neither these crest cells nor those in ganglion rudiments bound anti-Ng-CAM antibodies. The earliest neurons in the PNS stained by anti-Ng-CAM appeared by 4 d of development in the cranial ganglia. At later stages and progressively, all the neurons and neurities of the PNS were found to contain Ng-CAM both in vitro and in vivo. Many central nervous system (CNS) neurons also showed Ng-CAM at these later stages, but in the CNS, the molecule was mostly associated with neuronal processes (mainly axons) rather than with cell bodies; this regional distribution at the neuronal cell surface is an example of polarity modulation. In contrast to the neural cell adhesion molecule and the liver cell adhesion molecule, both of which are found very early in derivatives of more than one germ layer, Ng-CAM is expressed only on neurons of the CNS and the PNS during the later epoch of development concerned with neural histogenesis. Ng-CAM is thus a specific differentiation product of neuroectoderm. Ng-CAM was found on developing neurons at approximately the same time that neurofilaments first appear, times at which glial cells are still undergoing differentiation from neuroepithelial precursors. The present findings and those of previous studies suggest that together the neural cell adhesion molecule and Ng-CAM mediate specific cellular interactions during the formation of neuronal networks by means of modulation events that govern their prevalence and polarity on neuronal cell surfaces.

Modulation of synaptic transmission and plasticity by cell adhesion and repulsion molecules

2008 ◽  
Vol 4 (3) ◽  
pp. 197-209 ◽  
Author(s):  
Alexander Dityatev ◽  
Olena Bukalo ◽  
Melitta Schachner
Keyword(s):  
Cell Adhesion ◽  
Synaptic Plasticity ◽  
Synaptic Transmission ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Neuronal Cell ◽  
Long Term Potentiation ◽  
Synaptic Function ◽  
Immunoglobulin Superfamily

Adhesive and repellent molecular cues guide migrating cells and growing neurites during development. They also contribute to synaptic function, learning and memory in adulthood. Here, we review the roles of cell adhesion molecules of the immunoglobulin superfamily (Ig-CAMs) and semaphorins (some of which also contain Ig-like domains) in regulation of synaptic transmission and plasticity. Interestingly, among the seven studied Ig-CAMs, the neuronal cell adhesion molecule proved to be important for all tested forms of hippocampal plasticity, while its associated unusual glycan polysialic acid is necessary and sufficient part for synaptic plasticity only at CA3-CA1 synapses. In contrast, Thy-1 and L1 specifically regulate long-term potentiation (LTP) at synapses formed by entorhinal axons in the dentate gyrus and cornu ammonis, respectively. Contactin-1 is important for long-term depression but not for LTP at CA3-CA1 synapses. Analysis of CHL1-deficient mice illustrates that at intermediate stages of development a deficit in a cell adhesion molecule is compensated but appears as impaired LTP during early and late postnatal development. The emerging mechanisms by which adhesive Ig-CAMs contribute to synaptic plasticity involve regulation of activities of NMDA receptors and L-type Ca2+ channels, signaling via mitogen-activated protein kinase p38, changes in GABAergic inhibition and motility of synaptic elements. Regarding repellent molecules, available data for semaphorins demonstrate their activity-dependent regulation in normal and pathological conditions, synaptic localization of their receptors and their potential to elevate or inhibit synaptic transmission either directly or indirectly.

A Fab fragment directed against the neural cell adhesion molecule L1 enhances functional recovery after injury of the adult mouse spinal cord

2014 ◽  
Vol 460 (3) ◽  
pp. 437-446 ◽  
Author(s):  
Gabriele Loers ◽  
Yi-Fang Cui ◽  
Irmgard Neumaier ◽  
Melitta Schachner ◽  
Arne Skerra
Keyword(s):  
Spinal Cord ◽  
Cell Adhesion ◽  
Adhesion Molecule ◽  
Functional Recovery ◽  
Cell Adhesion Molecule ◽  
Fab Fragment ◽  
Cord Injury ◽  
Cell Adhesion Molecule L1 ◽  
Fibronectin Type Iii Domain

A recombinant monovalent Fab fragment recognizing a functional epitope within the third fibronectin type III domain of murine cell adhesion molecule L1 induces neurite outgrowth and neuronal survival in vitro and enhances functional recovery after spinal cord injury in mice.

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