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1.
Melitta Schachner 《Journal of neurochemistry》1982,39(1):1-8
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Stefano Carenini Dirk Montag Harold Cremer Melitta Schachner Rudolf Martini 《Cell and tissue research》1996,287(1):3-9
We have previously shown that mice deficient in the gene for the myelin-associated glycoprotein (MAG) develop normal myelin
in the peripheral nerves, but show axon and myelin degeneration at eight months of age, suggesting that MAG is involved in
the maintenance of axon-Schwann cell integrity. The search for molecules that might replace MAG during myelination revealed
an overexpression of the neural cell adhesion molecule (N-CAM) at those aspects where MAG is detectable in wild type mice.
To test whether N-CAM might compensate for MAG during myelination in MAG-deficient mice, double mutants deficient in both
MAG and N-CAM (MAG−/N-CAM−mice) were generated by cross-breeding the single mutants. Whereas alterations of myelin development were not detectable in
either of the single or double mutants, degeneration of myelin and axons occurred approximately 4 weeks earlier in MAG−/N-CAM−than in MAG−mutants. Furthermore, at 8 weeks of age, single fiber preparation and electron microscopy revealed that the number of profiles
indicative of degeneration was substantially increased in MAG−/N-CAM−mutants when compared to MAG−mice. These data suggest that in MAG-deficient mice N-CAM does not compensate for MAG in myelin formation but partially substitutes
for it in the maintenance of axon-myelin integrity.
Received: 20 May 1996 / Accepted: 19 July 1996 相似文献
5.
L1 is among the few adhesion molecules that favors repair after trauma in the adult central nervous system of vertebrates by promoting neuritogenesis and neuronal survival, among other beneficial features. In the peripheral nervous system, L1 is up-regulated in Schwann cells and regrowing axons after nerve damage, but the functional consequences of this expression remain unclear. Our previous study of L1-deficient mice in a femoral nerve injury model showed an unexpected improved functional recovery, attenuated motoneuronal cell death, and enhanced Schwann cell proliferation, being attributed to the persistent synthesis of neurotrophic factors. On the other hand, transgenic mice over-expressing L1 in neurons led to improved remyelination, but not improved functional recovery. The present study was undertaken to investigate whether the monoclonal L1 antibody 557 that triggers beneficial L1 functions in vitro would trigger these also in femoral nerve repair. We analyzed femoral nerve regeneration in C57BL/6J mice that received this antibody in a hydrogel filled conduit connecting the cut and sutured nerve before its bifurcation, leading to short-term release of antibody by diffusion. Video-based quantitative analysis of motor functions showed improved recovery when compared to mice treated with conduits containing PBS in the hydrogel scaffold, as a vehicle control. This improved recovery was associated with attenuated motoneuron loss, remyelination and improved precision of preferential motor reinnervation. We suggest that function-triggering L1 antibodies applied to the lesion site at the time of injury over a limited time period will not only be beneficial in peripheral, but also central nervous system regeneration. 相似文献
6.
Monoclonal antibodies used as probes for the structural organization of the central region of fibronectin 总被引:6,自引:0,他引:6
Two monoclonal mouse antibodies against human plasma fibronectin were compared in their reactivity for proteolytic fragments of the antigen by enzyme immunoassay and immunoblotting. These antibodies were shown to react with two different structures within a short segment (about 30 kDa) located about one-third away from the C-terminus of the fibronectin chains. 相似文献
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Nina Stemmer Elena Strekalova Nevena Djogo Frank Pl?ger Gabriele Loers David Lutz Friedrich Buck Marek Michalak Melitta Schachner Ralf Kleene 《PloS one》2013,8(4)
Dysregulation of the proteolytic processing of amyloid precursor protein by γ-secretase and the ensuing generation of amyloid-β is associated with the pathogenesis of Alzheimer''s disease. Thus, the identification of amyloid precursor protein binding proteins involved in regulating processing of amyloid precursor protein by the γ-secretase complex is essential for understanding the mechanisms underlying the molecular pathology of the disease. We identified calreticulin as novel amyloid precursor protein interaction partner that binds to the γ-secretase cleavage site within amyloid precursor protein and showed that this Ca2+- and N-glycan-independent interaction is mediated by amino acids 330–344 in the C-terminal C-domain of calreticulin. Co-immunoprecipitation confirmed that calreticulin is not only associated with amyloid precursor protein but also with the γ-secretase complex members presenilin and nicastrin. Calreticulin was detected at the cell surface by surface biotinylation of cells overexpressing amyloid precursor protein and was co-localized by immunostaining with amyloid precursor protein and presenilin at the cell surface of hippocampal neurons. The P-domain of calreticulin located between the N-terminal N-domain and the C-domain interacts with presenilin, the catalytic subunit of the γ-secretase complex. The P- and C-domains also interact with nicastrin, another functionally important subunit of this complex. Transfection of amyloid precursor protein overexpressing cells with full-length calreticulin leads to a decrease in amyloid-β42 levels in culture supernatants, while transfection with the P-domain increases amyloid-β40 levels. Similarly, application of the recombinant P- or C-domains and of a synthetic calreticulin peptide comprising amino acid 330–344 to amyloid precursor protein overexpressing cells result in elevated amyloid-β40 and amyloid-β42 levels, respectively. These findings indicate that the interaction of calreticulin with amyloid precursor protein and the γ-secretase complex regulates the proteolytic processing of amyloid precursor protein by the γ-secretase complex, pointing to calreticulin as a potential target for therapy in Alzheimer''s disease. 相似文献
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Xenogeneic immunization of rabbits with cells of a mouse undifferentiated neural tumor, MUNTAD, produces antisera which after appropriate absorption bind to the cell surfaces of MUNTAD cells and to three normal adult mouse tissues: brain, kidney, and spermatozoa. Any one of these tissues quantitatively absorbs all of the activity for MUNTAD cells from the antisera, indicating that a single antigen or antigens is shared. This is designated NS-7. The adult tissues positive for NS-7 are the same as those that carry NS-6, but NS-7 is distinguished serologically from NS-6 by being present on many embryonic tissues, tumors, and cell lines which completely lack NS-6. Blocking and capping studies show that on the MUNTAD cell surface, some NS-7 antigenic sites and all NS-6 sites are physically related. 相似文献
10.
NADPH oxidases 1 and 4 mediate cellular senescence induced by resveratrol in human endothelial cells
Yvonne D.C. Schilder Elke H. Heiss Daniel Schachner Jürgen Ziegler Gottfried Reznicek Dan Sorescu Verena M. Dirsch 《Free radical biology & medicine》2009,46(12):1598-1606
Resveratrol is believed to be partially responsible for the French paradox—the low risk of cardiovascular disease despite a high-fat diet in the French population. Recently, resveratrol has also been discussed as a life-span booster in several organisms. Age-related diseases are associated on the cellular level with senescence. We, therefore, hypothesized that resveratrol is vasoprotective by counteracting endothelial cell senescence. Surprisingly, we observed that chronic treatment with resveratrol (10 μM) was prosenescent in primary human endothelial cells. Resveratrol induced elevated reactive oxygen species (ROS) levels that were associated with and causally linked to an accumulation of cells in the S phase of the cell cycle, as measured by flow cytometry. We further show that cell accumulation in S phase leads to increased ROS and finally senescence. Using an siRNA approach, we clearly identified two NADPH oxidases, Nox1 and Nox4, as major targets of resveratrol and primary sources of ROS that act upstream of the observed S-phase accumulation. 相似文献