Schwann Cell Differentiation in vitro: Extracellular Matrix Deposition and Interaction

1986 ◽  
Vol 8 (3) ◽  
pp. 182-196 ◽  
Author(s):  
A. Baron-Van Evercooren ◽  
A. Gansmüller ◽  
M. Gumpel ◽  
N. Baumann ◽  
H.K. Kleinman
2014 ◽  
Vol 3 (5) ◽  
pp. 217-225 ◽  
Author(s):  
Renjith P. Nair ◽  
Jasmin Joseph ◽  
V.S. Harikrishnan ◽  
V.K. Krishnan ◽  
Lissy Krishnan

2021 ◽  
Vol 8 ◽  
Author(s):  
Francesco Cinetto ◽  
Jessica Ceccato ◽  
Ilaria Caputo ◽  
Daniela Cangiano ◽  
Barbara Montini ◽  
...  

Idiopathic pulmonary fibrosis (IPF) is mainly characterized by aberrant extracellular matrix deposition, consequent to epithelial lung injury and myofibroblast activation, and inflammatory response. Glycogen synthase kinase 3 (GSK-3) is a serine–threonine kinase involved in several pathways, and its inhibition has been already suggested as a therapeutic strategy for IPF patients. There is evidence that GSK-3 is able to induce matrix metalloproteinase (MMP) expression and that its inhibition modulates MMP expression in the tissues. The aim of our study was to investigate the role of GSK-3 and its inhibition in the modulation of MMP-9 and -2 in an in vivo mouse model of lung fibrosis and in vitro using different cell lines exposed to pro-inflammatory or pro-fibrotic stimuli. We found that GSK-3 inhibition down-modulates gene expression and protein levels of MMP-9, MMP-2, and their inhibitors TIMP-1 and TIMP-2 in inflammatory cells harvested from bronchoalveolar lavage fluid (BALF) of mice treated with bleomycin as well as in interstitial alveolar macrophages and cuboidalized epithelial alveolar cells. To the same extent, GSK-3 inhibition blunted the increased MMP-9 and MMP-2 activity induced by pro-fibrotic stimuli in a human lung fibroblast cell line. Moreover, the αSMA protein level, a marker of fibroblast-to-myofibroblast transition involved in fibrosis, was decreased in primary fibroblasts treated with TGFβ following GSK-3 inhibition. Our results confirm the implication of GSK-3 in lung inflammation and fibrosis, suggesting that it might play its role by modulating MMP expression and activity but also pushing fibroblasts toward a myofibroblast phenotype and therefore enhancing extracellular matrix deposition. Thus, its inhibition could represent a possible therapeutic strategy.


2018 ◽  
Vol 10 (3) ◽  
pp. 174-183 ◽  
Author(s):  
Paola Occhetta ◽  
Giuseppe Isu ◽  
Marta Lemme ◽  
Chiara Conficconi ◽  
Philipp Oertle ◽  
...  

Our 3D-scar-on-a-chip model resembles fibroblast proliferation and activation, extracellular matrix deposition and stiffening upon application of only cyclic mechanical stretching.


1989 ◽  
Vol 109 (6) ◽  
pp. 3095-3103 ◽  
Author(s):  
B Seilheimer ◽  
E Persohn ◽  
M Schachner

To investigate whether neural adhesion molecules are involved in neuron-induced Schwann cell differentiation, cocultures of pure dorsal root ganglion neurons, and Schwann cells were maintained in the presence of antibodies to evaluate possible perturbing effects. Several parameters characteristic of differentiating Schwann cells were studied, such as transition of spindle-shaped to flattened, i.e., more epithelioid morphology, association with neuronal cell bodies, ensheathment of neurites, production of basal lamina and collagen fibrils, and expression of the myelin associated glycoprotein (MAG). A complete ablation of Schwann cell differentiation in all features studied was seen with antibodies to the neural adhesion molecule L1. Antibodies to N-CAM did not reduce the association of Schwann cells with neurites but abolished the interdigitation of Schwann cell processes into neurite bundles, while leaving the other parameters studied unaffected. Fab fragments of antibodies to J1, MAG, and mouse liver membranes did not interfere with the manifestation of any of these parameters. None of the antibodies changed incorporation of [3H]thymidine into Schwann cells.


PLoS ONE ◽  
2017 ◽  
Vol 12 (2) ◽  
pp. e0172592 ◽  
Author(s):  
Thomas Stahnke ◽  
Bhavani S. Kowtharapu ◽  
Oliver Stachs ◽  
Klaus-Peter Schmitz ◽  
Johannes Wurm ◽  
...  

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