scholarly journals Calmodulin Regulates L-Selectin Adhesion Molecule Expression and Function through a Protease-Dependent Mechanism

Cell ◽  
1998 ◽  
Vol 92 (6) ◽  
pp. 809-818 ◽  
Author(s):  
Julius Kahn ◽  
Bruce Walcheck ◽  
Grace I Migaki ◽  
Mark A Jutila ◽  
Takashi Kei Kishimoto
1992 ◽  
Vol 1 (2) ◽  
pp. 101-106 ◽  
Author(s):  
Kevin D. Forsyth ◽  
Vivienne Talbot

Glucocorticoids are very effective inhibitors of both the acute and chronic inflammatory response. In this study the hypothesis that glucocorticoids inhibit an early component of the inflammatory response, neutrophil adhesion to endothelium, by down-regulation of adhesion molecules on neutrophils or endothelium was examined. No effect of dexamethasone on neutrophil adhesion to endothelium or of antigen expression by neutrophils or endothelium was found. The mechanism of action of glucocorticoids in the inflammatory response is probably not mediated by alterations in adhesion molecules.


1993 ◽  
Vol 13 (10) ◽  
pp. 6530-6536
Author(s):  
S L Eck ◽  
N D Perkins ◽  
D P Carr ◽  
G J Nabel

Adhesive interactions between cells are essential for the organization and function of differentiated tissues and organs and are mediated by inducible cell surface glycoproteins. In normal tissues, cell adhesion molecules contribute to immune regulation, inflammation, and embryogenesis. Additionally, they play an important role in a variety of pathogenic processes. Cell adhesion molecule expression can be induced by stimuli known to activate NF-kappa B, a ubiquitous transcription factor found in a variety of cell types. To investigate the role of NF-kappa B in cell adhesion molecule expression, we treated HL-60 cells with a double-stranded oligonucleotide which specifically inhibits NF-kappa B-mediated transcription. This treatment resulted in the inhibition of phorbol 12-myristate 13-acetate (PMA)-induced cellular adhesion, morphological changes, and the expression of leukocyte integrin CD11b. In a similar fashion, expression of intercellular adhesion molecule 1 on human endothelial cells induced by PMA was specifically inhibited by the NF-kappa B antagonist. We suggest that NF-kappa B activation is a necessary event for the PMA-induced differentiation of HL-60 cells and the expression of certain activation is a necessary event for the PMA-induced differentiation of HL-60 cells and the expression of certain adhesion molecules. Furthermore, the inhibition of transcription factor functions by this generally applicable mechanism can be used to define their role in cellular differentiation and function.


2020 ◽  
Author(s):  
Justin H. Trotter ◽  
Zahra Dargaei ◽  
Markus Wöhr ◽  
Kif Liakath-Ali ◽  
Karthik Raju ◽  
...  

ABSTRACTAt tripartite synapses, astrocytes surround synaptic contacts, but how astrocytes contribute to the assembly and function of synapses remains unclear. Here we show that neurexin-1α, a presynaptic adhesion molecule that controls synapse properties, is also abundantly expressed by astrocytes. Strikingly, astrocytic neurexin-1α, but not neuronal neurexin-1α, is highly modified by heparan sulfate. Moreover, astrocytic neurexin-1α is uniquely alternatively spliced and invariably contains an insert in splice-site #4, thereby restricting the range of ligands to which it binds. Deletion of neurexin-1 from astrocytes or neurons does not alter synapse numbers or synapse ultrastructure, but differentially impairs synapse function. At hippocampal Schaffer-collateral synapses, neuronal neurexin-1 is essential for normal NMDA-receptor-mediated synaptic responses, whereas astrocytic neurexin-1 is required for normal AMPA-receptor-mediated synaptic responses and for long-term potentiation of these responses. Thus, astrocytes directly shape synapse properties via a neurexin-1-dependent mechanism that involves a specific molecular program distinct from that of neuronal neurexin-1.


PLoS ONE ◽  
2014 ◽  
Vol 9 (3) ◽  
pp. e91808 ◽  
Author(s):  
Wolfgang Sievert ◽  
Soile Tapio ◽  
Stephanie Breuninger ◽  
Udo Gaipl ◽  
Nicolaus Andratschke ◽  
...  

1993 ◽  
Vol 13 (10) ◽  
pp. 6530-6536 ◽  
Author(s):  
S L Eck ◽  
N D Perkins ◽  
D P Carr ◽  
G J Nabel

Adhesive interactions between cells are essential for the organization and function of differentiated tissues and organs and are mediated by inducible cell surface glycoproteins. In normal tissues, cell adhesion molecules contribute to immune regulation, inflammation, and embryogenesis. Additionally, they play an important role in a variety of pathogenic processes. Cell adhesion molecule expression can be induced by stimuli known to activate NF-kappa B, a ubiquitous transcription factor found in a variety of cell types. To investigate the role of NF-kappa B in cell adhesion molecule expression, we treated HL-60 cells with a double-stranded oligonucleotide which specifically inhibits NF-kappa B-mediated transcription. This treatment resulted in the inhibition of phorbol 12-myristate 13-acetate (PMA)-induced cellular adhesion, morphological changes, and the expression of leukocyte integrin CD11b. In a similar fashion, expression of intercellular adhesion molecule 1 on human endothelial cells induced by PMA was specifically inhibited by the NF-kappa B antagonist. We suggest that NF-kappa B activation is a necessary event for the PMA-induced differentiation of HL-60 cells and the expression of certain activation is a necessary event for the PMA-induced differentiation of HL-60 cells and the expression of certain adhesion molecules. Furthermore, the inhibition of transcription factor functions by this generally applicable mechanism can be used to define their role in cellular differentiation and function.


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