S100A8 inhibits PDGF-induced proliferation of airway smooth muscle cells dependent on the receptor for advanced glycation end-products
Biol. Res
; 50: 23, 2017. graf
Article
de En
| LILACS
| ID: biblio-950874
Bibliothèque responsable:
CL1.1
ABSTRACT
BACKGROUND:
Airway remodeling is a key feature of asthma, characterized by increased proliferation of airway smooth muscle cells (ASMCs). S100A8 is a calcium-binding protein with a potential to regulate cell proliferation. Here, the effect of exogenous S100A8 protein on the proliferation of ASMCs induced by platelet-derived growth factor (PDGF) and the underlying molecular mechanism was investigated.METHODS:
Rat ASMCs were cultured with or without a neutralizing antibody to the receptor for advanced glycation end-products (RAGE), a potential receptor for S100A8 protein. Purified recombinant rat S100A8 protein was then added into the cultured cells, and the proliferation of ASMCs induced by PDGF was detected by colorimetric-based WST-8 assay and ampedance-based xCELLigence proliferation assay. The expression levels of RAGE in ASMCs were analyzed using western blotting assay.RESULTS:
Results showed that exogenous S100A8 inhibited the PDGF-induced proliferation of rat ASMCs in a dose- dependent manner with the maximal effect at 1 µg/ml in vitro. Furthermore, when ASMCs was pre-treated with anti-RAGE neutralizing antibody, the inhibitory effect of S100A8 on PDGF-induced proliferation was significantly suppressed. In addition, neither the treatment with S100A8 or PDGF alone nor the pre-treatment with rS100A8 followed by PDGF stimulation affected the expression levels of RAGE.CONCLUSIONS:
Our study demonstrated that S100A8 inhibits PDGF-induced ASMCs proliferation in a manner dependent on membrane receptor RAGE.Mots clés
Texte intégral:
1
Indice:
LILACS
Sujet Principal:
Facteur de croissance dérivé des plaquettes
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Myocytes du muscle lisse
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Calgranuline A
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Prolifération cellulaire
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Récepteur spécifique des produits finaux de glycosylation avancée
Limites du sujet:
Animals
langue:
En
Texte intégral:
Biol Res
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Biol. Res
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Biol. Res. (Online)
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Biological Research
Thème du journal:
BIOLOGIA
Année:
2017
Type:
Article