📇 Rhumatologue ·
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📰 Hommage NB · 30/09/2020
<a href="https://news.google.com/rss/articles/CBMifkFVX3lxTE8wYzEzRUtndU45WTJJSjlMSktlNnBWVjVnR1NuNXpaWm00dTNOdkN0NG1jdnQzd1FTa2hTbmZOODdOTjNjSjJOYmdnNEpVWmFMc2hvaUg4clBYN1dtUW9XdTFmRF9LakcwVWVteld6LUpjZWE0bXFqR3pmYXlTQQ?oc=5" target="_blank">Wilfred Bryar (1922-2020) Robertville</a> <font color="#6
International journal of molecular sciences · 2021
Sjögren’s syndrome (SS) is an exocrinopathy characterized by the hypofunction of salivary glands (SGs). Aquaporin-5 (AQP5); a water channel involved in saliva formation; is aberrantly distributed in SS SG acini and contributes to glandular dysfunction. We aimed to investigate the role of ezrin in AQP5 mislocalization in SS SGs. The AQP5–ezrin interaction was assessed by immunoprecipitation and proteome analysis and by proximity ligation assay in immortalized human SG cells. We demonstrated, for the first time, an interaction between ezrin and AQP5. A model of the complex was derived by computer modeling and in silico docking; suggesting that AQP5 interacts with the ezrin FERM-domain via its C-terminus. The interaction was also investigated in human minor salivary gland (hMSG) acini from SS patients (SICCA-SS); showing that AQP5–ezrin complexes were absent or mislocalized to the basolateral side of SG acini rather than the apical region compared to controls (SICCA-NS). Furthermore, in SICCA-SS hMSG acinar cells, ezrin immunoreactivity was decreased at the acinar apical region and higher at basal or lateral regions, accounting for altered AQP5–ezrin co-localization. Our data reveal that AQP5–ezrin interactions in human SGs could be involved in the regulation of AQP5 trafficking and may contribute to AQP5-altered localization in SS patients
International journal of molecular sciences · 2024
In primary Sjögren’s syndrome (pSS) patients, salivary gland (SG) epithelial cells (SGECs) could be exposed to chronic hyperosmotic stress (HOS), consecutive to their destruction and deregulation, that exacerbates an inflammatory response. The aims of this study were to assess the mechanism accounting for C-C motif chemokine ligand 2 (CCL2) expression in an immortalized human salivary gland epithelial acinar cell line (NS-SV-AC) subjected to HOS, as well as the involvement of CCL2 in pSS. CCL2 mRNA and protein levels were determined via RT-qPCR and ELISA. Reporter plasmids and a promoter pull-down assay were used to identify transcription factors associated with CCL2 mRNA increase. Our data showed that HOS-induced CCL2 mRNA increase was independent of the nuclear factor of activated T-cells 5 (NFAT5) and nuclear factor-kappa B (NFkB) but involved Kruppel-like factor 5 (KLF5). CCL2 protein levels, quantified by enzyme-linked immunosorbent assay (ELISA) in sera samples from pSS patients, correlated with the European Alliance of Associations for Rheumatology’s Sjogren’s syndrome disease activity index (ESSDAI) score for systemic activity. In addition, CCL2 protein levels were higher in patients with biological activity, cutaneous manifestations, and ESSDAI score superior or equal to five. Our data suggest that chronic HOS could exacerbate pSS disease by contributing to the inflammatory process induced by the expression and secretion of CCL2.
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Cell communication and signaling : CCS · 2025 · Journal Article
D'Agostino C, Filipovic N, Zindy E, Conrard L, et al.
International journal of molecular sciences · 2024 · Journal Article
Chivasso C, Parisis D, Cabrol X, Datlibagi A, et al.
International journal of molecular sciences · 2021 · Journal Article
Chivasso C, Hagströmer CJ, Rose KL, Lhotellerie F, et al.