Enhanced chemokine-receptor expression, function, and signaling in healthy African American and scleroderma-patient monocytes are regulated by caveolin-1.
Rebecca LeeCharles ReeseBeth PerryJonathan HeywoodMichael BonnerMarina ZemskovaRichard M SilverStanley HoffmanElena TourkinaPublished in: Fibrogenesis & tissue repair (2015)
To the best of our knowledge, this is the first report that the expression and function of CCR1, CCR2, and CCR3 are upregulated in monocytes from healthy AA and from SSc patients via molecular mechanisms involving caveolin-1, Src/Lyn, and MEK/ERK. The results suggest that the migration/recruitment of monocytes and fibrocytes into fibrotic tissues, mediated at least in part by CCR1, CCR2, and CCR3, plays a major role in the progression of lung and skin fibrosis and in the predisposition of AA to fibrotic diseases. Our findings further suggest that chemokine receptors and signaling molecules, particularly caveolin-1, that control their expression/function are promising targets for treating fibrotic diseases.
Keyphrases
- dendritic cells
- regulatory t cells
- systemic sclerosis
- african american
- end stage renal disease
- poor prognosis
- chronic kidney disease
- idiopathic pulmonary fibrosis
- immune response
- peripheral blood
- ejection fraction
- newly diagnosed
- interstitial lung disease
- gene expression
- prognostic factors
- signaling pathway
- peritoneal dialysis
- rheumatoid arthritis
- patient reported outcomes
- wound healing