Fibroblast growth factor-2 and interleukin-4 synergistically induce eotaxin-1 expression in adipose tissue-derived stromal cells.

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

The relationships between eosinophils and adipose tissues are involved in metabolic homeostasis. Eotaxin is a chemokine with potent effects on eosinophil migration. To clarify the mechanisms of eotaxin expression in adipose tissues, we examined the effects of fibroblast growth factor-2 (FGF-2) and interleukin-4 (IL-4) stimulation on eotaxin expression in adipose tissue-derived stromal cells (ASCs), a type of adipocyte progenitor, in vitro. ASCs expressed eotaxin-1 and did not express eotaxin-2 or -3. Eotaxin-1 expression was increased in a concentration-dependent manner following FGF-2 treatment. Additionally, ASCs expressed FGF receptor-1 (FGFR-1) and did not express FGFR-2, -3, or -4. Eotaxin-1 expression was inhibited in cells treated with the FGFR tyrosine kinase inhibitor and extracellular signal-regulated kinase (ERK) inhibitor U0126, even in the presence of FGF-2. Moreover, eotaxin-1 expression was synergistically enhanced by combined treatment with FGF-2 and IL-4 and inhibited in the presence of U0126. Eotaxin-1 expression induced by FGF-2 and IL-4 was involved in ERK activation via FGFR-1 in ASCs. Upregulation of eotaxin expression in adipose tissues could increase eosinophil migration, thereby inducing IL-4 secretion and activation of alternative macrophages and improving glucose homeostasis. These findings provide insights into the mechanisms through which eotaxin me

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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