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An isoform of decorin is a resistin receptor on the surface of adipose progenitor cells.

机译:核心蛋白聚糖的同工型是脂肪祖细胞表面的抵抗素受体。

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Adipose stromal cells (ASCs) serve as mesenchymal progenitors in white adipose tissue (WAT). Intercellular interactions involving ASCs have remained obscure. By merging phage display technology with fluorescence-activated cell sorting (FACS), we screened a combinatorial library for peptides that target mouse ASCs in vivo. We isolated peptide CSWKYWFGEC that specifically homes to ASCs, used it as bait to purify the corresponding ASC surface receptor, and identified it as a previously unreported cleavage product of decorin (DCN) lacking the glycanation site (termed DeltaDCN). We demonstrate that DeltaDCN is differentially expressed on ASC surface. In a screen for DeltaDCN-binding proteins, we identified resistin, an adipokine for which the receptor has been unknown. Expression of DeltaDCN in 3T3-L1 cells promoted proliferation and migration but suppressed lipid accumulation upon adipogenesis induction, which was resistin dependent. We conclude that DeltaDCN serves as a functional receptor of resistin in adipocyte progenitors and may regulate WAT expansion.
机译:脂肪基质细胞(ASC)充当白色脂肪组织(WAT)中的间充质祖细胞。涉及ASC的细胞间相互作用仍然不清楚。通过将噬菌体展示技术与荧光激活细胞分选术(FACS)合并,我们筛选了一个组合文库,用于体内靶向小鼠ASC的肽。我们分离了专门归巢于ASC的肽CSWKYWFGEC,将其用作诱饵来纯化相应的ASC表面受体,并将其鉴定为先前未报道的缺乏糖基化位点的得体(DCN)裂解产物(称为DeltaDCN)。我们证明DeltaDCN在ASC表面上差异表达。在针对DeltaDCN结合蛋白的筛选中,我们鉴定了抵抗素,这是一种未知的脂肪因子。 DeltaDCN在3T3-L1细胞中的表达促进了增殖和迁移,但抑制了脂肪生成,这是抵抗素依赖性的,在脂肪形成诱导时。我们得出的结论是,DeltaDCN在脂肪细胞祖细胞中充当抵抗素的功能受体,并可能调节WAT的扩展。

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