کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
8450696 1547686 2018 28 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Reduced substrate stiffness promotes M2-like macrophage activation and enhances peroxisome proliferator-activated receptor γ expression
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی تحقیقات سرطان
پیش نمایش صفحه اول مقاله
Reduced substrate stiffness promotes M2-like macrophage activation and enhances peroxisome proliferator-activated receptor γ expression
چکیده انگلیسی
The increased stiffness of the extracellular microenvironment observed in cancer and atherosclerosis is thought to regulate the activation of tissue-resident immune cells. However, it remains to be determined whether such substrate stiffness affects macrophage activation phenotypes. Here, we have studied the impact of substrate stiffness on in vitro activation phenotypes of the human monocyte cell line THP-1. THP-1 cells were activated while being cultured on 1%, 4%, 10% agarose gel (soft substrate) or on a plastic plate (stiff substrate). We have shown that a soft, versus a stiff, substrate attenuates the pro-inflammatory activity of M1 promoting-activated THP-1 cells. In addition, we have found that M1-related marker expression and phagocytic activity was lower in THP-1 cells activated on a soft substrate compared to cells on stiff substrates. THP-1 cells alternatively activated on soft substrates showed enhanced M2-like phenotypes. We have found that peroxisome proliferator-activated receptor γ (PPARγ) expression was up-regulated in THP-1 cells activated on a soft substrate. We have shown that the PPARγ antagonist GW9662 partially suppresses M2-like activation of THP-1 cells activated on a soft substrate. Substrate stiffness is, therefore, an important factor in regulating the balance of the pro-inflammatory M1 and anti-inflammatory M2 activation phenotypes.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Experimental Cell Research - Volume 367, Issue 2, 15 June 2018, Pages 264-273
نویسندگان
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