کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2130004 1086516 2016 12 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Mouse macrophage polarity and ROCK1 activity depend on RhoA and non-apoptotic Caspase 3
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی تحقیقات سرطان
پیش نمایش صفحه اول مقاله
Mouse macrophage polarity and ROCK1 activity depend on RhoA and non-apoptotic Caspase 3
چکیده انگلیسی


• Macrophage functions depend on actin cytoskeleton controlled by RhoA/ROCK pathway.
• Macrophage-specific deletion of RhoA affects macrophage polarity.
• Macrophage-specific deletion of RhoA up-regulates its downstream effector ROCK1.
• ROCK1 activity and macrophage polarity depend on non-apoptotic Caspase-3 pathway.

The macrophages have different subtypes with different functions in immune response and disease. It has been generally accepted that M1 macrophages are responsible for stimulation of immune system and inflammation while M2 macrophages play a role in tissue repair. Irrespective of the type, macrophage functions depend on actin cytoskeleton, which is under the control of small GTPase RhoA pathway and its downstream effector ROCK1. We generated RhoA-deleted macrophages and compared the effect of RhoA deletion on M0, M1 and M2 macrophage phenotype. Our studies showed that, unexpectedly, the RhoA deletion did not eliminate macrophage ROCK1 expression and increased ROCK1 activity. The RhoA deletion effect on macrophage phenotype, structure and polarity was different for each subtype. Moreover, our study indicates that the up-regulation of ROCK1 activity in RhoA-deleted macrophages and macrophage phenotype/polarity are dependent on non-apoptotic Caspase-3 and are sensitive to Caspase-3 inhibition. These novel findings will revise/complement our understanding of RhoA pathway regulation of cell structure and polarity.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Experimental Cell Research - Volume 341, Issue 2, 15 February 2016, Pages 225–236
نویسندگان
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