کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2827085 1570402 2016 6 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
SDF-1/CXCL12 modulates mitochondrial respiration of immature blood cells in a bi-phasic manner
ترجمه فارسی عنوان
SDF-1 / CXCL12 ، تنفس میتوكندری سلول های خونی نابالغ را به شیوه ای دوبعدی تعدیل کند
کلمات کلیدی
SDF-1 / CXCL12؛ میتوکندریا؛ مصرف اکسیژن؛ سلولهای خونی
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی زیست شناسی مولکولی
چکیده انگلیسی

SDF-1/CXCL12 is a potent chemokine required for the homing and engraftment of hematopoietic stem and progenitor cells. Previous data from our group has shown that in an SDF-1/CXCL12 transgenic mouse model, lineage− Sca-1+ c-Kit+ (LSK) bone marrow cells have reduced mitochondrial membrane potential versus wild-type. These results suggested that SDF-1/CXCL12 may function to keep mitochondrial respiration low in immature blood cells in the bone marrow. Low mitochondrial metabolism helps to maintain low levels of reactive oxygen species (ROS), which can influence differentiation. To test whether SDF-1/CXCL12 regulates mitochondrial metabolism, we employed the human leukemia cell line HL-60, that expresses high levels of the SDF-1/CXCL12 receptor, CXCR4, as a model of hematopoietic progenitor cells in vitro. We treated HL-60 cells with SDF-1/CXCL12 for 2 and 24 h. Oxygen consumption rates (OCR), mitochondrial-associated ATP production, mitochondrial mass, and mitochondrial membrane potential of HL-60 cells were significantly reduced at 2 h and increased at 24 h as compared to untreated control cells. These biphasic effects of SDF-1/CXCL12 were reproduced with lineage negative primary mouse bone marrow cells, suggesting a novel function of SDF-1/CXCL12 in modulating mitochondrial respiration by regulating mitochondrial oxidative phosphorylation, ATP production and mitochondrial content.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Blood Cells, Molecules, and Diseases - Volume 58, May 2016, Pages 13–18
نویسندگان
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