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10.1111/acel.12571 http://scihub22266oqcxt.onion/10.1111/acel.12571 C5418207!5418207!28229533     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28229533&cmd=llinks): Failed to open stream: HTTP request failed! 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Expansion of myeloid?derived suppressor cells with aging in the bone marrow of mice through a NF??B?dependent mechanism |pdf=|usr=}}{{28229533}} gab.com Text Expansion of myeloid derived suppressor cells with aging in the bone marrow of mice through a NF B dependent mechanism JO: Aging Cell http://www.kidney.de/pget.php?&tw=1&pmid=28229533 #FOAvip With aging, there is progressive loss of tissue homeostasis and functional reserve, leading to an impaired response to stress and an increased risk of morbidity and mortality. A key mediator of the cellular response to damage and stress is the transcription factor NF??B. We demonstrated previously that NF??B transcriptional activity is upregulated in tissues from both natural aged mice and in a mouse model of a human progeroid syndrome caused by defective repair of DNA damage (ERCC1?deficient mice). We also demonstrated that genetic reduction in the level of the NF??B subunit p65(RelA) in the Ercc1?/? progeroid mouse model of accelerated aging delayed the onset of age?related pathology including muscle wasting, osteoporosis, and intervertebral disk degeneration. Here, we report that the largest fraction of NF??B ?expressing cells in the bone marrow (BM) of aged (>2 year old) mice (C57BL/6?NF??BEGFP reporter mice) are Gr?1+CD11b+myeloid?derived suppressor cells (MDSCs). There was a significant increase in the overall percentage of MDSC present in the BM of aged animals compared with young, a trend also observed in the spleen. However, the function of these cells appears not to be compromised in aged mice. A similar increase of MDSC was observed in BM of progeroid Ercc1?/? and BubR1H/H mice. The increase in MDSC in Ercc1?/? mice was abrogated by heterozygosity in the p65/RelA subunit of NF??B. These results suggest that NF??B activation with aging, at least in part, drives an increase in the percentage of MDSCs, a cell type able to suppress immune cell responses. Twit Text FOAVip Expansion of myeloid derived suppressor cells with aging in the bone marrow of mice through a NF B dependent mechanism ????Aging Cell http://www.kidney.de/pget.php?&tw=1&pmid=28229533 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28229533 #FOAvip English Wikipedia <ref>{{Cite pmid|28229533}}</ref> Expansion of myeloid?derived suppressor cells with aging in the bone marrow of mice through a NF??B?dependent mechanism #MMPMID28229533 Flores RR; Clauson CL; Cho J; Lee B; McGowan SJ; Baker DJ; Niedernhofer LJ; Robbins PD Aging Cell 2017[Jun]; 16 (3): 480-7 PMID28229533show ga With aging, there is progressive loss of tissue homeostasis and functional reserve, leading to an impaired response to stress and an increased risk of morbidity and mortality. A key mediator of the cellular response to damage and stress is the transcription factor NF??B. We demonstrated previously that NF??B transcriptional activity is upregulated in tissues from both natural aged mice and in a mouse model of a human progeroid syndrome caused by defective repair of DNA damage (ERCC1?deficient mice). We also demonstrated that genetic reduction in the level of the NF??B subunit p65(RelA) in the Ercc1?/? progeroid mouse model of accelerated aging delayed the onset of age?related pathology including muscle wasting, osteoporosis, and intervertebral disk degeneration. Here, we report that the largest fraction of NF??B ?expressing cells in the bone marrow (BM) of aged (>2 year old) mice (C57BL/6?NF??BEGFP reporter mice) are Gr?1+CD11b+myeloid?derived suppressor cells (MDSCs). There was a significant increase in the overall percentage of MDSC present in the BM of aged animals compared with young, a trend also observed in the spleen. However, the function of these cells appears not to be compromised in aged mice. A similar increase of MDSC was observed in BM of progeroid Ercc1?/? and BubR1H/H mice. The increase in MDSC in Ercc1?/? mice was abrogated by heterozygosity in the p65/RelA subunit of NF??B. These results suggest that NF??B activation with aging, at least in part, drives an increase in the percentage of MDSCs, a cell type able to suppress immune cell responses. äExpansion of myeloid?derived suppressor cells with aging in the bone m(epmc).pdf DeepDyve Pubget Overpricing