Volume 7 Issue 5
Sep.  2016
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Yao chen, Li Shuxin, Yu Tao, et al. Changes of renal resident dendritic cells during kidney ischemia-reperfusion injury[J]. ORGAN TRANSPLANTATION, 2016, 7(5): 360-364. doi: 10.3969/j.issn.1674-7445.2016.05.006
Citation: Yao chen, Li Shuxin, Yu Tao, et al. Changes of renal resident dendritic cells during kidney ischemia-reperfusion injury[J]. ORGAN TRANSPLANTATION, 2016, 7(5): 360-364. doi: 10.3969/j.issn.1674-7445.2016.05.006

Changes of renal resident dendritic cells during kidney ischemia-reperfusion injury

doi: 10.3969/j.issn.1674-7445.2016.05.006
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  • Corresponding author: Shi Bingyi, E-mail:shibingyi@medmail.com.cn
  • Received Date: 2016-06-02
    Available Online: 2021-01-19
  • Publish Date: 2016-09-15
  •   Objective  To investigate the changes of renal resident dendritic cells (rDC) during kidney ischemia-reperfusion injury(IRI).  Methods  C57BL/6J mice models with bilateral renal warm ischemia were established. The kidney tissue was prepared for single cell suspension at 24 h and 48 h after reperfusion. The changes in the percentage of CD45+ cells and CD11c+rDCs were evaluated by flow cytometry. The renal tissues of mice labeled with green fluorescent protein and diphtheria toxin receptor (CD11c+GDTR) were prepared for single cell suspension. The percentage and phenotype of CD11c+rDCs were analyzed by flow cytometry. CD11c+GDTR mice models with bilateral renal warm ischemia were established. The renal tissue was prepared for single cell suspension at 24 h after reperfusion. CD45+ cells was gathered by magnetic-activated cell separation (MACS). The expression levels of co-stimulatory molecules on the rDC surface were analyzed by flow cytometry.  Results  At 24 h after reperfusion, the percentage of CD45+ cells in the kidney of C57BL/6J mice was significantly elevated, and further increased at 48 h after reperfusion. At 24 h after reperfusion, the quantity of CD11c+rDCs was equally increased, whereas the percentage of CD11c+rDCs in CD45+ cells was dramatically declined and restored at 48 h after reperfusion, slightly higher compared with that in the sham group. In healthy CD11c+GDTR mice, the percentage of CD45+ cells in the kidney was lower than 1%, consisting of approximately 40% of CD11c+rDCs, which mainly presented as CD11bintF4/80-MHCⅡ+. At 24 h after reperfusion, the percentage of CD11c+F4/80- subset rDC surface co-stimulatory molecules was significantly enhanced, such as CD40, CD80 and CD86.  Conclusions  Following warm IRI, the percentage and quantity of rDCs, and the expression level of rDC surface co-stimulatory molecule are significantly increased, prompting that renal rDC infiltration is increased and phenotype becomes matured.

     

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  • [1]
    Mir MC, Pavan N, Parekh DJ. Current paradigm for ischemia in kidney surgery[J]. J Urol, 2016, 195(6):1655-1663. doi: 10.1016/j.juro.2015.09.099
    [2]
    De Rosa S, Antonelli M, Ronco C. Hypothermia and kidney: a focus on ischaemia-reperfusion injury[J]. Nephrol Dial Transplant, 2016, DOI: 10.1093/ndt/gfw038[Epub ahead of print].
    [3]
    Mas VR, Le TH, Maluf DG. Epigenetics in kidney transplantation: current evidence, predictions, and future research directions[J]. Transplantation, 2016, 100(1):23-38. doi: 10.1097/TP.0000000000000878
    [4]
    Requião-Moura LR, Durão Junior Mde S, Matos AC, et al. Ischemia and reperfusion injury in renal transplantation: hemodynamic and immunological paradigms[J]. Einstein, 2015, 13(1): 129-135. doi: 10.1590/S1679-45082015RW3161
    [5]
    Dong X, Swaminathan S, Bachman LA, et al. Resident dendritic cells are the predominant TNF-secreting cell in early renal ischemia-reperfusion injury[J]. Kidney Int, 2007, 71(7): 619-628. doi: 10.1038/sj.ki.5002132
    [6]
    Scholz J, Lukacs-Kornek V, Engel DR, et al. Renal dendritic cells stimulate IL-10 production and attenuate nephrotoxic nephritis[J]. J Am Soc Nephrol, 2008, 19(3):527-537. doi: 10.1681/ASN.2007060684
    [7]
    Soos TJ, Sims TN, Barisoni L, et al. CX3CR1+ interstitial dendritic cells form a contiguous network throughout the entire kidney[J]. Kidney Int, 2006, 70(3): 591-596. doi: 10.1038/sj.ki.5001567
    [8]
    Bajwa A, Huang L, Ye H, et al. Dendritic cell sphingosine 1-phosphate receptor-3 regulates Th1-Th2 polarity in kidney ischemia-reperfusion injury[J]. J Immunol, 2012, 189(5):2584-2596. doi: 10.4049/jimmunol.1200999
    [9]
    Dean PG, Park WD, Cornell LD, et al. Early subclinical inflammation correlates with outcomes in positive crossmatch kidney allografts[J]. Clin Transplant, 2016, 30(8):925-933. doi: 10.1111/ctr.2016.30.issue-8
    [10]
    Yapici V, Kers J, Slavujevic-Letic I, et al. Intragraft blood dendritic cell antigen-1-positive myeloid dendritic cells increase during BK polyomavirus-associated nephropathy[J]. J Am Soc Nephrol, 2016, 27(8):2502-2510. doi: 10.1681/ASN.2015040442
    [11]
    Podestà MA, Cucchiari D, Ponticelli C. The diverging roles of dendritic cells in kidney allotransplantation[J]. Transplant Rev, 2015, 29(3):114-120. doi: 10.1016/j.trre.2015.04.001
    [12]
    Zhuang Q, Lakkis FG. Dendritic cells and innate immunity in kidney transplantation[J]. Kidney Int, 2015, 87(4):712-718. doi: 10.1038/ki.2014.430
    [13]
    骆志清, 王毅, 钱坤, 等. zVAD-fmk对未成熟树突状细胞诱导初始性CD4+ T细胞分化为调节性T细胞影响的体外研究[J/CD].中华细胞与干细胞杂志(电子版), 2011, 1(1):44-51.

    Luo ZQ, Wang Y, Qian K, et al. Role of apoptosis signal pathway during immature dendritic cell-induced differentiation of T cell[J/CD]. Chin J Cell Stem Cell (Electr Edit), 2011, 1(1):44-51.
    [14]
    Ponticelli C. Ischaemia-reperfusion injury: a major protagonist in kidney transplantation[J]. Nephrol Dial Transplant, 2014, 29(6):1134-1140. doi: 10.1093/ndt/gft488
    [15]
    Rogers NM, Matthews TJ, Kausman JY, et al. Review article: kidney dendritic cells: their role in homeostasis, inflammation and transplantation[J]. Nephrology, 2009, 14(7):625-635. doi: 10.1111/nep.2009.14.issue-7
    [16]
    Bar-On L, Jung S. Defining in vivo dendritic cell function using CD11c-DTR transgenic mice[J]. Methods Mol Biol, 2010, 595:429-442. doi: 10.1007/978-1-60761-421-0
    [17]
    Ozaki KS, Kimura S, Nalesnik MA, et al. The loss of renal dendritic cells and activation of host adaptive immunity are long-term effects of ischemia/reperfusion injury following syngenic kidney transplantation[J]. Kidney Int, 2012, 81(10):1015-1025. doi: 10.1038/ki.2011.458
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