红细胞衰亡及其在肝脏中的识别与清除机制
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摘要
红细胞衰亡(eryptosis)是指成熟红细胞在各种因素刺激下发生的自杀性程序性死亡,表现为膜内侧的磷脂酰丝氨酸(phosphatidylserine, PS)外翻、细胞皱缩体积变小以及细胞膜囊泡化等。衰亡红细胞由于PS外翻暴露而被巨噬细胞表面的PS受体识别,进而被吞噬并降解。肝脏是清除衰亡红细胞的主要器官,深入研究红细胞衰亡及其在肝脏中的识别与清除机制,有助于明确红细胞衰亡在肝脏疾病中的作用及病理生理学意义。
Erythrocytes undergo programmed cell death, similar to apoptosis, known as eryptosis. Eryptosis results from a wide variety of contributors and is characterized by phosphatidylserine(PS) exposure, cell shrinkage, and the presence of membrane blebbing. Erythrocytes with PS exposure are bound to and engulfed by macrophages in a PS-dependent manner. The liver as the primary organ supports rapid erythrocyte removal.Research on molecular mechanisms dictating eryptosis would help reveal the physiological and pathological significance of eryptosis in liver.
Erythrocytes undergo programmed cell death, similar to apoptosis, known as eryptosis. Eryptosis results from a wide variety of contributors and is characterized by phosphatidylserine(PS) exposure, cell shrinkage, and the presence of membrane blebbing. Erythrocytes with PS exposure are bound to and engulfed by macrophages in a PS-dependent manner. The liver as the primary organ supports rapid erythrocyte removal.Research on molecular mechanisms dictating eryptosis would help reveal the physiological and pathological significance of eryptosis in liver.
引文
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[35]GAO C,JI S,DONG W,et al.Indolic uremic solutes enhance procoagulant activity of red blood cells through phosphatidylserine exposure and microparticle release[J].Toxins,2015,7(11):4390-4403.
[36]STEFANOVA D,RAYCHEV A,AREZES J,et al.Endogenous hepcidin and its agonist mediate resistance to selected infections by clearing non-transferrin-bound iron[J].Blood,2017,130(3):245-257.
[37]TOSTI J,MANKELOW R E G,SARA T,et al.Autophagic vesicles on mature human reticulocytes explain phosphatidylserine-positive red cells in sickle cell disease[J].Blood,2015,126(15):1831-1834.
[38]TAKATSU H T M,NATIO T,TAKADA N,et al.Phospholipid flippase ATP11C is endocytosed and downregulated following Ca2+-mediated protein kinase C activation[J].Nature Communications,2017,8(1):1423-1437.
[2]THEURL I,HILGENDROF I,NAIRZ M,et al.On-demand erythrocyte disposal and iron recycling requires transient macrophages in the liver[J].Nature Medicine,2016,22(8):945-951.
[3]LANG E,GATIDIS S,FREISE N F,et al.Conjugated bilirubin triggers anemia by inducing erythrocyte death[J].Hepatology,2015,61(1):275-284.
[4]XIA S,CHEN G,WANG B,et al.Addition of sodium pyruvate to stored red blood cells attenuates liver injury in a murine transfusion model[J].Mediators of Inflammation,2016,2016:3549207.
[5]AUNG H H,TUNG J P,DEAN M M,et al.Procoagulant role of microparticles in routine storage of packed red blood cells:potential risk for prothrombotic post-transfusion complications[J].Pathology,2016,49(1):62-69.
[6]WESSELING M C,WAGNER-BRITZ L,HUPPERT H,et al.Phosphatidylserine exposure in human red blood cells depending on cell age[J].Cellular Physiology and Biochemistry,2016,38(4):1376-1390.
[7]GLASSMAN F Y,SCHNEIDER J L,RAMAKRISHNAN R,et al.Phosphatidylserine is not just a cleanup crew but also a wellmeaning teacher[J].Journal of Pharmaceutical Sciences,2018,107(8):2048-2054.
[8]WESSELING M C,WAGNER-BRITZ L,NGUYEN D B,et al.Novel insights in the regulation of phosphatidylserine exposure in human red blood cells[J].Cellular Physiology and Biochemistry,2016,39(5):1941-1954.
[9]ARASHIKI N T Y,MOHANDAS N,HALE J,et al.ATP11C is a major flippase in human erythrocytes and its defect causes congenital hemolytic anemia[J].Haematologica,2016,100(11):559-565.
[10]LI H,ZHANG Y,HA V,et al.Modeling of band-3 protein diffusion in the normal and defective red blood cell membrane[J].Soft Matter,2016,12(15):3643-3653.
[11]ARASHIKI N,KIMATA N,MANNO S,et al.Membrane peroxidation and methemoglobin formation are both necessary for band 3 clustering:mechanistic insights into human erythrocyte senescence[J].Biochemistry,2013,52(34):5760-5769.
[12]AUNG H H,TUNG J P,DEAN M M,et al.Procoagulant role of microparticles in routine storage of packed red blood cells:potential risk for prothrombotic post-transfusion complications[J].Pathology,2016,49(1):62-69.
[13]LEAL J K F,ADJOBO-HERMANS M J W,BOSMAN G J C GM.Red blood cell homeostasis:mechanisms and effects of microvesicle generation in health and disease[J].Frontiers in Physiology,2018,9:703.
[14]YANG C,GAO S,DAGNAES-HANSEN F,et al.Impact of PEG chain length on the physical properties and bioactivity of PEGylated chitosan/siRNA nanoparticles in vitro and in vivo[J].ACS Applied Materials&Interfaces,2017,9(14):12203-12206.
[15]TANG Q,GUO W,ZHENG L,et al.Structure of the receptoractivated human TRPC6 and TRPC3 ion channels[J].Cell Research,2018,28(7):746-755.
[16]ZIPSER Y,PIADE A,BARBUL A,et al.Ca2+promotes erythrocyte band 3 tyrosine phosphorylation via dissociation of phosphotyrosine phosphatase from band 3[J].Biochemical Journal,2002,368(1):137-144.
[17]WAGNER-BRITZ L,WANG J,KAESTNER L,et al.Protein kinase C alpha and P-type Ca2+channel Cav2.1 in red blood cell calcium signalling[J].Cellular Physiology and Biochemistry,2013,31(6):883-891.
[18]MA CZAKA,CYRKLER M,BUKOWSKA B,et al.Eryptosisinducing activity of bisphenol A and its analogs in human red blood cells(in vitro study)[J].Journal of Hazardous Materials,2016,307:328-335.
[19]LW,XU J,WANG X,et al.Bioengineered boronic ester modified dextran polymer nanoparticles as reactive oxygen species responsive nanocarrier for ischemic stroke treatment[J].ACSNano,2018,12(6):5417-5426.
[20]MANDAL D,MAZUMDER A,DAS P,et al.Fas-,caspase 8-,and caspase 3-dependent signaling regulates the activity of the aminophospholipid translocase and phosphatidylserine externalization in human erythrocytes[J].The Journal of Biological Chemistry,2005,280(47):39460-39467.
[21]LANG E,BISSINGER R,GULBINS E,et al.Ceramide in the regulation of eryptosis,the suicidal erythrocyte death[J].Apoptosis,2015,20(5):758-767.C
[22]RIVERA A,JAROLIM P,BRUGNARA C.Modulation of Gardos channel activity by cytokines in sickle erythrocytes[J].Blood,2002,99(1):357-603.
[23]LEE S J,PARK S Y,JUNG M Y,et al.Mechanism for phosphatidylserine-dependent erythrophagocytosis in mouse liver[J].Blood,2018,117(19):5215-5223.
[24]EGAMI Y,KAWAI K,ARAKI N.RhoC regulates the actin remodeling required for phagosome formation during FcγR-mediated phagocytosis[J].Journal of Cell Science,2017,130(24):4168-4179.
[25]ALLHORN M,BRICENO J G,BAUDINO L,et al.The IgG-specific endoglycosidase EndoS inhibits both cellular and complement-mediated autoimmune hemolysis[J].Blood,2010,115(24):5080-5088.
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[27]WANG C Y,KNUTSON M D.Hepatocyte divalent metal-ion transporter-1 is dispensable for hepatic iron accumulation and non-transferrin-bound iron uptake in mice[J].Hepatology,2013,58(2):788-798.
[28]AYI K,LU Z Y,SERGHIDES L,et al.CD47-SIRPαinteractions regulate macrophage uptake of plasmodium falciparuminfected erythrocytes and clearance of malaria in vivo[J].Infection and Immunity,2016,84:2002-2011.
[29]TAKESHI N,IMAI Y.Capture of microparticles by bolus flow of red blood cells in capillaries[J].Scientific Reports,2017,7:5381.
[30]MUANGSOMBUT V,WITHATANUNG P,SRINON V,et al.Burkholderia pseudomallei evades Nramp1(Slc11a1)-and NA-DPH oxidase-mediated killing in macrophages and exhibits Nramp1-dependent virulence gene expression[J].Frontiers in Cellular and Infection Microbiology,2017,7:350.
[31]LI X,RHEE D K,MALHOTRA R,et al.Progesterone receptor membrane component-1 regulates hepcidin biosynthesis[J].The Journal of Clinical Investigation,2016,126(1):389-401.
[32]MITCHELL D K.Non-transferrin-bound iron transporters[J].Free Radical Biology and Medicine,2019,133(2019):101-111.
[33]WU T,WANF L,AN J,et al.Noninvasive imaging of stored red blood cell-transfusion aggravating sepsis-induced liver injury associated with increased activation of M1-polarized kupffer cells[J].Shock,2017,48(4):459-466.
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[35]GAO C,JI S,DONG W,et al.Indolic uremic solutes enhance procoagulant activity of red blood cells through phosphatidylserine exposure and microparticle release[J].Toxins,2015,7(11):4390-4403.
[36]STEFANOVA D,RAYCHEV A,AREZES J,et al.Endogenous hepcidin and its agonist mediate resistance to selected infections by clearing non-transferrin-bound iron[J].Blood,2017,130(3):245-257.
[37]TOSTI J,MANKELOW R E G,SARA T,et al.Autophagic vesicles on mature human reticulocytes explain phosphatidylserine-positive red cells in sickle cell disease[J].Blood,2015,126(15):1831-1834.
[38]TAKATSU H T M,NATIO T,TAKADA N,et al.Phospholipid flippase ATP11C is endocytosed and downregulated following Ca2+-mediated protein kinase C activation[J].Nature Communications,2017,8(1):1423-1437.