Patch-clamp analysis of the "new permeability pathways" in malaria-infected erythrocytes

被引:38
作者
Huber, SM [1 ]
Duranton, C [1 ]
Lang, F [1 ]
机构
[1] Univ Tubingen, Dept Physiol, D-72076 Tubingen, Germany
来源
INTERNATIONAL REVIEW OF CYTOLOGY - A SURVEY OF CELL BIOLOGY, VOL 246 | 2005年 / 246卷
关键词
whole-cell recording; ion channels; RBCs; Plasmodium falciparum;
D O I
10.1016/S0074-7696(05)46003-9
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The intraerythrocytic amplification of the malaria parasite Plasmodium falciparum induces new pathways of solute permeability in the host cell's membrane. These pathways play a pivotal role in parasite development by supplying the parasite with nutrients, disposing of the parasite's metabolic waste and organic osmolytes, and adapting the host's electrolyte composition to the parasite's needs. The "new permeability pathways" allow the fast electrogenic diffusion of ions and thus can be analyzed by patch-clamp single-channel or whole-cell recording. By employing these techniques, several ion-channel types with different electrophysiological profiles have been identified in P. falciparum-infected erythrocytes; they have also been identified in noninfected cells. This review discusses a possible contribution of these channels to the new permeability pathways on the one hand and their supposed functions in noninfected erythrocytes on the other.
引用
收藏
页码:59 / +
页数:77
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共 293 条
  • [1] Erythrocyte membrane ATP binding cassette (ABC) proteins: MRP1 and CFTR as well as CD39 (ecto-apyrase) involved in RBC ATP transport and elevated blood plasma ATP of cystic fibrosis
    Abraham, EH
    Sterling, KM
    Kim, RJ
    Salikhova, AY
    Huffman, HB
    Crockett, MA
    Johnston, N
    Parker, HW
    Boyle, WE
    Hartov, A
    Demidenko, E
    Efird, J
    Kahn, J
    Grubman, SA
    Jefferson, DM
    Robson, SC
    Thakar, JH
    Lorico, A
    Rappa, G
    Sartorelli, AC
    Okunieff, P
    [J]. BLOOD CELLS MOLECULES AND DISEASES, 2001, 27 (01) : 165 - 180
  • [2] CYTOSOLIC FREE CALCIUM IN PLASMODIUM-FALCIPARUM-INFECTED ERYTHROCYTES AND THE EFFECT OF VERAPAMIL - A CYTOFLUOROMETRIC STUDY
    ADOVELANDE, J
    BASTIDE, B
    DELEZE, J
    SCHREVEL, J
    [J]. EXPERIMENTAL PARASITOLOGY, 1993, 76 (03) : 247 - 258
  • [3] Plasmodium falciparum likely encodes the principal anion channel on infected human erythrocytes
    Alkhalil, A
    Cohn, JV
    Wagner, MA
    Cabrera, JS
    Rajapandi, T
    Desai, SA
    [J]. BLOOD, 2004, 104 (13) : 4279 - 4286
  • [4] HUMAN RED BLOOD CELLS - PROSTAGLANDIN-E2, EPINEPHRINE, AND ISOPROTERENOL ALTER DEFORMABILITY
    ALLEN, JE
    RASMUSSEN, H
    [J]. SCIENCE, 1971, 174 (4008) : 512 - +
  • [5] The membrane potential of the intraerythrocytic malaria parasite Plasmodium falciparum
    Allen, RJW
    Kirk, K
    [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 2004, 279 (12) : 11264 - 11272
  • [6] HEXOSE-MONOPHOSPHATE SHUNT ACTIVITY IN INTACT PLASMODIUM-FALCIPARUM-INFECTED ERYTHROCYTES AND IN FREE PARASITES
    ATAMNA, H
    PASCARMONA, G
    GINSBURG, H
    [J]. MOLECULAR AND BIOCHEMICAL PARASITOLOGY, 1994, 67 (01) : 79 - 89
  • [7] ORIGIN OF REACTIVE OXYGEN SPECIES IN ERYTHROCYTES INFECTED WITH PLASMODIUM-FALCIPARUM
    ATAMNA, H
    GINSBURG, H
    [J]. MOLECULAR AND BIOCHEMICAL PARASITOLOGY, 1993, 61 (02) : 231 - 241
  • [8] The malaria parasite supplies glutathione to its host cell -: Investigation of glutathione transport and metabolism in human erythrocytes infected with Plasmodium falciparum
    Atamna, H
    Ginsburg, H
    [J]. EUROPEAN JOURNAL OF BIOCHEMISTRY, 1997, 250 (03): : 670 - 679
  • [9] Enhanced phagocytosis of ring-parasitized mutant erythrocytes: a common mechanism that may explain protection against falciparum malaria in sickle trait and beta-thalassemia trait
    Ayi, K
    Turrini, F
    Piga, A
    Arese, P
    [J]. BLOOD, 2004, 104 (10) : 3364 - 3371
  • [10] Pharmacology of the human red cell voltage-dependent cation channel - Part 1. Activation by clotrimazole and analogues
    Barksmann, TL
    Kristensen, BI
    Christophersen, P
    Bennekou, P
    [J]. BLOOD CELLS MOLECULES AND DISEASES, 2004, 32 (03) : 384 - 388