Central nervous system-infiltrated immune cells induce calcium increase in astrocytes via astroglial purinergic signaling
Samo za registrovane korisnike
2020
Autori
Bijelic, Dunja D.Milicević, Katarina
Lazarević, Milica N.
Miljković, Đorđe
Bogdanović Pristov, Jelena
Savić, Danijela Z
Petković, Branka
Andjus, Pavle R.
Momcilović, Miljana
Nikolić, Ljiljana M.
Članak u časopisu (Objavljena verzija)
Metapodaci
Prikaz svih podataka o dokumentuApstrakt
Interaction between autoreactive immune cells and astroglia is an important part of the pathologic processes that fuel neurodegeneration in multiple sclerosis. In this inflammatory disease, immune cells enter into the central nervous system (CNS) and they spread through CNS parenchyma, but the impact of these autoreactive immune cells on the activity pattern of astrocytes has not been defined. By exploiting naive astrocytes in culture and CNS-infiltrated immune cells (CNS IICs) isolated from rat with experimental autoimmune encephalomyelitis (EAE), here we demonstrate previously unrecognized properties of immune cell-astrocyte interaction. We show that CNS IICs but not the peripheral immune cell application, evokes a rapid and vigorous intracellular Ca(2+)increase in astrocytes by promoting glial release of ATP. ATP propagated Ca(2+)elevation through glial purinergic P2X7 receptor activation by the hemichannel-dependent nucleotide release mechanism. Astrocyte Ca(2+)increase is specific...ally triggered by the autoreactive CD4(+)T-cell application and these two cell types exhibit close spatial interaction in EAE. Therefore, Ca(2+)signals may mediate a rapid astroglial response to the autoreactive immune cells in their local environment. This property of immune cell-astrocyte interaction may be important to consider in studies interrogating CNS autoimmune disease.
Ključne reči:
SCR_014235 / SCR_011323 / SCR_003210 / SCR_002798 / SCR_002285 / RRID / RGD_21409752 / RGD_21409748 / purinergic receptors / nervous system autoimmune disease / cell communication / calcium signaling / astrocytes / AB_2828023 / AB_2629482 / AB_2538778 / AB_2535792 / AB_2534102 / AB_2534013 / AB_2224402 / AB_162543 / AB_162542 / AB_10682518 / AB_1018856 / AB_10050580 / AB_10013382Izvor:
Journal of Neuroscience Research, 2020, 98, 11, 2317-2332Izdavač:
- Wiley, Hoboken
Finansiranje / projekti:
- Centre for Leadership Development
- Ministarstvo nauke, tehnološkog razvoja i inovacija Republike Srbije, institucionalno finansiranje - 200007 (Univerzitet u Beogradu, Institut za biološka istraživanja 'Siniša Stanković') (RS-MESTD-inst-2020-200007)
- Ministarstvo nauke, tehnološkog razvoja i inovacija Republike Srbije, institucionalno finansiranje - 200178 (Univerzitet u Beogradu, Biološki fakultet) (RS-MESTD-inst-2020-200178)
- Ministarstvo nauke, tehnološkog razvoja i inovacija Republike Srbije, institucionalno finansiranje - 200053 (Univerzitet u Beogradu, Institut za multidisciplinarna istraživanja) (RS-MESTD-inst-2020-200053)
DOI: 10.1002/jnr.24699
ISSN: 0360-4012
PubMed: 32799373
WoS: 000563900600001
Scopus: 2-s2.0-85089392101
Institucija/grupa
Institut za multidisciplinarna istraživanjaTY - JOUR AU - Bijelic, Dunja D. AU - Milicević, Katarina AU - Lazarević, Milica N. AU - Miljković, Đorđe AU - Bogdanović Pristov, Jelena AU - Savić, Danijela Z AU - Petković, Branka AU - Andjus, Pavle R. AU - Momcilović, Miljana AU - Nikolić, Ljiljana M. PY - 2020 UR - http://rimsi.imsi.bg.ac.rs/handle/123456789/1317 AB - Interaction between autoreactive immune cells and astroglia is an important part of the pathologic processes that fuel neurodegeneration in multiple sclerosis. In this inflammatory disease, immune cells enter into the central nervous system (CNS) and they spread through CNS parenchyma, but the impact of these autoreactive immune cells on the activity pattern of astrocytes has not been defined. By exploiting naive astrocytes in culture and CNS-infiltrated immune cells (CNS IICs) isolated from rat with experimental autoimmune encephalomyelitis (EAE), here we demonstrate previously unrecognized properties of immune cell-astrocyte interaction. We show that CNS IICs but not the peripheral immune cell application, evokes a rapid and vigorous intracellular Ca(2+)increase in astrocytes by promoting glial release of ATP. ATP propagated Ca(2+)elevation through glial purinergic P2X7 receptor activation by the hemichannel-dependent nucleotide release mechanism. Astrocyte Ca(2+)increase is specifically triggered by the autoreactive CD4(+)T-cell application and these two cell types exhibit close spatial interaction in EAE. Therefore, Ca(2+)signals may mediate a rapid astroglial response to the autoreactive immune cells in their local environment. This property of immune cell-astrocyte interaction may be important to consider in studies interrogating CNS autoimmune disease. PB - Wiley, Hoboken T2 - Journal of Neuroscience Research T1 - Central nervous system-infiltrated immune cells induce calcium increase in astrocytes via astroglial purinergic signaling EP - 2332 IS - 11 SP - 2317 VL - 98 DO - 10.1002/jnr.24699 ER -
@article{ author = "Bijelic, Dunja D. and Milicević, Katarina and Lazarević, Milica N. and Miljković, Đorđe and Bogdanović Pristov, Jelena and Savić, Danijela Z and Petković, Branka and Andjus, Pavle R. and Momcilović, Miljana and Nikolić, Ljiljana M.", year = "2020", abstract = "Interaction between autoreactive immune cells and astroglia is an important part of the pathologic processes that fuel neurodegeneration in multiple sclerosis. In this inflammatory disease, immune cells enter into the central nervous system (CNS) and they spread through CNS parenchyma, but the impact of these autoreactive immune cells on the activity pattern of astrocytes has not been defined. By exploiting naive astrocytes in culture and CNS-infiltrated immune cells (CNS IICs) isolated from rat with experimental autoimmune encephalomyelitis (EAE), here we demonstrate previously unrecognized properties of immune cell-astrocyte interaction. We show that CNS IICs but not the peripheral immune cell application, evokes a rapid and vigorous intracellular Ca(2+)increase in astrocytes by promoting glial release of ATP. ATP propagated Ca(2+)elevation through glial purinergic P2X7 receptor activation by the hemichannel-dependent nucleotide release mechanism. Astrocyte Ca(2+)increase is specifically triggered by the autoreactive CD4(+)T-cell application and these two cell types exhibit close spatial interaction in EAE. Therefore, Ca(2+)signals may mediate a rapid astroglial response to the autoreactive immune cells in their local environment. This property of immune cell-astrocyte interaction may be important to consider in studies interrogating CNS autoimmune disease.", publisher = "Wiley, Hoboken", journal = "Journal of Neuroscience Research", title = "Central nervous system-infiltrated immune cells induce calcium increase in astrocytes via astroglial purinergic signaling", pages = "2332-2317", number = "11", volume = "98", doi = "10.1002/jnr.24699" }
Bijelic, D. D., Milicević, K., Lazarević, M. N., Miljković, Đ., Bogdanović Pristov, J., Savić, D. Z., Petković, B., Andjus, P. R., Momcilović, M.,& Nikolić, L. M.. (2020). Central nervous system-infiltrated immune cells induce calcium increase in astrocytes via astroglial purinergic signaling. in Journal of Neuroscience Research Wiley, Hoboken., 98(11), 2317-2332. https://doi.org/10.1002/jnr.24699
Bijelic DD, Milicević K, Lazarević MN, Miljković Đ, Bogdanović Pristov J, Savić DZ, Petković B, Andjus PR, Momcilović M, Nikolić LM. Central nervous system-infiltrated immune cells induce calcium increase in astrocytes via astroglial purinergic signaling. in Journal of Neuroscience Research. 2020;98(11):2317-2332. doi:10.1002/jnr.24699 .
Bijelic, Dunja D., Milicević, Katarina, Lazarević, Milica N., Miljković, Đorđe, Bogdanović Pristov, Jelena, Savić, Danijela Z, Petković, Branka, Andjus, Pavle R., Momcilović, Miljana, Nikolić, Ljiljana M., "Central nervous system-infiltrated immune cells induce calcium increase in astrocytes via astroglial purinergic signaling" in Journal of Neuroscience Research, 98, no. 11 (2020):2317-2332, https://doi.org/10.1002/jnr.24699 . .