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Calcium channel β3 subunit regulates ATP-dependent migration of dendritic cells

Standard

Calcium channel β3 subunit regulates ATP-dependent migration of dendritic cells. / Woo, Marcel S; Ufer, Friederike; Sonner, Jana K; Belkacemi, Anouar; Tintelnot, Joseph; Sáez, Pablo J; Krieg, Paula F; Mayer, Christina; Binkle-Ladisch, Lars; Engler, Jan Broder; Bauer, Simone; Kursawe, Nina; Vieira, Vanessa; Mannebach, Stefanie; Freichel, Marc; Flockerzi, Veit; Vargas, Pablo; Friese, Manuel A.

in: SCI ADV, Jahrgang 9, Nr. 38, eadh1653, 22.09.2023.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Woo, MS, Ufer, F, Sonner, JK, Belkacemi, A, Tintelnot, J, Sáez, PJ, Krieg, PF, Mayer, C, Binkle-Ladisch, L, Engler, JB, Bauer, S, Kursawe, N, Vieira, V, Mannebach, S, Freichel, M, Flockerzi, V, Vargas, P & Friese, MA 2023, 'Calcium channel β3 subunit regulates ATP-dependent migration of dendritic cells', SCI ADV, Jg. 9, Nr. 38, eadh1653. https://doi.org/10.1126/sciadv.adh1653

APA

Woo, M. S., Ufer, F., Sonner, J. K., Belkacemi, A., Tintelnot, J., Sáez, P. J., Krieg, P. F., Mayer, C., Binkle-Ladisch, L., Engler, J. B., Bauer, S., Kursawe, N., Vieira, V., Mannebach, S., Freichel, M., Flockerzi, V., Vargas, P., & Friese, M. A. (2023). Calcium channel β3 subunit regulates ATP-dependent migration of dendritic cells. SCI ADV, 9(38), [eadh1653]. https://doi.org/10.1126/sciadv.adh1653

Vancouver

Woo MS, Ufer F, Sonner JK, Belkacemi A, Tintelnot J, Sáez PJ et al. Calcium channel β3 subunit regulates ATP-dependent migration of dendritic cells. SCI ADV. 2023 Sep 22;9(38). eadh1653. https://doi.org/10.1126/sciadv.adh1653

Bibtex

@article{f6c0399fa12d478ea8a0aa97d9fd188c,
title = "Calcium channel β3 subunit regulates ATP-dependent migration of dendritic cells",
abstract = "Migratory dendritic cells (migDCs) continuously patrol tissues and are activated by injury and inflammation. Extracellular adenosine triphosphate (ATP) is released by damaged cells or actively secreted during inflammation and increases migDC motility. However, the underlying molecular mechanisms by which ATP accelerates migDC migration is not understood. Here, we show that migDCs can be distinguished from other DC subsets and immune cells by their expression of the voltage-gated calcium channel subunit β3 (Cavβ3; CACNB3), which exclusively facilitates ATP-dependent migration in vitro and during tissue damage in vivo. By contrast, CACNB3 does not regulate lipopolysaccharide-dependent migration. Mechanistically, CACNB3 regulates ATP-dependent inositol 1,4,5-trisphophate receptor-controlled calcium release from the endoplasmic reticulum. This, in turn, is required for ATP-mediated suppression of adhesion molecules, their detachment, and initiation of migDC migration. Thus, Cacnb3-deficient migDCs have an impaired migration after ATP exposure. In summary, we identified CACNB3 as a master regulator of ATP-dependent migDC migration that controls tissue-specific immunological responses during injury and inflammation.",
author = "Woo, {Marcel S} and Friederike Ufer and Sonner, {Jana K} and Anouar Belkacemi and Joseph Tintelnot and S{\'a}ez, {Pablo J} and Krieg, {Paula F} and Christina Mayer and Lars Binkle-Ladisch and Engler, {Jan Broder} and Simone Bauer and Nina Kursawe and Vanessa Vieira and Stefanie Mannebach and Marc Freichel and Veit Flockerzi and Pablo Vargas and Friese, {Manuel A}",
year = "2023",
month = sep,
day = "22",
doi = "10.1126/sciadv.adh1653",
language = "English",
volume = "9",
journal = "SCI ADV",
issn = "2375-2548",
publisher = "American Association for the Advancement of Science",
number = "38",

}

RIS

TY - JOUR

T1 - Calcium channel β3 subunit regulates ATP-dependent migration of dendritic cells

AU - Woo, Marcel S

AU - Ufer, Friederike

AU - Sonner, Jana K

AU - Belkacemi, Anouar

AU - Tintelnot, Joseph

AU - Sáez, Pablo J

AU - Krieg, Paula F

AU - Mayer, Christina

AU - Binkle-Ladisch, Lars

AU - Engler, Jan Broder

AU - Bauer, Simone

AU - Kursawe, Nina

AU - Vieira, Vanessa

AU - Mannebach, Stefanie

AU - Freichel, Marc

AU - Flockerzi, Veit

AU - Vargas, Pablo

AU - Friese, Manuel A

PY - 2023/9/22

Y1 - 2023/9/22

N2 - Migratory dendritic cells (migDCs) continuously patrol tissues and are activated by injury and inflammation. Extracellular adenosine triphosphate (ATP) is released by damaged cells or actively secreted during inflammation and increases migDC motility. However, the underlying molecular mechanisms by which ATP accelerates migDC migration is not understood. Here, we show that migDCs can be distinguished from other DC subsets and immune cells by their expression of the voltage-gated calcium channel subunit β3 (Cavβ3; CACNB3), which exclusively facilitates ATP-dependent migration in vitro and during tissue damage in vivo. By contrast, CACNB3 does not regulate lipopolysaccharide-dependent migration. Mechanistically, CACNB3 regulates ATP-dependent inositol 1,4,5-trisphophate receptor-controlled calcium release from the endoplasmic reticulum. This, in turn, is required for ATP-mediated suppression of adhesion molecules, their detachment, and initiation of migDC migration. Thus, Cacnb3-deficient migDCs have an impaired migration after ATP exposure. In summary, we identified CACNB3 as a master regulator of ATP-dependent migDC migration that controls tissue-specific immunological responses during injury and inflammation.

AB - Migratory dendritic cells (migDCs) continuously patrol tissues and are activated by injury and inflammation. Extracellular adenosine triphosphate (ATP) is released by damaged cells or actively secreted during inflammation and increases migDC motility. However, the underlying molecular mechanisms by which ATP accelerates migDC migration is not understood. Here, we show that migDCs can be distinguished from other DC subsets and immune cells by their expression of the voltage-gated calcium channel subunit β3 (Cavβ3; CACNB3), which exclusively facilitates ATP-dependent migration in vitro and during tissue damage in vivo. By contrast, CACNB3 does not regulate lipopolysaccharide-dependent migration. Mechanistically, CACNB3 regulates ATP-dependent inositol 1,4,5-trisphophate receptor-controlled calcium release from the endoplasmic reticulum. This, in turn, is required for ATP-mediated suppression of adhesion molecules, their detachment, and initiation of migDC migration. Thus, Cacnb3-deficient migDCs have an impaired migration after ATP exposure. In summary, we identified CACNB3 as a master regulator of ATP-dependent migDC migration that controls tissue-specific immunological responses during injury and inflammation.

U2 - 10.1126/sciadv.adh1653

DO - 10.1126/sciadv.adh1653

M3 - SCORING: Journal article

C2 - 37729408

VL - 9

JO - SCI ADV

JF - SCI ADV

SN - 2375-2548

IS - 38

M1 - eadh1653

ER -