Enhanced Membrane Fluidization and Cholesterol Displacement by 1-Heptanol Inhibit Mast Cell Effector Functions

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68378050%3A_____%2F23%3A00575881" target="_blank" >RIV/68378050:_____/23:00575881 - isvavai.cz</a>

Výsledek na webu

<a href="https://www.mdpi.com/2073-4409/12/16/2069" target="_blank" >https://www.mdpi.com/2073-4409/12/16/2069</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.3390/cells12162069" target="_blank" >10.3390/cells12162069</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Enhanced Membrane Fluidization and Cholesterol Displacement by 1-Heptanol Inhibit Mast Cell Effector Functions

Popis výsledku v původním jazyce

Signal transduction by the high-affinity IgE receptor (Fc epsilon RI) depends on membrane lipid and protein compartmentalization. Recently published data show that cells treated with 1-heptanol, a cell membrane fluidizer, exhibit changes in membrane properties. However, the functional consequences of 1-heptanol-induced changes on mast cell signaling are unknown. This study shows that short-term exposure to 1-heptanol reduces membrane thermal stability and dysregulates mast cell signaling at multiple levels. Cells treated with 1-heptanol exhibited increased lateral mobility and decreased internalization of the Fc epsilon RI. However, this did not affect the initial phosphorylation of the Fc epsilon RI-beta chain and components of the SYK/LAT1/PLC gamma 1 signaling pathway after antigen activation. In contrast, 1-heptanol inhibited SAPK/JNK phosphorylation and effector functions such as calcium response, degranulation, and cytokine production. Membrane hyperfluidization induced a heat shock-like response via increased expression of the heat shock protein 70, increased lateral diffusion of ORAI1-mCherry, and unsatisfactory performance of STIM1-ORAI1 coupling, as determined by flow-FRET. Furthermore, 1-heptanol inhibited the antigen-induced production of reactive oxygen species and potentiated stress-induced plasma membrane permeability by interfering with heat shock protein 70 activity. The combined data suggest that 1-heptanol-mediated membrane fluidization does not interfere with the earliest biochemical steps of Fc epsilon RI signaling, such as phosphorylation of the Fc epsilon RI-beta chain and components of the SYK/LAT/PLC gamma 1 signaling pathway, instead inhibiting the Fc epsilon RI internalization and mast cell effector functions, including degranulation and cytokine production.

Název v anglickém jazyce

Enhanced Membrane Fluidization and Cholesterol Displacement by 1-Heptanol Inhibit Mast Cell Effector Functions

Popis výsledku anglicky

Signal transduction by the high-affinity IgE receptor (Fc epsilon RI) depends on membrane lipid and protein compartmentalization. Recently published data show that cells treated with 1-heptanol, a cell membrane fluidizer, exhibit changes in membrane properties. However, the functional consequences of 1-heptanol-induced changes on mast cell signaling are unknown. This study shows that short-term exposure to 1-heptanol reduces membrane thermal stability and dysregulates mast cell signaling at multiple levels. Cells treated with 1-heptanol exhibited increased lateral mobility and decreased internalization of the Fc epsilon RI. However, this did not affect the initial phosphorylation of the Fc epsilon RI-beta chain and components of the SYK/LAT1/PLC gamma 1 signaling pathway after antigen activation. In contrast, 1-heptanol inhibited SAPK/JNK phosphorylation and effector functions such as calcium response, degranulation, and cytokine production. Membrane hyperfluidization induced a heat shock-like response via increased expression of the heat shock protein 70, increased lateral diffusion of ORAI1-mCherry, and unsatisfactory performance of STIM1-ORAI1 coupling, as determined by flow-FRET. Furthermore, 1-heptanol inhibited the antigen-induced production of reactive oxygen species and potentiated stress-induced plasma membrane permeability by interfering with heat shock protein 70 activity. The combined data suggest that 1-heptanol-mediated membrane fluidization does not interfere with the earliest biochemical steps of Fc epsilon RI signaling, such as phosphorylation of the Fc epsilon RI-beta chain and components of the SYK/LAT/PLC gamma 1 signaling pathway, instead inhibiting the Fc epsilon RI internalization and mast cell effector functions, including degranulation and cytokine production.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

10601 - Cell biology

Projekt

Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2023

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Cells

ISSN

2073-4409

e-ISSN

2073-4409

Svazek periodika

12

Číslo periodika v rámci svazku

16

Stát vydavatele periodika

CH - Švýcarská konfederace

Počet stran výsledku

31

Strana od-do

2069

Kód UT WoS článku

001055284800001

EID výsledku v databázi Scopus

2-s2.0-85169090698