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PI(18:1/18:1) is a SCD1-derived lipokine that limits stress signaling

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PI(18:1/18:1) is a SCD1-derived lipokine that limits stress signaling. / Thürmer, Maria; Gollowitzer, André; Pein, Helmut; Neukirch, Konstantin; Gelmez, Elif; Waltl, Lorenz; Wielsch, Natalie; Winkler, René; Löser, Konstantin; Grander, Julia; Hotze, Madlen; Harder, Sönke; Döding, Annika; Meßner, Martina; Troisi, Fabiana; Ardelt, Maximilian; Schlüter, Hartmut; Pachmayr, Johanna; Gutiérrez-Gutiérrez, Óscar; Rudolph, Karl Lenhard; Thedieck, Kathrin; Schulze-Späte, Ulrike; González-Estévez, Cristina; Kosan, Christian; Svatoš, Aleš; Kwiatkowski, Marcel; Koeberle, Andreas.

In: NAT COMMUN, Vol. 13, No. 1, 2982, 27.05.2022.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Thürmer, M, Gollowitzer, A, Pein, H, Neukirch, K, Gelmez, E, Waltl, L, Wielsch, N, Winkler, R, Löser, K, Grander, J, Hotze, M, Harder, S, Döding, A, Meßner, M, Troisi, F, Ardelt, M, Schlüter, H, Pachmayr, J, Gutiérrez-Gutiérrez, Ó, Rudolph, KL, Thedieck, K, Schulze-Späte, U, González-Estévez, C, Kosan, C, Svatoš, A, Kwiatkowski, M & Koeberle, A 2022, 'PI(18:1/18:1) is a SCD1-derived lipokine that limits stress signaling', NAT COMMUN, vol. 13, no. 1, 2982. https://doi.org/10.1038/s41467-022-30374-9

APA

Thürmer, M., Gollowitzer, A., Pein, H., Neukirch, K., Gelmez, E., Waltl, L., Wielsch, N., Winkler, R., Löser, K., Grander, J., Hotze, M., Harder, S., Döding, A., Meßner, M., Troisi, F., Ardelt, M., Schlüter, H., Pachmayr, J., Gutiérrez-Gutiérrez, Ó., ... Koeberle, A. (2022). PI(18:1/18:1) is a SCD1-derived lipokine that limits stress signaling. NAT COMMUN, 13(1), [2982]. https://doi.org/10.1038/s41467-022-30374-9

Vancouver

Thürmer M, Gollowitzer A, Pein H, Neukirch K, Gelmez E, Waltl L et al. PI(18:1/18:1) is a SCD1-derived lipokine that limits stress signaling. NAT COMMUN. 2022 May 27;13(1). 2982. https://doi.org/10.1038/s41467-022-30374-9

Bibtex

@article{ffe99322230e48159a8313be465467b1,
title = "PI(18:1/18:1) is a SCD1-derived lipokine that limits stress signaling",
abstract = "Cytotoxic stress activates stress-activated kinases, initiates adaptive mechanisms, including the unfolded protein response (UPR) and autophagy, and induces programmed cell death. Fatty acid unsaturation, controlled by stearoyl-CoA desaturase (SCD)1, prevents cytotoxic stress but the mechanisms are diffuse. Here, we show that 1,2-dioleoyl-sn-glycero-3-phospho-(1'-myo-inositol) [PI(18:1/18:1)] is a SCD1-derived signaling lipid, which inhibits p38 mitogen-activated protein kinase activation, counteracts UPR, endoplasmic reticulum-associated protein degradation, and apoptosis, regulates autophagy, and maintains cell morphology and proliferation. SCD1 expression and the cellular PI(18:1/18:1) proportion decrease during the onset of cell death, thereby repressing protein phosphatase 2 A and enhancing stress signaling. This counter-regulation applies to mechanistically diverse death-inducing conditions and is found in multiple human and mouse cell lines and tissues of Scd1-defective mice. PI(18:1/18:1) ratios reflect stress tolerance in tumorigenesis, chemoresistance, infection, high-fat diet, and immune aging. Together, PI(18:1/18:1) is a lipokine that links fatty acid unsaturation with stress responses, and its depletion evokes stress signaling.",
keywords = "Animals, Apoptosis, Fatty Acids, Mice, Signal Transduction, Stearoyl-CoA Desaturase/genetics, Unfolded Protein Response",
author = "Maria Th{\"u}rmer and Andr{\'e} Gollowitzer and Helmut Pein and Konstantin Neukirch and Elif Gelmez and Lorenz Waltl and Natalie Wielsch and Ren{\'e} Winkler and Konstantin L{\"o}ser and Julia Grander and Madlen Hotze and S{\"o}nke Harder and Annika D{\"o}ding and Martina Me{\ss}ner and Fabiana Troisi and Maximilian Ardelt and Hartmut Schl{\"u}ter and Johanna Pachmayr and {\'O}scar Guti{\'e}rrez-Guti{\'e}rrez and Rudolph, {Karl Lenhard} and Kathrin Thedieck and Ulrike Schulze-Sp{\"a}te and Cristina Gonz{\'a}lez-Est{\'e}vez and Christian Kosan and Ale{\v s} Svato{\v s} and Marcel Kwiatkowski and Andreas Koeberle",
note = "{\textcopyright} 2022. The Author(s).",
year = "2022",
month = may,
day = "27",
doi = "10.1038/s41467-022-30374-9",
language = "English",
volume = "13",
journal = "NAT COMMUN",
issn = "2041-1723",
publisher = "NATURE PUBLISHING GROUP",
number = "1",

}

RIS

TY - JOUR

T1 - PI(18:1/18:1) is a SCD1-derived lipokine that limits stress signaling

AU - Thürmer, Maria

AU - Gollowitzer, André

AU - Pein, Helmut

AU - Neukirch, Konstantin

AU - Gelmez, Elif

AU - Waltl, Lorenz

AU - Wielsch, Natalie

AU - Winkler, René

AU - Löser, Konstantin

AU - Grander, Julia

AU - Hotze, Madlen

AU - Harder, Sönke

AU - Döding, Annika

AU - Meßner, Martina

AU - Troisi, Fabiana

AU - Ardelt, Maximilian

AU - Schlüter, Hartmut

AU - Pachmayr, Johanna

AU - Gutiérrez-Gutiérrez, Óscar

AU - Rudolph, Karl Lenhard

AU - Thedieck, Kathrin

AU - Schulze-Späte, Ulrike

AU - González-Estévez, Cristina

AU - Kosan, Christian

AU - Svatoš, Aleš

AU - Kwiatkowski, Marcel

AU - Koeberle, Andreas

N1 - © 2022. The Author(s).

PY - 2022/5/27

Y1 - 2022/5/27

N2 - Cytotoxic stress activates stress-activated kinases, initiates adaptive mechanisms, including the unfolded protein response (UPR) and autophagy, and induces programmed cell death. Fatty acid unsaturation, controlled by stearoyl-CoA desaturase (SCD)1, prevents cytotoxic stress but the mechanisms are diffuse. Here, we show that 1,2-dioleoyl-sn-glycero-3-phospho-(1'-myo-inositol) [PI(18:1/18:1)] is a SCD1-derived signaling lipid, which inhibits p38 mitogen-activated protein kinase activation, counteracts UPR, endoplasmic reticulum-associated protein degradation, and apoptosis, regulates autophagy, and maintains cell morphology and proliferation. SCD1 expression and the cellular PI(18:1/18:1) proportion decrease during the onset of cell death, thereby repressing protein phosphatase 2 A and enhancing stress signaling. This counter-regulation applies to mechanistically diverse death-inducing conditions and is found in multiple human and mouse cell lines and tissues of Scd1-defective mice. PI(18:1/18:1) ratios reflect stress tolerance in tumorigenesis, chemoresistance, infection, high-fat diet, and immune aging. Together, PI(18:1/18:1) is a lipokine that links fatty acid unsaturation with stress responses, and its depletion evokes stress signaling.

AB - Cytotoxic stress activates stress-activated kinases, initiates adaptive mechanisms, including the unfolded protein response (UPR) and autophagy, and induces programmed cell death. Fatty acid unsaturation, controlled by stearoyl-CoA desaturase (SCD)1, prevents cytotoxic stress but the mechanisms are diffuse. Here, we show that 1,2-dioleoyl-sn-glycero-3-phospho-(1'-myo-inositol) [PI(18:1/18:1)] is a SCD1-derived signaling lipid, which inhibits p38 mitogen-activated protein kinase activation, counteracts UPR, endoplasmic reticulum-associated protein degradation, and apoptosis, regulates autophagy, and maintains cell morphology and proliferation. SCD1 expression and the cellular PI(18:1/18:1) proportion decrease during the onset of cell death, thereby repressing protein phosphatase 2 A and enhancing stress signaling. This counter-regulation applies to mechanistically diverse death-inducing conditions and is found in multiple human and mouse cell lines and tissues of Scd1-defective mice. PI(18:1/18:1) ratios reflect stress tolerance in tumorigenesis, chemoresistance, infection, high-fat diet, and immune aging. Together, PI(18:1/18:1) is a lipokine that links fatty acid unsaturation with stress responses, and its depletion evokes stress signaling.

KW - Animals

KW - Apoptosis

KW - Fatty Acids

KW - Mice

KW - Signal Transduction

KW - Stearoyl-CoA Desaturase/genetics

KW - Unfolded Protein Response

U2 - 10.1038/s41467-022-30374-9

DO - 10.1038/s41467-022-30374-9

M3 - SCORING: Journal article

C2 - 35624087

VL - 13

JO - NAT COMMUN

JF - NAT COMMUN

SN - 2041-1723

IS - 1

M1 - 2982

ER -