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Article ; Online: Increased Activation of Innate Immunity and Pro-Apoptotic CXCR3B in Normal-Appearing Skin on the Lesional Site of Patients with Segmental Vitiligo.

Passeron, Thierry / Malmqvst, Valentina E A / Bzioueche, Hanene / Marchetti, Sandrine / Rocchi, Stephane / Tulic, Meri K

The Journal of investigative dermatology

2021 Volume 142, Issue 2, Page(s) 480–483.e2

MeSH term(s)	Adult ; Apoptosis/immunology ; Biopsy ; Case-Control Studies ; Disease Progression ; Female ; Healthy Volunteers ; Humans ; Immunity, Innate ; Male ; Melanocytes/immunology ; Melanocytes/pathology ; Middle Aged ; Receptors, CXCR3/metabolism ; Skin/immunology ; Skin/metabolism ; Skin/pathology ; Vitiligo/immunology ; Vitiligo/pathology ; Young Adult
Chemical Substances	CXCR3 protein, human ; Receptors, CXCR3
Language	English
Publishing date	2021-07-31
Publishing country	United States
Document type	Letter ; Observational Study
ZDB-ID	80136-7
ISSN	1523-1747 ; 0022-202X
ISSN (online)	1523-1747
ISSN	0022-202X
DOI	10.1016/j.jid.2021.07.157
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Article ; Online: No Parkin Zone: Mitophagy without Parkin.

Villa, Elodie / Marchetti, Sandrine / Ricci, Jean-Ehrland

Trends in cell biology

2018 Volume 28, Issue 11, Page(s) 882–895

Abstract: Mitochondria are essential highly dynamic organelles that provide the necessary energy for a variety of different processes, such as survival, proliferation, and migration. In order to maintain an intact mitochondrial network, cells have developed ... ...

Abstract	Mitochondria are essential highly dynamic organelles that provide the necessary energy for a variety of different processes, such as survival, proliferation, and migration. In order to maintain an intact mitochondrial network, cells have developed quality control systems that allow the removal of damaged or superfluous mitochondria by selective mitochondrial autophagy called mitophagy. Although the parkin/PINK1 axis is often considered the main regulator of mitophagy, a growing body of evidence has shown that this pathway is not unique and that mitophagy can still be functional in the absence of parkin. Here, we will review recent literature describing parkin-independent mitophagy and its role in various physiopathological conditions, therefore representing potential new targets to treat diseases affected by dysregulated mitophagy.
MeSH term(s)	Animals ; Humans ; Mitochondria/metabolism ; Mitochondrial Degradation ; Ubiquitin-Protein Ligases/deficiency ; Ubiquitin-Protein Ligases/metabolism
Chemical Substances	Ubiquitin-Protein Ligases (EC 2.3.2.27) ; parkin protein (EC 2.3.2.27)
Language	English
Publishing date	2018-08-13
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	30122-x
ISSN	1879-3088 ; 0962-8924
ISSN (online)	1879-3088
ISSN	0962-8924
DOI	10.1016/j.tcb.2018.07.004
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Article ; Online: Impact of house dust mite in vitiligo skin: environmental contribution to increased cutaneous immunity and melanocyte detachment.

Bzioueche, Hanene / Boniface, Katia / Drullion, Claire / Marchetti, Sandrine / Chignon-Sicard, Bérengère / Sormani, Laura / Rocchi, Stéphane / Seneschal, Julien / Passeron, Thierry / Tulic, Meri K

The British journal of dermatology

2023 Volume 189, Issue 3, Page(s) 312–327

Abstract: Background: Vitiligo is an autoimmune skin disorder characterized by loss of melanocytes. Protease-mediated disruption of junctions between keratinocytes and/or keratinocyte intrinsic dysfunction may directly contribute to melanocyte loss. House dust ... ...

Abstract	Background: Vitiligo is an autoimmune skin disorder characterized by loss of melanocytes. Protease-mediated disruption of junctions between keratinocytes and/or keratinocyte intrinsic dysfunction may directly contribute to melanocyte loss. House dust mite (HDM), an environmental allergen with potent protease activity, contributes to respiratory and gut disease but also to atopic dermatitis and rosacea. Objectives: To verify if HDM can contribute to melanocyte detachment in vitiligo and if so, by which mechanism(s). Methods: Using primary human keratinocytes, human skin biopsies from healthy donors and patients with vitiligo, and 3D reconstructed human epidermis, we studied the effect of HDM on cutaneous immunity, tight and adherent junction expression and melanocyte detachment. Results: HDM increased keratinocyte production of vitiligo-associated cytokines and chemokines and increased expression of toll-like receptor (TLR)-4. This was associated with increased in situ matrix-metalloproteinase (MMP)-9 activity, reduced cutaneous expression of adherent protein E-cadherin, increased soluble E-cadherin in culture supernatant and significantly increased number of suprabasal melanocytes in the skin. This effect was dose-dependent and driven by cysteine protease Der p1 and MMP-9. Selective MMP-9 inhibitor, Ab142180, restored E-cadherin expression and inhibited HDM-induced melanocyte detachment. Keratinocytes from patients with vitiligo were more sensitive to HDM-induced changes than healthy keratinocytes. All results were confirmed in a 3D model of healthy skin and in human skin biopsies. Conclusions: Our results highlight that environmental mite may act as an external source of pathogen-associated molecular pattern molecules in vitiligo and topical MMP-9 inhibitors may be useful therapeutic targets. Whether HDM contributes to the onset of flares in vitiligo remains to be tested in carefully controlled trials.
MeSH term(s)	Animals ; Humans ; Vitiligo/metabolism ; Matrix Metalloproteinase 9/metabolism ; Matrix Metalloproteinase 9/pharmacology ; Pyroglyphidae ; Melanocytes/metabolism ; Keratinocytes/metabolism ; Cadherins/metabolism
Chemical Substances	Matrix Metalloproteinase 9 (EC 3.4.24.35) ; Cadherins
Language	English
Publishing date	2023-05-04
Publishing country	England
Document type	Journal Article
ZDB-ID	80076-4
ISSN	1365-2133 ; 0007-0963
ISSN (online)	1365-2133
ISSN	0007-0963
DOI	10.1093/bjd/ljad148
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Article: Pharmacological preconditioning protects from ischemia/reperfusion‐induced apoptosis by modulating Bcl‐xL expression through a ROS‐dependent mechanism

Rozier, Romain / Paul, Rachel / Madji Hounoum, Blandine / Villa, Elodie / Mhaidly, Rana / Chiche, Johanna / Verhoeyen, Els / Marchetti, Sandrine / Vandenberghe, Ashaina / Raucoules, Marc / Carles, Michel / Ricci, Jean‐Ehrland

FEBS journal. 2021 June, v. 288, no. 11

2021

Abstract: Myocardial ischemia/reperfusion (I/R) injury is a frequent perioperative threat, with numerous strategies developed to limit and/or prevent it. One interesting axis of research is the anesthetic preconditioning (APc) agent’s hypothesis (such as ... ...

Abstract	Myocardial ischemia/reperfusion (I/R) injury is a frequent perioperative threat, with numerous strategies developed to limit and/or prevent it. One interesting axis of research is the anesthetic preconditioning (APc) agent’s hypothesis (such as sevoflurane, SEV). However, APc’s mode of action is still poorly understood and volatile anesthetics used as preconditioning agents are often not well suited in clinical practice. Here, in vitro using H9C2 cells lines (in myeloblast state or differentiated toward cardiomyocytes) and in vivo in mice, we identified that SEV‐induced APc is mediated by a mild induction of reactive oxygen species (ROS) that activates Akt and induces the expression of the anti‐apoptotic protein B‐cell lymphoma‐extra large (Bcl‐xL), therefore protecting cardiomyocytes from I/R‐induced death. Furthermore, we extended these results to human cardiomyocytes (derived from induced pluripotent stem ‐ IPS ‐ cells). Importantly, we demonstrated that this protective signaling pathway induced by SEV could be stimulated using the antidiabetic agent metformin (MET), suggesting the preconditioning properties of MET. Altogether, our study identified a signaling pathway allowing APc of cardiac injuries as well as a rational for the use of MET as a pharmacological preconditioning agent to prevent I/R injuries.
Keywords	B-lymphocytes ; apoptosis ; cardiomyocytes ; death ; humans ; mechanism of action ; metformin ; myocardial ischemia ; pro-apoptotic proteins ; reactive oxygen species ; sevoflurane
Language	English
Dates of publication	2021-06
Size	p. 3547-3569.
Publishing place	John Wiley & Sons, Ltd
Document type	Article
Note	NAL-AP-2-clean ; JOURNAL ARTICLE
ZDB-ID	2173655-8
ISSN	1742-4658 ; 1742-464X
ISSN (online)	1742-4658
ISSN	1742-464X
DOI	10.1111/febs.15675
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Tumoral microenvironment prevents de novo asparagine biosynthesis in B cell lymphoma, regardless of ASNS expression.

Grima-Reyes, Manuel / Vandenberghe, Ashaina / Nemazanyy, Ivan / Meola, Pauline / Paul, Rachel / Reverso-Meinietti, Julie / Martinez-Turtos, Adriana / Nottet, Nicolas / Chan, Wai-Kin / Lorenzi, Philip L / Marchetti, Sandrine / Ricci, Jean-Ehrland / Chiche, Johanna

Science advances

2022 Volume 8, Issue 27, Page(s) eabn6491

Abstract: Depletion of circulating asparagine with l-asparaginase (ASNase) is a mainstay of leukemia treatment and is under investigation in many cancers. Expression levels of asparagine synthetase (ASNS), which catalyzes asparagine synthesis, were considered ... ...

Abstract	Depletion of circulating asparagine with l-asparaginase (ASNase) is a mainstay of leukemia treatment and is under investigation in many cancers. Expression levels of asparagine synthetase (ASNS), which catalyzes asparagine synthesis, were considered predictive of cancer cell sensitivity to ASNase treatment, a notion recently challenged. Using [U-
MeSH term(s)	Animals ; Antineoplastic Agents/therapeutic use ; Asparaginase/therapeutic use ; Asparagine/metabolism ; Aspartate-Ammonia Ligase/genetics ; Aspartate-Ammonia Ligase/metabolism ; Cell Line, Tumor ; Glutaminase/therapeutic use ; Lymphoma, B-Cell/drug therapy ; Mice ; Precursor Cell Lymphoblastic Leukemia-Lymphoma ; Tumor Microenvironment
Chemical Substances	Antineoplastic Agents ; Asparagine (7006-34-0) ; Asparaginase (EC 3.5.1.1) ; Glutaminase (EC 3.5.1.2) ; Aspartate-Ammonia Ligase (EC 6.3.1.1)
Language	English
Publishing date	2022-07-06
Publishing country	United States
Document type	Journal Article
ZDB-ID	2810933-8
ISSN	2375-2548 ; 2375-2548
ISSN (online)	2375-2548
ISSN	2375-2548
DOI	10.1126/sciadv.abn6491
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Article ; Online: IRE1α overexpression in malignant cells limits tumor progression by inducing an anti-cancer immune response.

Martinez-Turtos, Adriana / Paul, Rachel / Grima-Reyes, Manuel / Issaoui, Hussein / Krug, Adrien / Mhaidly, Rana / Bossowski, Jozef P / Chiche, Johanna / Marchetti, Sandrine / Verhoeyen, Els / Chevet, Eric / Ricci, Jean-Ehrland

Oncoimmunology

2022 Volume 11, Issue 1, Page(s) 2116844

Abstract: IRE1α is one of the three ER transmembrane transducers of the Unfolded Protein Response (UPR) activated under endoplasmic reticulum (ER) stress. IRE1α activation has a dual role in cancer as it may be either pro- or anti-tumoral depending on the studied ... ...

Abstract	IRE1α is one of the three ER transmembrane transducers of the Unfolded Protein Response (UPR) activated under endoplasmic reticulum (ER) stress. IRE1α activation has a dual role in cancer as it may be either pro- or anti-tumoral depending on the studied models. Here, we describe the discovery that exogenous expression of IRE1α, resulting in IRE1α auto-activation, did not affect cancer cell proliferation
MeSH term(s)	Animals ; Endoribonucleases/genetics ; Endoribonucleases/metabolism ; Immunity ; Mice ; Neoplasms ; Neoplastic Processes ; Protein Serine-Threonine Kinases/genetics ; Signal Transduction ; X-Box Binding Protein 1/genetics ; X-Box Binding Protein 1/metabolism
Chemical Substances	X-Box Binding Protein 1 ; Protein Serine-Threonine Kinases (EC 2.7.11.1) ; Endoribonucleases (EC 3.1.-)
Language	English
Publishing date	2022-08-27
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2645309-5
ISSN	2162-402X ; 2162-4011
ISSN (online)	2162-402X
ISSN	2162-4011
DOI	10.1080/2162402X.2022.2116844
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Article: The prohibitin-binding compound fluorizoline inhibits mitophagy in cancer cells.

Núñez-Vázquez, Sonia / Saura-Esteller, José / Sánchez-Vera, Ismael / Guilbaud, Emma / Cosialls, Ana M / Pons, Gabriel / Ricci, Jean-Ehrland / Iglesias-Serret, Daniel / Marchetti, Sandrine / Gil, Joan

Oncogenesis

2021 Volume 10, Issue 9, Page(s) 64

Abstract: Fluorizoline is a prohibitin-binding compound that triggers apoptosis in several cell lines from murine and human origin, as well as in primary cells from hematologic malignancies by inducing the integrated stress response and ER stress. Recently, it was ...

Abstract	Fluorizoline is a prohibitin-binding compound that triggers apoptosis in several cell lines from murine and human origin, as well as in primary cells from hematologic malignancies by inducing the integrated stress response and ER stress. Recently, it was described that PHB (Prohibitin) 1 and 2 are crucial mitophagy receptors involved in mediating the autophagic degradation of mitochondria. We measured mitophagy in HeLa cells expressing Parkin and in A549, a lung cancer cell line that can undergo mitophagy in a Parkin-independent manner, and we demonstrated that both fluorizoline and rocaglamide A, another PHB-binding molecule, inhibit CCCP- and OA-induced mitophagy. Moreover, we demonstrated that PHBs are mediating Parkin-dependent mitophagy. In conclusion, besides being a potent pro-apoptotic compound, we present fluorizoline as a promising new mitophagy modulator that could be used as anticancer agent.
Language	English
Publishing date	2021-09-27
Publishing country	United States
Document type	Journal Article
ZDB-ID	2674437-5
ISSN	2157-9024
ISSN	2157-9024
DOI	10.1038/s41389-021-00352-9
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Article ; Online: Pharmacological preconditioning protects from ischemia/reperfusion-induced apoptosis by modulating Bcl-xL expression through a ROS-dependent mechanism.

The FEBS journal

2021 Volume 288, Issue 11, Page(s) 3547–3569

Abstract	Myocardial ischemia/reperfusion (I/R) injury is a frequent perioperative threat, with numerous strategies developed to limit and/or prevent it. One interesting axis of research is the anesthetic preconditioning (APc) agent's hypothesis (such as sevoflurane, SEV). However, APc's mode of action is still poorly understood and volatile anesthetics used as preconditioning agents are often not well suited in clinical practice. Here, in vitro using H9C2 cells lines (in myeloblast state or differentiated toward cardiomyocytes) and in vivo in mice, we identified that SEV-induced APc is mediated by a mild induction of reactive oxygen species (ROS) that activates Akt and induces the expression of the anti-apoptotic protein B-cell lymphoma-extra large (Bcl-xL), therefore protecting cardiomyocytes from I/R-induced death. Furthermore, we extended these results to human cardiomyocytes (derived from induced pluripotent stem - IPS - cells). Importantly, we demonstrated that this protective signaling pathway induced by SEV could be stimulated using the antidiabetic agent metformin (MET), suggesting the preconditioning properties of MET. Altogether, our study identified a signaling pathway allowing APc of cardiac injuries as well as a rational for the use of MET as a pharmacological preconditioning agent to prevent I/R injuries.
MeSH term(s)	Animals ; Apoptosis/drug effects ; Cell Survival/drug effects ; Humans ; Hypoglycemic Agents/pharmacology ; Metformin/pharmacology ; Myocardial Reperfusion Injury/drug therapy ; Myocardial Reperfusion Injury/genetics ; Myocardial Reperfusion Injury/pathology ; Myocytes, Cardiac/drug effects ; Rats ; Reactive Oxygen Species/metabolism ; Reperfusion Injury/drug therapy ; Reperfusion Injury/genetics ; Reperfusion Injury/pathology ; Sevoflurane/pharmacology ; Signal Transduction/drug effects ; bcl-X Protein/genetics
Chemical Substances	Hypoglycemic Agents ; Reactive Oxygen Species ; bcl-X Protein ; Sevoflurane (38LVP0K73A) ; Metformin (9100L32L2N)
Language	English
Publishing date	2021-01-04
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2173655-8
ISSN	1742-4658 ; 1742-464X
ISSN (online)	1742-4658
ISSN	1742-464X
DOI	10.1111/febs.15675
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Article ; Online: Cholesterol efflux pathways hinder KRAS-driven lung tumor progenitor cell expansion.

Guilbaud, Emma / Barouillet, Thibault / Ilie, Marius / Borowczyk, Coraline / Ivanov, Stoyan / Sarrazy, Vincent / Vaillant, Nathalie / Ayrault, Marion / Castiglione, Alexia / Rignol, Guylène / Brest, Patrick / Bazioti, Venetia / Zaitsev, Konstantin / Lebrigand, Kevin / Dussaud, Sébastien / Magnone, Virginie / Bertolotto, Corine / Marchetti, Sandrine / Irondelle, Marie /

Goldberg, Ira / Huby, Thierry / Westerterp, Marit / Gautier, Emmanuel L / Mari, Bernard / Barbry, Pascal / Hofman, Paul / Yvan-Charvet, Laurent

Cell stem cell

2023 Volume 30, Issue 6, Page(s) 800–817.e9

Abstract: Cholesterol efflux pathways could be exploited in tumor biology to unravel cancer vulnerabilities. A mouse model of lung-tumor-bearing ... ...

Abstract	Cholesterol efflux pathways could be exploited in tumor biology to unravel cancer vulnerabilities. A mouse model of lung-tumor-bearing KRAS
MeSH term(s)	Humans ; Mice ; Animals ; Proto-Oncogene Proteins p21(ras)/genetics ; Proto-Oncogene Proteins p21(ras)/metabolism ; Cholesterol/metabolism ; Lung Neoplasms/genetics ; Cell Proliferation ; Lung ; Stem Cells/metabolism ; Apolipoprotein A-I/metabolism ; Tumor Microenvironment
Chemical Substances	Proto-Oncogene Proteins p21(ras) (EC 3.6.5.2) ; Cholesterol (97C5T2UQ7J) ; Apolipoprotein A-I ; KRAS protein, human
Language	English
Publishing date	2023-05-25
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2375354-7
ISSN	1875-9777 ; 1934-5909
ISSN (online)	1875-9777
ISSN	1934-5909
DOI	10.1016/j.stem.2023.05.005
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Article: Endoplasmic reticulum stress mediates resistance to BCL-2 inhibitor in uveal melanoma cells.

Bellini, Lara / Strub, Thomas / Habel, Nadia / Pandiani, Charlotte / Marchetti, Sandrine / Martel, Arnaud / Baillif, Stéphanie / Bailly-Maitre, Béatrice / Gual, Philippe / Ballotti, Robert / Bertolotto, Corine

Cell death discovery

2020 Volume 6, Page(s) 22

Abstract: To address unmet clinical need for uveal melanomas, we assessed the effects of BH3-mimetic molecules, the ABT family, known to exert pro-apoptotic activities in cancer cells. Our results uncovered that ABT-263 (Navitoclax), a potent and orally ... ...

Abstract	To address unmet clinical need for uveal melanomas, we assessed the effects of BH3-mimetic molecules, the ABT family, known to exert pro-apoptotic activities in cancer cells. Our results uncovered that ABT-263 (Navitoclax), a potent and orally bioavailable BCL-2 family inhibitor, induced antiproliferative effects in metastatic human uveal melanoma cells through cell cycle arrest at the G0/G1 phase, loss of mitochondrial membrane potential, and subsequently apoptotic cell death monitored by caspase activation and poly-ADP ribose polymerase cleavage. ABT-263-mediated reduction in tumor growth was also observed in vivo. We observed in some cells that ABT-263 treatment mounted a pro-survival response through activation of the ER stress signaling pathway. Blocking the PERK signaling pathway increased the pro-apoptotic ABT-263 effect. We thus uncovered a resistance mechanism in uveal melanoma cells mediated by activation of endoplasmic reticulum stress pathway. Therefore, our study identifies ABT-263 as a valid therapeutic option for patients suffering from uveal melanoma.
Language	English
Publishing date	2020-04-17
Publishing country	United States
Document type	Journal Article
ISSN	2058-7716
ISSN	2058-7716
DOI	10.1038/s41420-020-0259-2
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