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Article ; Online: Novel, non-conventional pathways of necroptosis in the heart and other organs: Molecular mechanisms, regulation and inter-organelle interplay.

Horvath, Csaba / Jarabicova, Izabela / Kura, Branislav / Kalocayova, Barbora / Faurobert, Eva / Davidson, Sean M / Adameova, Adriana

Biochimica et biophysica acta. Molecular cell research

2023 Volume 1870, Issue 7, Page(s) 119534

Abstract: Necroptosis, a cell death modality that is defined as a necrosis-like cell death depending on the receptor-interacting protein kinase 3 (RIPK3) and mixed lineage kinase domain-like pseudokinase (MLKL), has been found to underlie the injury of various ... ...

Abstract	Necroptosis, a cell death modality that is defined as a necrosis-like cell death depending on the receptor-interacting protein kinase 3 (RIPK3) and mixed lineage kinase domain-like pseudokinase (MLKL), has been found to underlie the injury of various organs. Nevertheless, the molecular background of this cell loss seems to also involve, at least under certain circumstances, some novel axes, such as RIPK3-PGAM5-Drp1 (mitochondrial protein phosphatase 5-dynamin-related protein 1), RIPK3-CaMKII (Ca
MeSH term(s)	Humans ; Necroptosis/genetics ; Protein Kinases/genetics ; Protein Kinases/metabolism ; Necrosis ; Cell Death/genetics ; Organelles/metabolism
Chemical Substances	Protein Kinases (EC 2.7.-)
Language	English
Publishing date	2023-07-01
Publishing country	Netherlands
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	60-7
ISSN	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbamcr.2023.119534
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Article ; Online: Recent insights into cerebral cavernous malformations.

Faurobert, Eva

The FEBS journal

2010 Volume 277, Issue 5, Page(s) 1069

MeSH term(s)	Animals ; Disease Models, Animal ; Genetic Predisposition to Disease ; Hemangioma, Cavernous, Central Nervous System/genetics ; Hemangioma, Cavernous, Central Nervous System/physiopathology ; Humans ; KRIT1 Protein ; Microtubule-Associated Proteins/genetics ; Proto-Oncogene Proteins/genetics
Chemical Substances	KRIT1 Protein ; KRIT1 protein, human ; Microtubule-Associated Proteins ; Proto-Oncogene Proteins
Language	English
Publishing date	2010-03
Publishing country	England
Document type	Introductory Journal Article
ZDB-ID	2173655-8
ISSN	1742-4658 ; 1742-464X
ISSN (online)	1742-4658
ISSN	1742-464X
DOI	10.1111/j.1742-4658.2009.07534.x
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Article ; Online: Calcium signaling mediates a biphasic mechanoadaptive response of endothelial cells to cyclic mechanical stretch.

Miroshnikova, Yekaterina A / Manet, Sandra / Li, Xinping / Wickström, Sara A / Faurobert, Eva / Albiges-Rizo, Corinne

Molecular biology of the cell

2021 Volume 32, Issue 18, Page(s) 1724–1736

Abstract: The vascular system is precisely regulated to adjust blood flow to organismal demand, thereby guaranteeing adequate perfusion under varying physiological conditions. Mechanical forces, such as cyclic circumferential stretch, are among the critical ... ...

Abstract	The vascular system is precisely regulated to adjust blood flow to organismal demand, thereby guaranteeing adequate perfusion under varying physiological conditions. Mechanical forces, such as cyclic circumferential stretch, are among the critical stimuli that dynamically adjust vessel distribution and diameter, but the precise mechanisms of adaptation to changing forces are unclear. We find that endothelial monolayers respond to cyclic stretch by transient remodeling of the vascular endothelial cadherin-based adherens junctions and the associated actomyosin cytoskeleton. Time-resolved proteomic profiling reveals that this remodeling is driven by calcium influx through the mechanosensitive Piezo1 channel, triggering Rho activation to increase actomyosin contraction. As the mechanical stimulus persists, calcium signaling is attenuated through transient down-regulation of Piezo1 protein. At the same time, filamins are phosphorylated to increase monolayer stiffness, allowing mechanoadaptation to restore junctional integrity despite continuing exposure to stretch. Collectively, this study identifies a biphasic response to cyclic stretch, consisting of an initial calcium-driven junctional mechanoresponse, followed by mechanoadaptation facilitated by monolayer stiffening.
MeSH term(s)	Actin Cytoskeleton/metabolism ; Actomyosin/metabolism ; Adherens Junctions/physiology ; Antigens, CD/genetics ; Antigens, CD/metabolism ; Biomechanical Phenomena ; Cadherins/genetics ; Cadherins/metabolism ; Calcimycin/pharmacology ; Calcium Ionophores/pharmacology ; Calcium Signaling/drug effects ; Cytochalasin D/pharmacology ; Filamins/metabolism ; Human Umbilical Vein Endothelial Cells ; Humans ; Ion Channels/genetics ; Ion Channels/metabolism ; Mechanotransduction, Cellular ; Phosphoproteins/analysis ; Phosphoproteins/metabolism ; Protein Interaction Maps ; p21-Activated Kinases/metabolism ; rac GTP-Binding Proteins/metabolism ; rhoA GTP-Binding Protein/metabolism
Chemical Substances	Antigens, CD ; Cadherins ; Calcium Ionophores ; Filamins ; Ion Channels ; PIEZO1 protein, human ; Phosphoproteins ; cadherin 5 ; RHOA protein, human (124671-05-2) ; Cytochalasin D (22144-77-0) ; Calcimycin (37H9VM9WZL) ; Actomyosin (9013-26-7) ; PAK1 protein, human (EC 2.7.11.1) ; p21-Activated Kinases (EC 2.7.11.1) ; rac GTP-Binding Proteins (EC 3.6.5.2) ; rhoA GTP-Binding Protein (EC 3.6.5.2)
Language	English
Publishing date	2021-06-03
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1098979-1
ISSN	1939-4586 ; 1059-1524
ISSN (online)	1939-4586
ISSN	1059-1524
DOI	10.1091/mbc.E21-03-0106
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Article ; Online: Impaired retinoic acid signaling in cerebral cavernous malformations.

Grdseloff, Nastasja / Boulday, Gwenola / Rödel, Claudia J / Otten, Cécile / Vannier, Daphné Raphaelle / Cardoso, Cécile / Faurobert, Eva / Dogra, Deepika / Tournier-Lasserve, Elisabeth / Abdelilah-Seyfried, Salim

Scientific reports

2023 Volume 13, Issue 1, Page(s) 5572

Abstract: The capillary-venous pathology cerebral cavernous malformation (CCM) is caused by loss of CCM1/Krev interaction trapped protein 1 (KRIT1), CCM2/MGC4607, or CCM3/PDCD10 in some endothelial cells. Mutations of CCM genes within the brain vasculature can ... ...

Abstract	The capillary-venous pathology cerebral cavernous malformation (CCM) is caused by loss of CCM1/Krev interaction trapped protein 1 (KRIT1), CCM2/MGC4607, or CCM3/PDCD10 in some endothelial cells. Mutations of CCM genes within the brain vasculature can lead to recurrent cerebral hemorrhages. Pharmacological treatment options are urgently needed when lesions are located in deeply-seated and in-operable regions of the central nervous system. Previous pharmacological suppression screens in disease models of CCM led to the discovery that treatment with retinoic acid improved CCM phenotypes. This finding raised a need to investigate the involvement of retinoic acid in CCM and test whether it has a curative effect in preclinical mouse models. Here, we show that components of the retinoic acid synthesis and degradation pathway are transcriptionally misregulated across disease models of CCM. We complemented this analysis by pharmacologically modifying retinoic acid levels in zebrafish and human endothelial cell models of CCM, and in acute and chronic mouse models of CCM. Our pharmacological intervention studies in CCM2-depleted human umbilical vein endothelial cells (HUVECs) and krit1 mutant zebrafish showed positive effects when retinoic acid levels were increased. However, therapeutic approaches to prevent the development of vascular lesions in adult chronic murine models of CCM were drug regiment-sensitive, possibly due to adverse developmental effects of this hormone. A treatment with high doses of retinoic acid even worsened CCM lesions in an adult chronic murine model of CCM. This study provides evidence that retinoic acid signaling is impaired in the CCM pathophysiology and suggests that modification of retinoic acid levels can alleviate CCM phenotypes.
MeSH term(s)	Adult ; Humans ; Animals ; Mice ; Hemangioma, Cavernous, Central Nervous System/genetics ; Zebrafish/metabolism ; Proto-Oncogene Proteins/metabolism ; Brain/metabolism ; Human Umbilical Vein Endothelial Cells/metabolism ; Microtubule-Associated Proteins/metabolism
Chemical Substances	Proto-Oncogene Proteins ; Microtubule-Associated Proteins
Language	English
Publishing date	2023-04-05
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-023-31905-0
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Article ; Online: Correction to: VEGF

Boudria, Asma / Faycal, Cherine Abou / Jia, Tao / Gout, Stephanie / Keramidas, Michelle / Didier, Chloé / Lemaître, Nicolas / Manet, Sandra / Coll, Jean-Luc / Toffart, Anne-Claire / Moro-Sibilot, Denis / Albiges-Rizo, Corinne / Josserand, Véronique / Faurobert, Eva / Brambilla, Christian / Brambilla, Elisabeth / Gazzeri, Sylvie / Eymin, Beatrice

Oncogene

2023 Volume 42, Issue 32, Page(s) 2471–2472

Language	English
Publishing date	2023-07-07
Publishing country	England
Document type	Published Erratum
ZDB-ID	639046-8
ISSN	1476-5594 ; 0950-9232
ISSN (online)	1476-5594
ISSN	0950-9232
DOI	10.1038/s41388-023-02764-w
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Article ; Online: Immunofluorescence of Cell-Cell and Cell-Extracellular Matrix Adhesive Defects in In Vitro Endothelial CCM Model: Juxtacrine Role of Mutant Extracellular Matrix on Wild-Type Endothelial Cells.

Manet, Sandra / Vannier, Daphné / Bouin, Anne-Pascale / Lisowska, Justyna / Albiges-Rizo, Corinne / Faurobert, Eva

Methods in molecular biology (Clifton, N.J.)

2020 Volume 2152, Page(s) 401–416

Abstract: Endothelial cells lining cerebral cavernous malformations (CCM) present strong adhesive and mechanical defects. Increased cell contractility is a driver to the onset and the expansion of the CCM lesions. 2D in vitro endothelial models have been developed ...

Abstract	Endothelial cells lining cerebral cavernous malformations (CCM) present strong adhesive and mechanical defects. Increased cell contractility is a driver to the onset and the expansion of the CCM lesions. 2D in vitro endothelial models have been developed from either endothelial cells isolated from ccm1-3 knock-out mice or CCM1-3-silenced primary endothelial cells. These in vitro models faithfully recapitulate the adhesive and contractile defects of the CCM-deficient endothelial cells such as increased cell-extracellular matrix (ECM) adhesion through β1 integrin-anchored actin stress fibers, abnormal remodeling of the ECM, and destabilized VE-cadherin-dependent cell-cell junctions. Using such 2D in vitro CCM models, we have shown that the ECM remodeled by CCM-depleted endothelial cells can propagate CCM-like adhesive defects to wild-type endothelial cells, a process potentially pertinent to CCM lesion expansion. Here, we detail methods for studying the morphology of focal adhesions, actomyosin cytoskeleton, and VE-cadherin-dependent Adherens junctions by immunofluorescence and morphometric analyses. Moreover, we detail the protocols to produce and purify remodeled ECM and to test its effect on endothelial cell adhesion.
MeSH term(s)	Adherens Junctions/metabolism ; Animals ; Biomarkers ; Cell Adhesion ; Cell Communication ; Cytoskeleton/metabolism ; Endothelial Cells/metabolism ; Endothelium, Vascular/metabolism ; Extracellular Matrix/metabolism ; Fluorescent Antibody Technique ; Focal Adhesions/metabolism ; Hemangioma, Cavernous, Central Nervous System/etiology ; Hemangioma, Cavernous, Central Nervous System/metabolism ; Hemangioma, Cavernous, Central Nervous System/pathology ; Human Umbilical Vein Endothelial Cells ; Humans ; Intercellular Junctions/metabolism ; Mechanotransduction, Cellular ; Models, Biological
Chemical Substances	Biomarkers
Language	English
Publishing date	2020-06-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-0716-0640-7_29
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Article ; Online: β1 integrin monoclonal antibody treatment ameliorates cerebral cavernous malformations.

McCurdy, Sara / Lin, Jenny / Shenkar, Robert / Moore, Thomas / Lightle, Rhonda / Faurobert, Eva / Lopez-Ramirez, Miguel-Alejandro / Awad, Issam / Ginsberg, Mark H

FASEB journal : official publication of the Federation of American Societies for Experimental Biology

2022 Volume 36, Issue 12, Page(s) e22629

Abstract: β1 integrins are important in blood vessel formation and function, finely tuning the adhesion of endothelial cells to each other and to the extracellular matrix. The role of integrins in the vascular disease, cerebral cavernous malformation (CCM) has yet ...

Abstract	β1 integrins are important in blood vessel formation and function, finely tuning the adhesion of endothelial cells to each other and to the extracellular matrix. The role of integrins in the vascular disease, cerebral cavernous malformation (CCM) has yet to be explored in vivo. Endothelial loss of the gene KRIT1 leads to brain microvascular defects, resulting in debilitating and often fatal consequences. We tested administration of a monoclonal antibody that enforces the active β1 integrin conformation, (clone 9EG7), on a murine neonatal CCM mouse model, Krit1
MeSH term(s)	Animals ; Humans ; Mice ; Hemangioma, Cavernous, Central Nervous System/metabolism ; Integrin beta1/metabolism ; Antibodies, Monoclonal/metabolism ; Integrins/metabolism ; Human Umbilical Vein Endothelial Cells/metabolism ; Microtubule-Associated Proteins/metabolism
Chemical Substances	Integrin beta1 ; Antibodies, Monoclonal ; Integrins ; Microtubule-Associated Proteins
Language	English
Publishing date	2022-11-05
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	639186-2
ISSN	1530-6860 ; 0892-6638
ISSN (online)	1530-6860
ISSN	0892-6638
DOI	10.1096/fj.202200907RR
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Zs.A 2266: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Impaired retinoic acid signaling in cerebral cavernous malformations

Nastasja Grdseloff / Gwenola Boulday / Claudia J. Rödel / Cécile Otten / Daphné Raphaelle Vannier / Cécile Cardoso / Eva Faurobert / Deepika Dogra / Elisabeth Tournier-Lasserve / Salim Abdelilah-Seyfried

Scientific Reports, Vol 13, Iss 1, Pp 1-

2023 Volume 11

Abstract: Abstract The capillary-venous pathology cerebral cavernous malformation (CCM) is caused by loss of CCM1/Krev interaction trapped protein 1 (KRIT1), CCM2/MGC4607, or CCM3/PDCD10 in some endothelial cells. Mutations of CCM genes within the brain ... ...

Abstract	Abstract The capillary-venous pathology cerebral cavernous malformation (CCM) is caused by loss of CCM1/Krev interaction trapped protein 1 (KRIT1), CCM2/MGC4607, or CCM3/PDCD10 in some endothelial cells. Mutations of CCM genes within the brain vasculature can lead to recurrent cerebral hemorrhages. Pharmacological treatment options are urgently needed when lesions are located in deeply-seated and in-operable regions of the central nervous system. Previous pharmacological suppression screens in disease models of CCM led to the discovery that treatment with retinoic acid improved CCM phenotypes. This finding raised a need to investigate the involvement of retinoic acid in CCM and test whether it has a curative effect in preclinical mouse models. Here, we show that components of the retinoic acid synthesis and degradation pathway are transcriptionally misregulated across disease models of CCM. We complemented this analysis by pharmacologically modifying retinoic acid levels in zebrafish and human endothelial cell models of CCM, and in acute and chronic mouse models of CCM. Our pharmacological intervention studies in CCM2-depleted human umbilical vein endothelial cells (HUVECs) and krit1 mutant zebrafish showed positive effects when retinoic acid levels were increased. However, therapeutic approaches to prevent the development of vascular lesions in adult chronic murine models of CCM were drug regiment-sensitive, possibly due to adverse developmental effects of this hormone. A treatment with high doses of retinoic acid even worsened CCM lesions in an adult chronic murine model of CCM. This study provides evidence that retinoic acid signaling is impaired in the CCM pathophysiology and suggests that modification of retinoic acid levels can alleviate CCM phenotypes.
Keywords	Medicine ; R ; Science ; Q
Language	English
Publishing date	2023-04-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
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Article ; Online: Microenvironment, tumor cell plasticity, and cancer.

Faurobert, Eva / Bouin, Anne-Pascale / Albiges-Rizo, Corinne

Current opinion in oncology

2015 Volume 27, Issue 1, Page(s) 64–70

Abstract: Purpose of review: Much effort has been devoted to determining how cellular and noncellular components of the tumoral niche initiate and promote cancer development. Cancer cells perceive biochemical signals from components of the extracellular matrix ( ... ...

Abstract	Purpose of review: Much effort has been devoted to determining how cellular and noncellular components of the tumoral niche initiate and promote cancer development. Cancer cells perceive biochemical signals from components of the extracellular matrix (ECM) and sense physical features, such as matrix stiffness and cell confinement. The past decade has seen a better understanding of the biophysics and mechanobiology associated with cancer cells. Indeed, loss of mechanisms controlling the production, the degradation, and the remodeling of ECM contributes to tumor growth or cell dissemination by affecting cell contractility in response to ECM stiffness and by stimulating mechanical dependence of growth factor activation. Results: Cell plasticity allows adaptative strategies for cancer cells to survive or eventually escape from tumoral environment through modification of the microenvironment-cell interface, internal tension increase, and nuclear deformation partly leading to intratumoral heterogeneity. However, although alteration of the biomechanical properties of the ECM are sufficient to promote cell migration and invasion in cancer cells, this microenvironment can also provide a hospitable niche for tumor dormancy and resistance to cancer therapy. Conclusion: The review will focus on how physicochemical properties of ECM might promote tumor growth or cell dissemination or on the contrary maintain quiescent state of cancer cells. It is crucial to clarify the molecular basis of mechanotransduction in the development and progression of tumors to identify new potential biomarkers and anticancer therapeutic targets.
MeSH term(s)	Disease Progression ; Elasticity/physiology ; Extracellular Matrix/physiology ; Humans ; Mechanotransduction, Cellular/physiology ; Neoplasm Invasiveness/physiopathology ; Neoplasms/physiopathology ; Tumor Microenvironment/physiology
Language	English
Publishing date	2015-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1049384-0
ISSN	1531-703X ; 1040-8746
ISSN (online)	1531-703X
ISSN	1040-8746
DOI	10.1097/CCO.0000000000000154
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Article ; Online: Control of SRC molecular dynamics encodes distinct cytoskeletal responses by specifying signaling pathway usage.

Kerjouan, Adèle / Boyault, Cyril / Oddou, Christiane / Hiriart-Bryant, Edwige / Grichine, Alexei / Kraut, Alexandra / Pezet, Mylène / Balland, Martial / Faurobert, Eva / Bonnet, Isabelle / Coute, Yohann / Fourcade, Bertrand / Albiges-Rizo, Corinne / Destaing, Olivier

Journal of cell science

2021 Volume 134, Issue 2

Abstract: Upon activation by different transmembrane receptors, the same signaling protein can induce distinct cellular responses. A way to decipher the mechanisms of such pleiotropic signaling activity is to directly manipulate the decision-making activity that ... ...

Abstract	Upon activation by different transmembrane receptors, the same signaling protein can induce distinct cellular responses. A way to decipher the mechanisms of such pleiotropic signaling activity is to directly manipulate the decision-making activity that supports the selection between distinct cellular responses. We developed an optogenetic probe (optoSRC) to control SRC signaling, an example of a pleiotropic signaling node, and we demonstrated its ability to generate different acto-adhesive structures (lamellipodia or invadosomes) upon distinct spatio-temporal control of SRC kinase activity. The occurrence of each acto-adhesive structure was simply dictated by the dynamics of optoSRC nanoclusters in adhesive sites, which were dependent on the SH3 and Unique domains of the protein. The different decision-making events regulated by optoSRC dynamics induced distinct downstream signaling pathways, which we characterized using time-resolved proteomic and network analyses. Collectively, by manipulating the molecular mobility of SRC kinase activity, these experiments reveal the pleiotropy-encoding mechanism of SRC signaling.
MeSH term(s)	Animals ; Cells, Cultured ; Cytoskeleton ; Molecular Dynamics Simulation ; Phosphorylation ; Proteomics ; Signal Transduction ; src Homology Domains ; src-Family Kinases/genetics ; src-Family Kinases/metabolism
Chemical Substances	src-Family Kinases (EC 2.7.10.2)
Language	English
Publishing date	2021-01-25
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2993-2
ISSN	1477-9137 ; 0021-9533
ISSN (online)	1477-9137
ISSN	0021-9533
DOI	10.1242/jcs.254599
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