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Article: Human dental pulp stem cells cultured in serum-free supplemented medium.

Bonnamain, Virginie / Thinard, Reynald / Sergent-Tanguy, Solène / Huet, Pascal / Bienvenu, Géraldine / Naveilhan, Philippe / Farges, Jean-Christophe / Alliot-Licht, Brigitte

Frontiers in physiology

2013 Volume 4, Page(s) 357

Abstract: Unlabelled: Growing evidence show that human dental pulp stem cells (DPSCs) could provide a source of adult stem cells for the treatment of neurodegenerative pathologies. In this study, DPSCs were expanded and cultured with a protocol generally used for ...

Abstract	Unlabelled: Growing evidence show that human dental pulp stem cells (DPSCs) could provide a source of adult stem cells for the treatment of neurodegenerative pathologies. In this study, DPSCs were expanded and cultured with a protocol generally used for the culture of neural stem/progenitor cells. Methodology: DPSC cultures were established from third molars. The pulp tissue was enzymatically digested and cultured in serum-supplemented basal medium for 12 h. Adherent (ADH) and non-adherent (non-ADH) cell populations were separated according to their differential adhesion to plastic and then cultured in serum-free defined N2 medium with epidermal growth factor (EGF) and basic fibroblast growth factor (bFGF). Both ADH and non-ADH populations were analyzed by FACS and/or PCR. Results: FACS analysis of ADH-DPSCs revealed the expression of the mesenchymal cell marker CD90, the neuronal marker CD56, the transferrin receptor CD71, and the chemokine receptor CXCR3, whereas hematopoietic stem cells markers CD45, CD133, and CD34 were not expressed. ADH-DPSCs expressed transcripts coding for the Nestin gene, whereas expression levels of genes coding for the neuronal markers β-III tubulin and NF-M, and the oligodendrocyte marker PLP-1 were donor dependent. ADH-DPSCs did not express the transcripts for GFAP, an astrocyte marker. Cells of the non-ADH population that grew as spheroids expressed Nestin, β-III tubulin, NF-M and PLP-1 transcripts. DPSCs that migrated out of the spheroids exhibited an odontoblast-like morphology and expressed a higher level of DSPP and osteocalcin transcripts than ADH-DPSCs. Conclusion: Collectively, these data indicate that human DPSCs can be expanded and cultured in serum-free supplemented medium with EGF and bFGF. ADH-DPSCs and non-ADH populations contained neuronal and/or oligodendrocyte progenitors at different stages of commitment and, interestingly, cells from spheroid structures seem to be more engaged into the odontoblastic lineage than the ADH-DPSCs.
Language	English
Publishing date	2013-12-11
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2564217-0
ISSN	1664-042X
ISSN	1664-042X
DOI	10.3389/fphys.2013.00357
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Article ; Online: Dendritic Cells Require TMEM176A/B Ion Channels for Optimal MHC Class II Antigen Presentation to Naive CD4

Lancien, Melanie / Bienvenu, Geraldine / Salle, Sonia / Gueno, Lucile / Feyeux, Magalie / Merieau, Emmanuel / Remy, Severine / Even, Amandine / Moreau, Aurelie / Molle, Alice / Fourgeux, Cynthia / Coulon, Flora / Beriou, Gaelle / Bouchet-Delbos, Laurence / Chiffoleau, Elise / Kirstetter, Peggy / Chan, Susan / Kerfoot, Steven M / Abdu Rahiman, Saeed /

De Simone, Veronica / Matteoli, Gianluca / Boncompain, Gaelle / Perez, Franck / Josien, Regis / Poschmann, Jeremie / Cuturi, Maria Cristina / Louvet, Cedric

Journal of immunology (Baltimore, Md. : 1950)

2021 Volume 207, Issue 2, Page(s) 421–435

Abstract: Intracellular ion fluxes emerge as critical actors of immunoregulation but still remain poorly explored. In this study, we investigated the role of the redundant cation channels TMEM176A and TMEM176B (TMEM176A/B) in retinoic acid-related orphan receptor ... ...

Abstract	Intracellular ion fluxes emerge as critical actors of immunoregulation but still remain poorly explored. In this study, we investigated the role of the redundant cation channels TMEM176A and TMEM176B (TMEM176A/B) in retinoic acid-related orphan receptor γt
MeSH term(s)	Animals ; Antigen Presentation/immunology ; CD4-Positive T-Lymphocytes/immunology ; Dendritic Cells/immunology ; Endosomes/immunology ; Female ; Genes, MHC Class II/immunology ; Golgi Apparatus/immunology ; Histocompatibility Antigens Class II/immunology ; Immunity, Innate/immunology ; Intestinal Mucosa/immunology ; Ion Channels/immunology ; Lymphocytes/immunology ; Lysosomes/immunology ; Male ; Membrane Proteins/immunology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Th17 Cells/immunology ; Tretinoin/immunology
Chemical Substances	Histocompatibility Antigens Class II ; Ion Channels ; Membrane Proteins ; Tmem176A protein, mouse ; Tmem176B protein, mouse ; Tretinoin (5688UTC01R)
Language	English
Publishing date	2021-07-07
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.2000498
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Article ; Online: RORγt+ cells selectively express redundant cation channels linked to the Golgi apparatus.

Drujont, Lucile / Lemoine, Aurélie / Moreau, Aurélie / Bienvenu, Géraldine / Lancien, Mélanie / Cens, Thierry / Guillot, Flora / Bériou, Gaëlle / Bouchet-Delbos, Laurence / Fehling, Hans Jörg / Chiffoleau, Elise / Nicot, Arnaud B / Charnet, Pierre / Martin, Jérôme C / Josien, Régis / Cuturi, Maria Cristina / Louvet, Cédric

Scientific reports

2016 Volume 6, Page(s) 23682

Abstract: Retinoid-related orphan receptor gamma t (RORγt) is a master transcription factor central to type 17 immunity involving cells such as T helper 17, group 3 innate lymphoid cells or IL-17-producing γδ T cells. Here we show that the intracellular ion ... ...

Abstract	Retinoid-related orphan receptor gamma t (RORγt) is a master transcription factor central to type 17 immunity involving cells such as T helper 17, group 3 innate lymphoid cells or IL-17-producing γδ T cells. Here we show that the intracellular ion channel TMEM176B and its homologue TMEM176A are strongly expressed in these RORγt(+) cells. We demonstrate that TMEM176A and B exhibit a similar cation channel activity and mainly colocalise in close proximity to the trans-Golgi network. Strikingly, in the mouse, the loss of Tmem176b is systematically associated with a strong upregulation of Tmem176a. While Tmem176b single-deficiency has no effect on the course of experimental autoimmune encephalomyelitis, T cell or DSS-induced colitis, it significantly reduces imiquimod-induced psoriasis-like skin inflammation. These findings shed light on a potentially novel specific process linked to post-Golgi trafficking for modulating the function of RORγt(+) cells and indicate that both homologues should be simultaneously targeted to clearly elucidate the role of this intracellular ion flow.
MeSH term(s)	Animals ; Cells, Cultured ; Colitis/chemically induced ; Colitis/genetics ; Colitis/immunology ; Disease Models, Animal ; Encephalomyelitis, Autoimmune, Experimental/chemically induced ; Encephalomyelitis, Autoimmune, Experimental/genetics ; Humans ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Mice ; Nuclear Receptor Subfamily 1, Group F, Member 3/metabolism ; Psoriasis/chemically induced ; Psoriasis/genetics ; T-Lymphocytes, Helper-Inducer/cytology ; T-Lymphocytes, Helper-Inducer/metabolism ; trans-Golgi Network/genetics ; trans-Golgi Network/metabolism
Chemical Substances	Membrane Proteins ; Nuclear Receptor Subfamily 1, Group F, Member 3 ; TMEM176A protein, human ; TMEM176B protein, human ; Tmem176A protein, mouse ; Tmem176B protein, mouse
Language	English
Publishing date	2016-03-24
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/srep23682
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Article: Insulin-like growth factor binding protein-6 transgenic mice: postnatal growth, brain development, and reproduction abnormalities.

Bienvenu, Géraldine / Seurin, Danielle / Grellier, Pascale / Froment, Pascal / Baudrimont, Marielle / Monget, Philippe / Le Bouc, Yves / Babajko, Sylvie

Endocrinology

2004 Volume 145, Issue 5, Page(s) 2412–2420

Abstract: In biological fluids, IGFs bind to six distinct binding proteins (IGFBP-1 to -6). IGFBP-6 is of particular interest because it has been shown to inhibit proliferation in many cell types and to be synthesized in the central nervous system (CNS). It also ... ...

Abstract	In biological fluids, IGFs bind to six distinct binding proteins (IGFBP-1 to -6). IGFBP-6 is of particular interest because it has been shown to inhibit proliferation in many cell types and to be synthesized in the central nervous system (CNS). It also has the strongest affinity for IGF-II among the IGFBPs. To study IGFBP-6 function in vivo, we established IGFBP-6 transgenic mice in which human IGFBP-6 (hIGFBP-6) cDNA is expressed under the control of the glial fibrillary acidic protein (GFAP) promoter. Northern and Western blot analysis revealed strong transgene expression in the CNS. With histological examination of the CNS, cerebellum size and weight proved to be reduced by about 25% and 35%, respectively, and there were smaller numbers of differentiated, GFAP-expressing astrocytes than in wild-type mice. Between birth and 1 month of age, transgenic mice had high levels of circulating hIGFBP-6 and reduced plasma IGF-I, and, as a result, body weight was significantly reduced. Reproductive physiology was also affected. Litter size was reduced by 27% when wild-type males were mated with 3-month-old transgenic females and by 66% when mated with 6-month-old transgenic females. Histological examination of ovaries of transgenic mice revealed a marked decrease in weight and in the number of corpora lutea, suggesting altered ovulation, and circulating LH levels were reduced by 50%. Our results indicate that this new model of transgenic mouse may prove to be a useful tool in elucidating the in vivo role of IGFBP-6 in the brain, especially in regard to hypothalamic control, and in reproductive physiology.
MeSH term(s)	Animals ; Astrocytes/chemistry ; Blotting, Northern ; Blotting, Western ; Brain/growth & development ; Cerebellum/anatomy & histology ; Female ; Fetal Death ; Follicle Stimulating Hormone/blood ; Gene Expression ; Glial Fibrillary Acidic Protein/genetics ; Growth ; Humans ; Hypothalamus/physiology ; Insulin-Like Growth Factor Binding Protein 6/genetics ; Insulin-Like Growth Factor Binding Protein 6/physiology ; Insulin-Like Growth Factor I/analysis ; Litter Size ; Luteinizing Hormone/blood ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Inbred DBA ; Mice, Transgenic ; Organ Size ; Ovary/anatomy & histology ; Promoter Regions, Genetic/genetics ; RNA, Messenger/analysis ; Reproduction
Chemical Substances	Glial Fibrillary Acidic Protein ; Insulin-Like Growth Factor Binding Protein 6 ; RNA, Messenger ; Insulin-Like Growth Factor I (67763-96-6) ; Luteinizing Hormone (9002-67-9) ; Follicle Stimulating Hormone (9002-68-0)
Language	English
Publishing date	2004-05
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	427856-2
ISSN	1945-7170 ; 0013-7227
ISSN (online)	1945-7170
ISSN	0013-7227
DOI	10.1210/en.2003-1196
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Article: Pleckstrin homology domain-interacting protein (PHIP) as a marker and mediator of melanoma metastasis

De Semir, David / Nosrati, Mehdi / Bezrookove, Vladimir / Dar, Altaf A / Federman, Scot / Bienvenu, Geraldine / Venna, Suraj / Rangel, Javier / Climent, Joan / Meyer Tamgüney, Tanja M / Thummala, Suresh / Tong, Schuyler / Leong, Stanley P. L / Haqq, Chris / Billings, Paul / Miller, James R. III / Sagebiel, Richard W / Debs, Robert / Kashani-Sabet, Mohammed

Proceedings of the National Academy of Sciences of the United States of America. 2012 May 1, v. 109, no. 18

2012

Abstract: Although melanomas with mutant v-Raf murine sarcoma viral oncogene homolog B1 (BRAF) can now be effectively targeted, there is no molecular target for most melanomas expressing wild-type BRAF. Here, we show that the activation of Pleckstrin homology ... ...

Abstract	Although melanomas with mutant v-Raf murine sarcoma viral oncogene homolog B1 (BRAF) can now be effectively targeted, there is no molecular target for most melanomas expressing wild-type BRAF. Here, we show that the activation of Pleckstrin homology domain-interacting protein (PHIP), promotes melanoma metastasis, can be used to classify a subset of primary melanomas, and is a prognostic biomarker for melanoma. Systemic, plasmid-based shRNA targeting of Phip inhibited the metastatic progression of melanoma, whereas stable suppression of Phip in melanoma cell lines suppressed metastatic potential and prolonged the survival of tumor-bearing mice. The human PHIP gene resides on 6q14.1, and although 6q loss has been observed in melanoma, the PHIP locus was preserved in melanoma cell lines and patient samples, and its overexpression was an independent adverse predictor of survival in melanoma patients. In addition, a high proportion of PHIP-overexpressing melanomas harbored increased PHIP copy number. PHIP-overexpressing melanomas include tumors with wild-type BRAF, neuroblastoma RAS viral (v-ras) oncogene homolog, and phosphatase and tensin homolog, demonstrating PHIP activation in triple-negative melanoma. These results describe previously unreported roles for PHIP in predicting and promoting melanoma metastasis, and in the molecular classification of melanoma.
Keywords	biomarkers ; gene overexpression ; humans ; loci ; melanoma ; metastasis ; mice ; mutants ; oncogenes ; patients ; pleckstrin ; sarcoma
Language	English
Dates of publication	2012-0501
Size	p. 7067-7072.
Publishing place	National Academy of Sciences
Document type	Article
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.1119949109
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Pleckstrin homology domain-interacting protein (PHIP) as a marker and mediator of melanoma metastasis.

De Semir, David / Nosrati, Mehdi / Bezrookove, Vladimir / Dar, Altaf A / Federman, Scot / Bienvenu, Geraldine / Venna, Suraj / Rangel, Javier / Climent, Joan / Meyer Tamgüney, Tanja M / Thummala, Suresh / Tong, Schuyler / Leong, Stanley P L / Haqq, Chris / Billings, Paul / Miller, James R / Sagebiel, Richard W / Debs, Robert / Kashani-Sabet, Mohammed

Proceedings of the National Academy of Sciences of the United States of America

2012 Volume 109, Issue 18, Page(s) 7067–7072

Abstract	Although melanomas with mutant v-Raf murine sarcoma viral oncogene homolog B1 (BRAF) can now be effectively targeted, there is no molecular target for most melanomas expressing wild-type BRAF. Here, we show that the activation of Pleckstrin homology domain-interacting protein (PHIP), promotes melanoma metastasis, can be used to classify a subset of primary melanomas, and is a prognostic biomarker for melanoma. Systemic, plasmid-based shRNA targeting of Phip inhibited the metastatic progression of melanoma, whereas stable suppression of Phip in melanoma cell lines suppressed metastatic potential and prolonged the survival of tumor-bearing mice. The human PHIP gene resides on 6q14.1, and although 6q loss has been observed in melanoma, the PHIP locus was preserved in melanoma cell lines and patient samples, and its overexpression was an independent adverse predictor of survival in melanoma patients. In addition, a high proportion of PHIP-overexpressing melanomas harbored increased PHIP copy number. PHIP-overexpressing melanomas include tumors with wild-type BRAF, neuroblastoma RAS viral (v-ras) oncogene homolog, and phosphatase and tensin homolog, demonstrating PHIP activation in triple-negative melanoma. These results describe previously unreported roles for PHIP in predicting and promoting melanoma metastasis, and in the molecular classification of melanoma.
MeSH term(s)	Animals ; Base Sequence ; Biomarkers, Tumor/genetics ; Biomarkers, Tumor/metabolism ; Cell Line, Tumor ; Female ; Humans ; Intracellular Signaling Peptides and Proteins/antagonists & inhibitors ; Intracellular Signaling Peptides and Proteins/genetics ; Intracellular Signaling Peptides and Proteins/metabolism ; Melanoma/genetics ; Melanoma/metabolism ; Melanoma/secondary ; Melanoma, Experimental/genetics ; Melanoma, Experimental/metabolism ; Melanoma, Experimental/secondary ; Mice ; Mice, Inbred C57BL ; Mice, Nude ; Nerve Tissue Proteins/antagonists & inhibitors ; Nerve Tissue Proteins/genetics ; Nerve Tissue Proteins/metabolism ; RNA, Small Interfering/genetics ; Signal Transduction
Chemical Substances	Biomarkers, Tumor ; Intracellular Signaling Peptides and Proteins ; Nerve Tissue Proteins ; PHIP protein, human ; Phip protein, mouse ; RNA, Small Interfering
Language	English
Publishing date	2012-04-17
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.1119949109
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Article: Pleckstrin homology domain-interacting protein (PHIP) as a marker and mediator of melanoma metastasis

De Semir, David / Nosrati, Mehdi / Bezrookove, Vladimir / Dar, Altaf A. / Federman, Scot / Bienvenu, Geraldine / Venna, Suraj / Rangel, Javier / Climent, Joan / Meyer Tamgüney, Tanja M. / Thummala, Suresh / Tong, Schuyler / Leong, Stanley P. L. / Haqq, Chris / Billings, Paul / Miller, James R. III / Sagebiel, Richard W. / Debs, Robert / Kashani-Sabet, Mohammed

Proceedings of the National Academy of Sciences of the United States of America

Volume v. 109,, Issue no. 1

Abstract	Although melanomas with mutant v-Raf murine sarcoma viral oncogene homolog B1 (BRAF) can now be effectively targeted, there is no molecular target for most melanomas expressing wild-type BRAF. Here, we show that the activation of Pleckstrin homology domain-interacting protein (PHIP), promotes melanoma metastasis, can be used to classify a subset of primary melanomas, and is a prognostic biomarker for melanoma. Systemic, plasmid-based shRNA targeting of Phip inhibited the metastatic progression of melanoma, whereas stable suppression of Phip in melanoma cell lines suppressed metastatic potential and prolonged the survival of tumor-bearing mice. The human PHIP gene resides on 6q14.1, and although 6q loss has been observed in melanoma, the PHIP locus was preserved in melanoma cell lines and patient samples, and its overexpression was an independent adverse predictor of survival in melanoma patients. In addition, a high proportion of PHIP-overexpressing melanomas harbored increased PHIP copy number. PHIP-overexpressing melanomas include tumors with wild-type BRAF, neuroblastoma RAS viral (v-ras) oncogene homolog, and phosphatase and tensin homolog, demonstrating PHIP activation in triple-negative melanoma. These results describe previously unreported roles for PHIP in predicting and promoting melanoma metastasis, and in the molecular classification of melanoma.
Keywords	mice ; patients ; oncogenes ; metastasis ; gene overexpression ; sarcoma ; pleckstrin ; loci ; melanoma ; humans ; biomarkers ; mutants
Language	English
Document type	Article
ISSN	0027-8424
Database	AGRIS - International Information System for the Agricultural Sciences and Technology

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Article: Human dental pulp stem cells cultured in serum-free supplemented medium.

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Article ; Online: Dendritic Cells Require TMEM176A/B Ion Channels for Optimal MHC Class II Antigen Presentation to Naive CD4

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Article ; Online: RORγt+ cells selectively express redundant cation channels linked to the Golgi apparatus.

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Article: Insulin-like growth factor binding protein-6 transgenic mice: postnatal growth, brain development, and reproduction abnormalities.

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Article: Pleckstrin homology domain-interacting protein (PHIP) as a marker and mediator of melanoma metastasis

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Article ; Online: Pleckstrin homology domain-interacting protein (PHIP) as a marker and mediator of melanoma metastasis.

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Article: Pleckstrin homology domain-interacting protein (PHIP) as a marker and mediator of melanoma metastasis

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