Maria-Luz Alvarez Gonzalez

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Acute Suppression of Gonadotropin-Releasing Hormone Secretion by Insulin-Like Growth Factor I and Subproducts: An Age-Dependent Endocrine Effect

Neuroendocrinology (1993)

Jean-Pierre Bourguignon Arlette Gérard Maria-Luz Alvarez Gonzalez Paul Franchimont

Using rat hypothalamic explants, we showed previously that activation of N-methyl-D-aspartate (NMDA) receptors was involved in the mechanism of gonadotropin-releasing hormone (GnRH) secretion. (1–3)Insulin-like growth factor I (IGF-I), the N-terminal tripeptide of IGF-I, was suggested to be a possible antagonist at NMDA receptors. Here, we study the effects of IGF-I and its subproducts, (1–3)IGF-I and (4-70)IGF-I, either given in vivo as a single subcutaneous injection or used in vitro, on the secretion of GnRH by hypothalamic explants. At the three ages studied (15, 25 and 50 days), (4–70)IGF-I does not show any effect. At 50 days, the in vivo administration or the in vitro use of IGF-I results in a dose-related inhibition of the GnRH secretion induced by veratridine, a depolarizing agent. In addition, the spontaneous pulsatile secretion of GnRH in vitro is transiently suppressed after the in vivo administration of IGF-I. (1–3)IGF-I results in an inhibitory effect similar to that of IGF-I. At 25 days, IGF-I and (1-3)IGF-I show the same effects as at 50 days though higher concentrations are required. At 15 days, IGF-I does not show any effect whereas a potent inhibition of GnRH secretion is observed using (1–3)IGF-I either in vivo or in vitro. At all ages, the effects of (1–3)IGF-I parallel those of AP-5, a competitive antagonist at NMDA receptors. We conclude that the acute systemic administration of IGF-I results in a suppression of GnRH secretion, presumably through a competitive antagonism at NMDA receptors by (1–3)IGF-I resulting from IGF-I degradation, a process developing between 15 and 25 days of age.

10.1159/000126586

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Citations (44)

ADAMTS-1 Metalloproteinase Promotes Tumor Development through the Induction of a Stromal Reaction In vivo

Cancer Research (2008)

Natacha Rocks Geneviève Paulissen Florence Quesada‐Calvo Carine Munaut Maria-Luz Alvarez Gonzalez

Abstract ADAMTS-1 (a disintegrin and metalloproteinase with thrombospondin motifs), the first described member of the ADAMTS family, is differentially expressed in various tumors. However, its exact role in tumor development and progression is still unclear. The aim of this study was to investigate the effects of ADAMTS-1 transfection in a bronchial epithelial tumor cell line (BZR) and its potential to modulate tumor development. ADAMTS-1 overexpression did not affect in vitro cell properties such as (a) proliferation in two-dimensional culture, (b) proliferation in three-dimensional culture, (c) anchorage-independent growth in soft agar, (d) cell migration and invasion in modified Boyden chamber assay, (e) angiogenesis in the aortic ring assay, and (f) cell apoptosis. In contrast, ADAMTS-1 stable transfection in BZR cells accelerated the in vivo tumor growth after s.c. injection into severe combined immunodeficient mice. It also promoted a stromal reaction characterized by myofibroblast infiltration and excessive matrix deposition. These features are, however, not observed in tumors derived from cells overexpressing a catalytically inactive mutant of ADAMTS-1. Conditioned media from ADAMTS-1–overexpressing cells display a potent chemotactic activity toward fibroblasts. ADAMTS-1 overexpression in tumors was associated with increased production of matrix metalloproteinase-13, fibronectin, transforming growth factor β (TGF-β), and interleukin-1β (IL-1β). Neutralizing antibodies against TGF-β and IL-1β blocked the chemotactic effect of medium conditioned by ADAMTS-1–expressing cells on fibroblasts, showing the contribution of these factors in ADAMTS-1–induced stromal reaction. In conclusion, we propose a new paradigm for catalytically active ADAMTS-1 contribution to tumor development, which consists of the recruitment of fibroblasts involved in tumor growth and tumor-associated stroma remodeling. [Cancer Res 2008;68(22):9541–50]

ADAMTS

10.1158/0008-5472.can-08-0548

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Citations (67)

[Endometriosis: from research to clinical practice].

Michelle Nisolle Maria-Luz Alvarez Gonzalez María Cecilia Colombo Jean‐Michel Foidart

L'endometriose, definie par la presence ectopique de tissu endometrial, est une affection benigne responsable d'infertilite ou de douleurs pelviennes. Un diagnostic precoce base sur une anamnese minutieuse et un examen clinique bien conduit permet une prise en charge precoce. Le traitement medical n'est pas approprie dans tous les cas, faisant place a la coelioscopie operatoire dont la morbidite est en relation avec la severite de la lesion. L'implantation ectopique de cellules endometriales est possible grâce a des interactions complexes entre le tissu hote et les cellules epitheliales endometriales. Les conditions necessaires au developpement de l'endometriose sont une proliferation oestrogeno-dependante des cellules endometriales, une induction d'angiogenese et d'une lymphangiogenese. Les principaux acteurs cellulaires et moleculaires de l'angiogenese, de la lymphangiogenese, et de la fibrose doivent etre identifies afin de permettre le developpement de nouvelles strategies therapeutiques de l'endometriose.

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Laser-induced choroidal neovascularization model to study age-related macular degeneration in mice

Nature Protocols (2013)

Vincent Lambert Julie Lecomte Sylvain Hansen Silvia Blacher Maria-Luz Alvarez Gonzalez

Choroid

Immunostaining

Laser capture microdissection

10.1038/nprot.2013.135

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Citations (327)

Hipertensión arterial de reciente diagnóstico secundaria a síndrome de Cushing ectópico agudo: presentación de un caso

Hipertensión y Riesgo Vascular (2004)

S. Suárez Ortega Marie‐Béatrice Saade Maria-Luz Alvarez Gonzalez Amparo Castellano G. Bautista Suárez

10.1016/s1889-1837(04)71829-2

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MicroRNA-21 Exhibits Antiangiogenic Function by Targeting RhoB Expression in Endothelial Cells

PLoS ONE (2011)

Céline Sabatel Ludovic Malvaux Nicolas Bovy Christophe Deroanne Vincent Lambert

Background MicroRNAs (miRNAs) are endogenously expressed small non-coding RNAs that regulate gene expression at post-transcriptional level. The recent discovery of the involvement of these RNAs in the control of angiogenesis renders them very attractive in the development of new approaches for restoring the angiogenic balance. Whereas miRNA-21 has been demonstrated to be highly expressed in endothelial cells, the potential function of this miRNA in angiogenesis has never been investigated. Methodology/Principal Findings We first observed in endothelial cells a negative regulation of miR-21 expression by serum and bFGF, two pro-angiogenic factors. Then using in vitro angiogenic assays, we observed that miR-21 acts as a negative modulator of angiogenesis. miR-21 overexpression reduced endothelial cell proliferation, migration and the ability of these cells to form tubes whereas miR-21 inhibition using a LNA-anti-miR led to opposite effects. Expression of miR-21 in endothelial cells also led to a reduction in the organization of actin into stress fibers, which may explain the decrease in cell migration. Further mechanistic studies showed that miR-21 targets RhoB, as revealed by a decrease in RhoB expression and activity in miR-21 overexpressing cells. RhoB silencing impairs endothelial cell migration and tubulogenesis, thus providing a possible mechanism for miR-21 to inhibit angiogenesis. Finally, the therapeutic potential of miR-21 as an angiogenesis inhibitor was demonstrated in vivo in a mouse model of choroidal neovascularization. Conclusions/Significance Our results identify miR-21 as a new angiogenesis inhibitor and suggest that inhibition of cell migration and tubulogenesis is mediated through repression of RhoB.

RHOB

10.1371/journal.pone.0016979

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Citations (243)

Announcement

Neuroendocrinology (1993)

Diane F. Matesic John Germak E. Dupont Burra V. Madhukar Cristina Matera

10.1159/000126596

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<title>Multiple immunophenotyping at the single-cell level</title>

Proceedings of SPIE, the International Society for Optical Engineering/Proceedings of SPIE (1997)

Jean‐Michel Paulus André Gothot Jean‐Claude Grosdent Maria-Luz Alvarez Gonzalez Françoise Tassin

There is a growing interest for flow and image cytometry analytes permitting the simultaneous discrimination of 6-10 fluorochromes. We have derived a strategy to optimize the factors affecting the sensitivity and specificity of multiple immunofluorescence analysis. Following a spectrophotometric analysis of 14 fluorochromes conjugated to streptavidin (SA), a set of 7 spectrally separable SA- dyes and appropriate filter combinations were selected for evaluation in image cytometry. The SA-dyes were bound to latex particles labeled with biotinilated mIgG1 and the emissions of all fluorochromes detected by each filter combination were measured. The resulting crosstalk matrix served as the basic tool for final selection of dyes, design of optimal trichroic beamsplitter and filter combination, modulation of illumination and mathematical correction of residual spectral overlap. Using this strategy we demonstrated that latex-bound SA conjugates of Cascade Blue, Lucifer Yellow, FITC, R-PE, Red613, PerCP and APC could be discriminated. More recently we extended the applicability of the technique by analyzing blood cells bound to glass slides. The same field could be initially measured for autofluorescence and non-specific IgG binding and then remeasured for specific binding of lineage markers. The ability to use paired measurements of background and total fluorescence is a significant advantage of image over flow cytometry.

Cytometry

Immunofluorescence

Autofluorescence

10.1117/12.273637

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Tumoral and Choroidal Vascularization

American Journal Of Pathology (2007)

Maud Jost Catherine Maillard Julie Lecomte Vincent Lambert Marc Tjwa

Plasminogen activator inhibitor-1

Lewis lung carcinoma

10.2353/ajpath.2007.070074