Creissels (Aveyron). Rue de la Poudrière

Une étude de bâti rue de la Poudrière, au pied du château qui surplombe le bourg ancien de Creissels, sur la rive gauche du Tarn, en aval de Millau, a permis d’observer une maison en bordure de rue. Au rez-de-chaussée, deux baies géminées ouvrent, au-dessus d’un bandeau de tuf, sur cour. Elles ont été en partie comblées par la voûte sous laquelle a été ménagée une cave. Une porte ogivale, qui ouvre aujourd’hui sur la maison contiguë, y donnait accès. À l’étage, aujourd’hui partagé à mi-hauteu..

Bibliographie régionale

Galés Françoise. Bibliographie régionale. In: Archéologie du Midi médiéval. Tome 21, 2003. pp. 245-257

Bibliographie régionale

Galés Françoise. Bibliographie régionale. In: Archéologie du Midi médiéval. Tome 22, 2004. pp. 219-243

Bibliographie régionale

Galés Françoise. Bibliographie régionale. In: Archéologie du Midi médiéval. Tome 21, 2003. pp. 245-257

Bibliographie régionale

Galés Françoise. Bibliographie régionale. In: Archéologie du Midi médiéval. Tome 22, 2004. pp. 219-243

Les résidences de Gaston Fébus en Béarn

Gaston III, born in 1331 of the mariage between Aliénor de Comminges and Gaston II de Foix-Béarn, inherits the county of Foix-Béarn in 1343. He thereby finds himself at the head of two distinct territories: the viscounty of Béarn and the county of Foix, where he owns about ten castles. After a victory won over the count of Armagnac, his financial means are now sufficient and his power well-recognized; he undertakes therefore in the years 1374-75 an ambitious campaign of castle. The previous era had mostly witnessed the reinforcement of existing edifices, inherited primarily from the viscount of Béarn, Gaston VII Moncade. While the castles built in the 13th century essentially serve a defensive purpose, those build by Fébus rather destined to be places of residence. A centered leyout serves as model for these castles. Because this leyout was used systematically, being only adjusted according to contraints, it became archetypal. He leaves an architectural mark on the landsape of Béarn by imposing a distinctive architectural style, original style for the viscounty and directly associated with the name of the count.Gaston III, né en 1331 du mariage d’Aliénor de Comminges et de Gaston II de Foix-Béarn, hérite du comté de Foix-Béarn en 1343. Alors, il se trouve à la tête de deux territoires distincts: la vicomté de Béarn et le comté de Foix, dans lesquels il possède une dizaine de châteaux. Après une victoire remportée sur le comte d’Armagnac, ses moyens financiers s’avérant suffisants et sa puissance étant reconnue, il entreprend, dans les années 1374-75, une ambitieuse campagne de construction de châteaux, la période antérieure ayant vu la consolidation des édifices hérités pour la plupart du vicomte de Béarn, Gaston VII Moncade. Alors que les châteaux érigés au XIIIe siècle sont essentiellement dévolus à la défense, ceux élevés par Fébus sont davantage destinés à la résidence. Un plan centré, dit fébusien, leur sert de modèle. Par son usage systématique, modulé en fonction des contraintes, il est érigé en archétype. Il marque architecturalement le paysage béarnais en imposant un style distinctif, original pour la vicomté, directement associé au nom du comte.Galés Françoise. Les résidences de Gaston Fébus en Béarn. In: Archéologie du Midi médiéval. Supplément n°4, 2006. Résidences aristocratiques, résidences du pouvoir entre Loire et Pyrénées, Xe-XVe siècles. Recherches archéologiques récentes, 1987-2002. pp. 151-164

Estrogen receptors and endothelium.

International audienceEstrogens, and in particular 17beta-estradiol (E2), play a pivotal role in sexual development and reproduction and are also implicated in a large number of physiological processes, including the cardiovascular system. Both acetylcholine-induced and flow-dependent vasodilation are preserved or potentiated by estrogen treatment in both animal models and humans. Indeed, E2 increases the endothelial production of nitric oxide and prostacyclin and prevents early atheroma through endothelial-mediated mechanisms. Furthermore, whereas it prevents endothelial activation, E2 potentiates the ability of several subpopulations of the circulating or resident immune cells to produce proinflammatory cytokines. The balance between these 2 actions could determine the final effect in a given pathophysiological process. E2 also promotes endothelial healing, as well as angiogenesis. Estrogen actions are essentially mediated by 2 molecular targets: estrogen receptor-alpha (ERalpha) and ERbeta. The analysis of mouse models targeted for ERalpha or ERbeta demonstrated a prominent role of ERalpha in vascular biology. ERalpha directly modulates transcription of target genes through 2 activation functions (AFs), AF-1 and AF-2. Interestingly, an AF-1-deficient ERalpha isoform can be physiologically expressed in the endothelium and appears sufficient to mediate most of the vasculoprotective actions of E2. In contrast, AF-1 is necessary for the E2 actions in reproductive targets. Thus, it appears conceivable to uncouple the vasculoprotective and sexual actions with appropriate selective ER modulators

Endothelial estrogen receptor-alpha plays a crucial role in the atheroprotective action of 17beta-estradiol in low-density lipoprotein receptor-deficient mice.

International audienceBACKGROUND: The prevention of early atheroma by estrogens has been clearly demonstrated in all animal models and appears to be mediated through a direct action on the arterial wall rather than through an effect on the lipoprotein profile. The goal of the present study was to evaluate which cellular target is crucial in this beneficial action of estradiol. METHODS AND RESULTS: We first confirmed the key role of estrogen receptor-alpha (ERalpha) in the atheroprotective effect of estradiol, because this action was completely abolished in mice deficient in both the low-density lipoprotein receptor (LDLr) and ERalpha. Second, using chimeric mice with an ERalpha deficiency in the hematopoietic lineage, we showed the persistence of the protective action of estradiol, which suggests the involvement of extrahematopoietic ERalpha. Third, we showed that loxP-flanked ERalpha mice (ERalpha(flox/flox)) bred with Tie2-Cre(+) mice on an LDLr(-/-) background had complete inactivation of ERalpha in most hematopoietic and all endothelial cells. Remarkably, in this mouse model, the atheroprotective effect of estradiol was completely abolished. Fourth, the atheroprotective effect of estradiol remained abolished in Tie2-Cre(+) ERalpha(flox/flox) LDLr(-/-) mice transplanted with either Tie2-Cre(+) ERalpha(flox/flox) or ERalpha(-/-) bone marrow, whereas it was present in analogous chimeric Tie2-Cre(-) ERalpha(flox/flox) LDLr(-/-) receivers expressing endothelial ERalpha. CONCLUSIONS: We demonstrate directly and for the first time that endothelial ERalpha represents a key target of the atheroprotective effect of estradiol, whereas hematopoietic ERalpha is dispensable. Selective estrogen receptor modulators that mimic the endothelial action of estradiol should now be considered in atheroprotection

Activation function 2 (AF2) of estrogen receptor-α is required for the atheroprotective action of estradiol but not to accelerate endothelial healing

17β-Estradiol (E2) regulates estrogen receptor-α (ERα) target gene transcription through the two independent activation functions (AFs), AF1 and AF2, located in the N-terminal and ligand binding domain of ERα, respectively. We previously reported that ERα is required for the E2 atheroprotective action as well as for its accelerative action on endothelial healing, but its AF1 function is dispensable. Here, we investigated the role of ERαAF2 in these two major beneficial actions of E2 by electively targeting ERαAF2 (named ERαAF20). Our results prove four points. (i) Compared with WT ERα, the ability of ERαAF20 to stimulate the C3 complement or the estrogen response element-thymidine kinase promoter in two cell lines was dramatically decreased, confirming the importance of AF2 in the E2-induced transcriptional activity of ERα. (ii) The uterotrophic action of E2 was totally absent in ERαAF20 mice, showing the crucial role of ERαAF2 in E2-induced uterus hyperplasia. (iii) ERαAF2 was dispensable for the accelerative action of E2 on endothelial healing, underlining the functionality of ERαAF20 in vivo. (iv) Finally, the atheroprotective effect of E2 was abrogated in ERαAF20 LDL-r−/− mice. Thus, whereas ERαAF1 and ERαAF2 are both required for the uterotrophic action of E2, we show that only ERαAF2 is necessary for its atheroprotective effect

The transactivating function 1 of estrogen receptor α is dispensable for the vasculoprotective actions of 17β-estradiol

Full-length 66-kDa estrogen receptor α (ERα) stimulates target gene transcription through two activation functions (AFs), AF-1 in the N-terminal domain and AF-2 in the ligand binding domain. Another physiologically expressed 46-kDa ERα isoform lacks the N-terminal A/B domains and is consequently devoid of AF-1. Previous studies in cultured endothelial cells showed that the N-terminal A/B domain might not be required for estradiol (E2)-elicited NO production. To evaluate the involvement of ERα AF-1 in the vasculoprotective actions of E2, we generated a targeted deletion of the ERα A/B domain in the mouse. In these ERαAF-10 mice, both basal endothelial NO production and reendothelialization process were increased by E2 administration to a similar extent than in control mice. Furthermore, exogenous E2 similarly decreased fatty streak deposits at the aortic root from both ovariectomized 18-week-old ERαAF-1+/+ LDLr−/− (low-density lipoprotein receptor) and ERαAF-10 LDLr −/− mice fed with a hypercholesterolemic diet. In addition, quantification of lesion size on en face preparations of the aortic tree of 8-month-old ovariectomized or intact female mice revealed that ERα AF-1 is dispensable for the atheroprotective action of endogenous estrogens. We conclude that ERα AF-1 is not required for three major vasculoprotective actions of E2, whereas it is necessary for the effects of E2 on its reproductive targets. Thus, selective ER modulators stimulating ERα with minimal activation of ERα AF-1 could retain beneficial vascular actions, while minimizing the sexual effects