Publications by authors named "Claudine Perret"
A major deleterious side effect of glucocorticoids is skin atrophy. Glucocorticoids activate the glucocorticoid and the mineralocorticoid (MR) receptor, both present in the epidermis. We hypothesized that glucocorticoid-induced epidermal atrophy may be related to inappropriate occupancy of MR by glucocorticoids.
View Article and Find Full Text PDFMineralocorticoid receptor (MR) activation may be deleterious to the cardiovascular system, and MR antagonists improve morbidity and mortality of patients with heart failure. However, mineralocorticoid signaling in the heart remains largely unknown. Using a pan-genomic transcriptomic analysis, we identified neutrophil gelatinase-associated lipocalin (NGAL or lipocalin 2) as a strongly induced gene in the heart of mice with conditional and targeted MR overexpression in cardiomyocytes (whereas induction was low in glucocorticoid receptor-overexpressing mice).
View Article and Find Full Text PDFPathophysiological aldosterone (aldo)/mineralocorticoid receptor signaling has a major impact on the cardiovascular system, resulting in hypertension and vascular remodeling. Mineralocorticoids induce endothelial dysfunction, decreasing vasorelaxation in response to acetylcholine and increasing the response to vasoconstrictors. Activation of the epidermal growth factor receptor (EGFR) is thought to mediate the vascular effects of aldo, but this has yet to be demonstrated in vivo.
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- The study investigates how maternal diabetes affects arterial structure, gene expression, and function in rat offspring before hypertension develops (at 3 months).
- No significant differences in the structure of the thoracic aorta were found between control and diabetic mother offspring, but the gene expression profile in diabetic offspring showed a notable underexpression of prostacyclin receptor, linked to reduced vasodilation capacity.
- The findings indicate that exposure to maternal hyperglycemia may lead to abnormal vascular programming in offspring, contributing to the risk of developing hypertension later on.
Article Synopsis
- Hypertension and chronic renal failure (CRF) lead to increased arterial stiffness, and the study aims to explore gene expression differences in the aorta between CRF patients and healthy controls.
- Analysis of aortic tissue using GeneChip Microarray revealed that CRF patients had 97 overexpressed transcripts, with a significant focus on the genes lumican (LUM) and ornithine decarboxylase (ODC1), which are linked to collagen regulation and cell growth.
- The findings suggest that early-stage CRF is associated with a unique aortic gene profile that may influence vascular smooth muscle cell behavior, highlighting potential pathways for further research in arterial health.
Article Synopsis
- SSAO-deficient mice show no significant changes in arterial structure, while treatment with semicarbazide (SCZ), an SSAO inhibitor, led to altered arterial phenotype in growing rats.
- After 6 weeks of SCZ treatment, SSAO activity was drastically reduced, and although lysyl oxidase was partially inhibited, significant arterial growth inhibition and increased stiffness were observed.
- SCZ treatment resulted in modifications to elastic fiber structure, reduced insoluble elastin, and increased extracellular proteins, suggesting that lysyl oxidase inhibition plays a key role in the vascular changes seen in treated rats.
Myocardial infarction causes neurohormonal activation involving aldosterone and angiotensin II (AngII). These hormones may increase arterial stiffness, an independent cardiovascular risk factor contributing to progression of congestive heart failure (CHF). This study aimed to determine the effect of aldosterone and AngII blockade on carotid artery distensibility and collagen density in adult Wistar rats with MI-induced CHF.
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