Untreated Rat Cardiac Ventricular tissue Age
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ABSTRACT:
ORGANISM(S): Rattus rattus
PROVIDER: GSE272911 | GEO | 2025/09/02
REPOSITORIES: GEO
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Project description:LRAT knockout mice on vitamin A sufficient or deficient diets were compared to age and gender matched wildtype mice on a vitamin A sufficient diet RNA was isolated from the left ventricle of the heart and one array was run for each sample.
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Project description:The molecular mechanism underlying cardiac remodeling following exercise have been incompletely understood. Until now, most studies have been performed in rodents. We studied cardiac remodeling in the physiologically more relevant animal model, the swine. Microarray analysis was performed on animals that underwent either and exercise protocol or remained sedentary. RNA was isolated from tissue samples from the endocardial layer of the free wall of the left ventricle. RNA was isolated from 8 exercise-trained and 8 sedentary animals 4-5 weeks after start of the protocol. Each group contained 4 males and 4 females. Animals used for the study were 2-3 months old Yorkshire x Landrace swine. Only neutered males entered the study.
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Project description:The molecular mechanism underlying cardiac remodeling following exercise have been incompletely understood. Until now, most studies have been performed in rodents. We studied cardiac remodeling in the physiologically more relevant animal model, the swine. Microarray analysis was performed on animals that underwent either and exercise protocol or remained sedentary. RNA was isolated from tissue samples from the endocardial layer of the free wall of the left ventricle.
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Project description:Background. Ageing is one of the main risk factors of cardiovascular disease. Pericytes are capillary-associated mural cells involved in the maintenance and stability of the vascular network. In the heart, the consequences of ageing on cardiac pericytes are unknown. Methods. In this study, we have combined single nucleus RNA sequencing and histological analysis to determine the effects of ageing on cardiac pericytes. Furthermore, we have conducted in vivo and in vitro analysis of RGS5 loss of function and finally have perfomed pericytes-fibroblasts co-culture studies to understand the effect of RGS5 loss of function in pericytes on the neighbouring fibroblasts. Results. We showed that ageing reduces the pericyte area and coverage. Single nucleus RNA sequencing analysis further revealed that the expression of the Regulator of G protein signalling 5 (Rgs5) is reduced in old cardiac pericytes. In vivo and in vitro studies showed that the deletion of RGS5 induces morphological changes and a pro-fibrotic gene expression signature characterized by the expression of different extracellular matrix components and growth factors like TGFB2 and PDGFB in pericytes. Indeed, the culture of fibroblasts with the supernatant of RGS5 deficient pericytes induced their activation characterized by the increased expression of α smooth muscle actin in a TFGβ2 dependent mechanism. Conclusions. Our results identify RGS5 as a crucial regulator of pericyte function during cardiac ageing. The deletion of RGS5 causes cardiac dysfunction and induces myocardial fibrosis, one of the hallmarks of cardiac ageing.
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