{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Punapart M"],"funding":["Eye Hope Foundation","Estonian Research Council","CELSA","European Regional Development Fund"],"pagination":["827"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10137641"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["14(4)"],"pubmed_abstract":["Biallelic mutations in the gene encoding WFS1 underlie the development of Wolfram syndrome (WS), a rare neurodegenerative disorder with no available cure. We have previously shown that <i>Wfs1</i> deficiency can impair the functioning of the renin-angiotensin-aldosterone system (RAAS). The expression of two key receptors, angiotensin II receptor type 2 (<i>Agtr2</i>) and bradykinin receptor B1 (<i>Bdkrb1</i>), was downregulated both in vitro and in vivo across multiple organs in a rat model of WS. Here, we show that the expression of key RAAS components is also dysregulated in neural tissue from aged WS rats and that these alterations are not normalized by pharmacological treatments (liraglutide (LIR), 7,8-dihydroxyflavone (7,8-DHF) or their combination). We found that the expression of an"],"journal":["Genes"],"pubmed_title":["Chronic Stress Alters Hippocampal Renin-Angiotensin-Aldosterone System Component Expression in an Aged Rat Model of Wolfram Syndrome."],"pmcid":["PMC10137641"],"funding_grant_id":["SJD90","2014-2020.4.01.15-0012","PSG471"],"pubmed_authors":["Gaur N","Kirillov S","Jagomae T","Plaas M","Seppa K","Reimets R","Punapart M","Eskla KL","Vasar E"],"additional_accession":[]},"is_claimable":false,"name":"Chronic Stress Alters Hippocampal Renin-Angiotensin-Aldosterone System Component Expression in an Aged Rat Model of Wolfram Syndrome.","description":"Biallelic mutations in the gene encoding WFS1 underlie the development of Wolfram syndrome (WS), a rare neurodegenerative disorder with no available cure. We have previously shown that <i>Wfs1</i> deficiency can impair the functioning of the renin-angiotensin-aldosterone system (RAAS). The expression of two key receptors, angiotensin II receptor type 2 (<i>Agtr2</i>) and bradykinin receptor B1 (<i>Bdkrb1</i>), was downregulated both in vitro and in vivo across multiple organs in a rat model of WS. Here, we show that the expression of key RAAS components is also dysregulated in neural tissue from aged WS rats and that these alterations are not normalized by pharmacological treatments (liraglutide (LIR), 7,8-dihydroxyflavone (7,8-DHF) or their combination). We found that the expression of an","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Mar","modification":"2025-04-18T17:33:39.226Z","creation":"2024-11-14T12:01:59.666Z"},"accession":"S-EPMC10137641","cross_references":{"pubmed":["37107585"],"doi":["10.3390/genes14040827"]}}