ArticleArteriosclerosis, thrombosis, and vascular biology2010
Bioinformatic analysis of gene sets regulated by ligand-activated and dominant-negative peroxisome proliferator-activated receptor gamma in mouse aorta.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
22 citing papers in PubMed, 26 citations in OpenAlex.
- Roles of the peroxisome proliferator-activated receptors (PPARs) in the pathogenesis of diabetic kidney disease (DKD).Cell death discovery · 2026Review
- The 2023 Walter B. Cannon Award Lecture: Mechanisms Regulating Vascular Function and Blood Pressure by the PPARγ-RhoBTB1-CUL3 Pathway.Function (Oxford, England) · 2024Review
- Role of the Peroxisome Proliferator Activated Receptors in Hypertension.Circulation research · 2021Review
- PPARγ and RhoBTB1 in hypertension.Current opinion in nephrology and hypertension · 2020Review
- RhoBTB1 protects against hypertension and arterial stiffness by restraining phosphodiesterase 5 activity.The Journal of clinical investigation · 2019Article
- PPARγ and retinol binding protein 7 form a regulatory hub promoting antioxidant properties of the endothelium.Physiological genomics · 2017Review
- Hypertension-Causing Mutation in Peroxisome Proliferator-Activated Receptor γ Impairs Nuclear Export of Nuclear Factor-κB p65 in Vascular Smooth Muscle.Hypertension (Dallas, Tex. : 1979) · 2017Article
- Retinol-binding protein 7 is an endothelium-specific PPARJCI insight · 2017Article
- Nervous System Expression of PPARγ and Mutant PPARγ Has Profound Effects on Metabolic Regulation and Brain Development.Endocrinology · 2016Article
- Effect of selective expression of dominant-negative PPARγ in pro-opiomelanocortin neurons on the control of energy balance.Physiological genomics · 2016Article
- Protective Role for Tissue Inhibitor of Metalloproteinase-4, a Novel Peroxisome Proliferator-Activated Receptor-γ Target Gene, in Smooth Muscle in Deoxycorticosterone Acetate-Salt Hypertension.Hypertension (Dallas, Tex. : 1979) · 2016Article
- Endothelial PPAR-γ protects against vascular thrombosis by downregulating P-selectin expression.Arteriosclerosis, thrombosis, and vascular biology · 2015Article
- Role of vascular smooth muscle PPARγ in regulating AT1 receptor signaling and angiotensin II-dependent hypertension.PloS one · 2014Article
- Dominant negative PPARγ promotes atherosclerosis, vascular dysfunction, and hypertension through distinct effects in endothelium and vascular muscle.American journal of physiology. Regulatory, integrative and comparative physiology · 2013Article
- Pioglitazone attenuates valvular calcification induced by hypercholesterolemia.Arteriosclerosis, thrombosis, and vascular biology · 2013Article
- PPARγ regulates resistance vessel tone through a mechanism involving RGS5-mediated control of protein kinase C and BKCa channel activity.Circulation research · 2012Article
- Cullin-3 regulates vascular smooth muscle function and arterial blood pressure via PPARγ and RhoA/Rho-kinase.Cell metabolism · 2012Article
- A second chance for a PPARγ targeted therapy?Circulation research · 2012Article
- The nuclear hormone receptor PPARγ counteracts vascular calcification by inhibiting Wnt5a signalling in vascular smooth muscle cells.Nature communications · 2012Article
- Disruption of endothelial peroxisome proliferator-activated receptor γ accelerates diet-induced atherogenesis in LDL receptor-null mice.Arteriosclerosis, thrombosis, and vascular biology · 2012Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
objectiveDrugs that activate peroxisome proliferator-activated receptor (PPAR) gamma improve glucose sensitivity and lower blood pressure, whereas dominant-negative mutations in PPARgamma cause severe insulin resistance and hypertension. We hypothesize that these PPARgamma mutants regulate target genes opposite to those of ligand-mediated activation, and we tested this hypothesis on a genomewide scale. METHODS AND
resultsWe integrated gene expression data in aorta specimens from mice treated with the PPARgamma ligand rosiglitazone with data from mice containing a globally expressed knockin of the PPARgamma P465L dominant-negative mutation. We also integrated our data with publicly available data sets containing the following: (1) gene expression profiles in many human tissues, (2) PPARgamma target genes in 3T3-L1 adipocytes, and (3) experimentally validated PPARgamma binding sites throughout the genome. Many classic PPARgamma target genes were induced by rosiglitazone and repressed by dominant-negative PPARgamma. A similar pattern was observed for about 90% of the gene sets regulated by both rosiglitazone and dominant-negative PPARgamma. Genes exhibiting this pattern of contrasting regulation were significantly enriched for nearby PPARgamma binding sites.
conclusionsThese results provide convincing evidence that the PPARgamma P465L mutation causes transcriptional effects that are opposite to those mediated by PPARgamma ligand, thus validating mice carrying the mutation as a model of PPARgamma interference.
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