NDLI: Vascular Smooth Muscle Cell–Selective Peroxisome Proliferator–Activated Receptor-γ Deletion Leads to Hypotension

Please wait, while we are loading the content...

Vascular Smooth Muscle Cell–Selective Peroxisome Proliferator–Activated Receptor-γ Deletion Leads to Hypotension

Content Provider	Scilit
Author	D'alecy, Louis G. Chang, Lin Villacorta, Luis Zhang, Jifeng Garcia-Barrio, Minerva T. Yang, Kun Hamblin, Milton Whitesall, Steven E. Chen, Y. Eugene
Copyright Year	2009
Description	Journal: Circulation Background— Peroxisome proliferator–activated receptor-γ (PPARγ) agonists are commonly used to treat diabetes, although their PPARγ-dependent effects transcend their role as insulin sensitizers. Thiazolidinediones lower blood pressure (BP) in diabetic patients, whereas results from conventional/tissue-specific PPARγ experimental models suggest an important pleiotropic role for PPARγ in BP control. Little evidence is available on the molecular mechanisms underlying the role of vascular smooth muscle cell–specific PPARγ in basal vascular tone. Methods and Results— We show that vascular smooth muscle cell–selective deletion of PPARγ impairs vasoactivity with an overall reduction in BP. Aortic contraction in response to norepinephrine is reduced and vasorelaxation is enhanced in response to β-adrenergic receptor (β-AdR) agonists in vitro. Similarly, vascular smooth muscle cell–selective PPARγ knockout mice display a biphasic response to norepinephrine in BP, reversible on administration of β-AdR blocker, and enhanced BP reduction on treatment with β-AdR agonists. Consistent with enhanced β2-AdR responsiveness, we found that the absence of PPARγ in vascular smooth muscle cells increased β2-AdR expression, possibly leading to the hypotensive phenotype during the rest phase. Conclusion— These data uncovered the β2-AdR as a novel target of PPARγ transcriptional repression in vascular smooth muscle cells and indicate that PPARγ regulation of β2-adrenergic signaling is important in the modulation of BP.
Related Links	https://www.ahajournals.org/doi/pdf/10.1161/CIRCULATIONAHA.108.815803 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2829656/pdf
Ending Page	2169
Page Count	9
Starting Page	2161
ISSN	00097322
e-ISSN	15244539
DOI	10.1161/circulationaha.108.815803
Journal	Circulation
Issue Number	16
Volume Number	119
Language	English
Publisher	Ovid Technologies (Wolters Kluwer Health)
Publisher Date	2009-04-28
Access Restriction	Open
Subject Keyword	Journal: Circulation Peripheral Vascular Disease Vascular Smooth Muscle Cells Β2-adrenergic Receptor Conditional Null Mice
Content Type	Text
Resource Type	Article
Subject	Physiology (medical) Cardiology and Cardiovascular Medicine

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

Vascular smooth muscle cell-selective peroxisome proliferator-activated receptor-gamma deletion leads to hypotension.

Bcr Kinase Activation by Angiotensin II Inhibits Peroxisome Proliferator-Activated Receptor γ Transcriptional Activity in Vascular Smooth Muscle Cells

Peroxisome Proliferator-Activated Receptor Gamma Activators Inhibit Gene Expression and Migration in Human Vascular Smooth Muscle Cells

Rescue of Cardiomyopathy in Peroxisome Proliferator-Activated Receptor-α Transgenic Mice by Deletion of Lipoprotein Lipase Identifies Sources of Cardiac Lipids and Peroxisome Proliferator-Activated Receptor-α Activators

Pannexin1 Regulates α1-Adrenergic Receptor– Mediated Vasoconstriction

Regulation of Peroxisome Proliferator–Activated Receptor-γ by Angiotensin II Via Transforming Growth Factor-β1–Activated p38 Mitogen-Activated Protein Kinase in Aortic Smooth Muscle Cells

Mice With Cardiac Overexpression of Peroxisome Proliferator–Activated Receptor γ Have Impaired Repolarization and Spontaneous Fatal Ventricular Arrhythmias

Vascular smooth muscle cell-selective PPARγ deletion leads to hypotension

Interference With Peroxisome Proliferator-Activated Receptor-γ in Vascular Smooth Muscle Causes Baroreflex Impairment and Autonomic Dysfunction

Vascular Smooth Muscle Cell–Selective Peroxisome Proliferator–Activated Receptor-γ Deletion Leads to Hypotension

Similar Documents

Vascular smooth muscle cell-selective peroxisome proliferator-activated receptor-gamma deletion leads to hypotension.

Bcr Kinase Activation by Angiotensin II Inhibits Peroxisome Proliferator-Activated Receptor γ Transcriptional Activity in Vascular Smooth Muscle Cells

Peroxisome Proliferator-Activated Receptor Gamma Activators Inhibit Gene Expression and Migration in Human Vascular Smooth Muscle Cells

Rescue of Cardiomyopathy in Peroxisome Proliferator-Activated Receptor-α Transgenic Mice by Deletion of Lipoprotein Lipase Identifies Sources of Cardiac Lipids and Peroxisome Proliferator-Activated Receptor-α Activators

Pannexin1 Regulates α1-Adrenergic Receptor– Mediated Vasoconstriction

Regulation of Peroxisome Proliferator–Activated Receptor-γ by Angiotensin II Via Transforming Growth Factor-β1–Activated p38 Mitogen-Activated Protein Kinase in Aortic Smooth Muscle Cells

Mice With Cardiac Overexpression of Peroxisome Proliferator–Activated Receptor γ Have Impaired Repolarization and Spontaneous Fatal Ventricular Arrhythmias

Vascular smooth muscle cell-selective PPARγ deletion leads to hypotension

Interference With Peroxisome Proliferator-Activated Receptor-γ in Vascular Smooth Muscle Causes Baroreflex Impairment and Autonomic Dysfunction

Vascular Smooth Muscle Cell–Selective Peroxisome Proliferator–Activated Receptor-γ Deletion Leads to Hypotension