Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Hypertension II: Pathophysiology01:29

Hypertension II: Pathophysiology

Hypertension is a chronic condition in which the blood's force against artery walls is excessively high, posing risks such as heart disease. The condition's underlying mechanisms involve complex interactions among the cardiovascular, kidney, and autonomic nervous systems.Renin-Angiotensin-Aldosterone System (RAAS): This system significantly influences blood pressure regulation. When blood pressure decreases, the kidneys secrete renin. This enzyme transforms angiotensinogen, a plasma protein,...
Peripheral Artery Disease I: Introduction01:30

Peripheral Artery Disease I: Introduction

Peripheral artery disease (PAD) predominantly results from atherosclerosis, which involves the accumulation of fatty deposits, or plaques, within the walls of arteries. This causes them to narrow and harden, significantly reducing blood flow. PAD predominantly affects the legs, particularly the arteries supplying the thighs and calves. In rare cases, it may involve other arteries, including those in the arms.Etiology of PAD:The principal cause of PAD is atherosclerosis, which results from fatty...
Treatment for Pulmonary Arterial Hypertension: Endothelin Receptor Antagonists01:18

Treatment for Pulmonary Arterial Hypertension: Endothelin Receptor Antagonists

Endothelins (ETs) are potent vasoactive peptides critical in the human body's various physiological and pathological processes. One of the most promising therapeutic strategies for treating pulmonary arterial hypertension (PAH) involves counteracting the effects of these endothelins using a class of drugs known as endothelin receptor antagonists.
ETs are synthesized through a complex sequence of enzymatic steps, primarily involving an enzyme referred to as endothelin-converting enzyme (ECE). Of...
Pulmonary Hypertension: Classification and Pathogenesis01:30

Pulmonary Hypertension: Classification and Pathogenesis

Pulmonary hypertension (PH) is a severe health condition in which the mean pulmonary arterial pressure increases to 25 mmHg or more, even when the body is at rest. This high pressure in the blood vessels that transport blood from the heart to the lungs can cause various symptoms, including shortness of breath, can lead to right heart failure, and significantly affect the overall quality of life.
There are various classifications for PH, each relating to different underlying causes and also...
Antihypertensive Drugs: Vasodilators01:23

Antihypertensive Drugs: Vasodilators

Vasodilators, primarily affecting the smooth muscles within arterial and venous walls, are commonly used for hypertension treatment. Medications such as minoxidil and hydralazine primarily target arteries and arterioles, while sodium nitroprusside acts on arterioles and venules. Minoxidil, functioning as a prodrug, is metabolized by hepatic sulfotransferase into its active form, minoxidil sulfate, after oral administration. This metabolite binds to the sulfonylurea receptor (SUR) component of...
Diabetic Nephropathy01:28

Diabetic Nephropathy

Definition Diabetic nephropathy is a chronic kidney complication that results from prolonged hyperglycemia.Prevalence It is the most common cause of chronic kidney disease (CKD) and end-stage renal disease (ESRD) worldwide, affecting up to half of individuals with diabetes.Pathophysiology • Sustained hyperglycemia triggers multiple hemodynamic and metabolic changes in the kidney. • Early in the disease, increased renal blood flow and glomerular hyperfiltration occur due to afferent arteriolar...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Barrierless proton and hydrogen atom migrations in photoionized benzaldehyde clusters result in benzyl alcohol formation: an ion-molecule perspective.

Physical chemistry chemical physics : PCCP·2026
Same author

Clinical failure of an extended-pulsed fidaxomicin regimen associated with emergence of a <i>Clostridioides difficile</i> isolate with reduced fidaxomicin susceptibility in an elderly man.

Antimicrobial agents and chemotherapy·2026
Same author

A comparative review of three cloud-based platforms for microbial whole genome sequencing analysis.

Antimicrobial stewardship & healthcare epidemiology : ASHE·2026
Same author

Copper (Cu) for Reducing Environmental Healthcare Associated Infections (CuRE HAI): A 10-year pragmatic copper surface implementation study.

American journal of infection control·2026
Same author

The Effects of Hypertension on Signaling Dynamics in Rare Renal Cell Types.

bioRxiv : the preprint server for biology·2026
Same author

Nephron-associated Support Cell Transcriptional Plasticity Expands in Hypertension.

bioRxiv : the preprint server for biology·2026

Related Experiment Video

Updated: May 30, 2026

Assessing Murine Resistance Artery Function Using Pressure Myography
07:25

Assessing Murine Resistance Artery Function Using Pressure Myography

Published on: June 7, 2013

Pin1 deficiency causes endothelial dysfunction and hypertension.

Valorie L Chiasson1, Nidhi Munshi, Piyali Chatterjee

  • 1Division of Nephrology & Hypertension, Department of Internal Medicine, Texas A&M Health Science Center College of Medicine, 702 SW HK Dodgen Loop, Temple, TX 76504, USA.

Hypertension (Dallas, Tex. : 1979)
|August 4, 2011
PubMed
Summary

Pin1 protein regulates endothelial NO synthase by enabling dephosphorylation at serine 116. This process is crucial for maintaining NO production, vascular function, and normal blood pressure.

More Related Videos

Precision Cut Lung Slices as an Efficient Tool for Ex vivo Pulmonary Vessel Structure and Contractility Studies
09:08

Precision Cut Lung Slices as an Efficient Tool for Ex vivo Pulmonary Vessel Structure and Contractility Studies

Published on: May 24, 2021

Assessing Endothelial Vasodilator Function with the Endo-PAT 2000
07:46

Assessing Endothelial Vasodilator Function with the Endo-PAT 2000

Published on: October 15, 2010

Related Experiment Videos

Last Updated: May 30, 2026

Assessing Murine Resistance Artery Function Using Pressure Myography
07:25

Assessing Murine Resistance Artery Function Using Pressure Myography

Published on: June 7, 2013

Precision Cut Lung Slices as an Efficient Tool for Ex vivo Pulmonary Vessel Structure and Contractility Studies
09:08

Precision Cut Lung Slices as an Efficient Tool for Ex vivo Pulmonary Vessel Structure and Contractility Studies

Published on: May 24, 2021

Assessing Endothelial Vasodilator Function with the Endo-PAT 2000
07:46

Assessing Endothelial Vasodilator Function with the Endo-PAT 2000

Published on: October 15, 2010

Area of Science:

  • Vascular Biology
  • Enzymology
  • Cardiovascular Physiology

Background:

  • Pin1 is a peptidyl prolyl cis-trans isomerase.
  • Endothelial NO synthase (eNOS) phosphorylation at serine 116 inhibits NO production.
  • Previous studies showed FK506 binding protein 12/12.6 deficiency impacts eNOS phosphorylation, endothelial dysfunction, and hypertension.

Purpose of the Study:

  • To investigate the role of Pin1 in regulating eNOS phosphorylation, vascular function, and blood pressure.
  • To test the hypothesis that Pin1 isomerizes phosphorylated eNOS serine 116, facilitating dephosphorylation and stimulating NO production.

Main Methods:

  • Immunoprecipitation of eNOS and probing for Pin1 in rat aortic endothelial cells.
  • Pin1 knockdown using small interfering RNA (siRNA) or inhibition with juglone.
  • Assessment of eNOS serine 116 phosphorylation, NO production, and vascular relaxation in isolated mouse aortas and in vivo studies with juglone-treated or Pin1 knockout mice.

Main Results:

  • Pin1 interacts with eNOS in rat aortic endothelial cells.
  • Pin1 knockdown or inhibition increased eNOS serine 116 phosphorylation and prevented vascular endothelial growth factor-induced dephosphorylation.
  • Acute and chronic inhibition or knockout of Pin1 led to increased eNOS serine 116 phosphorylation, endothelial dysfunction, and hypertension.

Conclusions:

  • Pin1 binds to eNOS and facilitates the dephosphorylation of serine 116.
  • This interaction increases NO production and endothelium-dependent dilation, contributing to blood pressure maintenance.
  • Pin1 plays a critical role in regulating vascular function and preventing hypertension.