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Related Experiment Video

Updated: May 10, 2026

An In Vitro 3D Model and Computational Pipeline to Quantify the Vasculogenic Potential of iPSC-Derived Endothelial Progenitors

An In Vitro 3D Model and Computational Pipeline to Quantify the Vasculogenic Potential of iPSC-Derived Endothelial Progenitors

Published on: May 13, 2019

Polymerase delta interacting protein 2 sustains vascular structure and function.

Roy L Sutliff¹, Lula L Hilenski, Angélica M Amanso

¹Department of Medicine, Division of Pulmonary and Critical Care Medicine, Atlanta Veterans Affairs Medical Center and Emory University School of Medicine, Decatur, GA, USA.

Arteriosclerosis, Thrombosis, and Vascular Biology

|July 5, 2013

Summary

Polymerase delta interacting protein 2 (Poldip2) knockdown reduces hydrogen peroxide (H2O2) production, increasing vascular stiffness and impairing contraction. Unaltered Poldip2 expression is vital for maintaining vascular integrity and function.

Keywords:

Nox4 Poldip2 blood vessel extracellular matrix hydrogen peroxide

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Last Updated: May 10, 2026

An In Vitro 3D Model and Computational Pipeline to Quantify the Vasculogenic Potential of iPSC-Derived Endothelial Progenitors

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Published on: November 1, 2024

Area of Science:

Vascular Biology
Biochemistry
Cardiovascular Research

Background:

Polymerase delta interacting protein 2 (Poldip2) is known to enhance NADPH oxidase 4 (Nox4) activity in vascular smooth muscle cells.
Reactive oxygen species (ROS) play a critical role in vascular homeostasis and disease.

Purpose of the Study:

To investigate the in vivo effects of Poldip2 knockdown on ROS production and vascular function.
To determine the role of Poldip2 in regulating vascular integrity and response to stimuli.

Main Methods:

Utilized Poldip2(+/-) mice due to the lethality of homozygous deletion.
Assessed Poldip2 mRNA and protein levels, NADPH oxidase activity, and aortic function (contractions, stiffness, compliance).
Examined collagen secretion in cultured vascular smooth muscle cells and evaluated protection against experimental aortic aneurysm.

Main Results:

Poldip2 knockdown reduced NADPH oxidase activity and hydrogen peroxide (H2O2) production in vivo.
Aortas from Poldip2(+/-) mice exhibited impaired contractions, increased stiffness, reduced compliance, disrupted elastic lamellae, and excessive extracellular matrix deposition.
Elevated collagen I secretion in Poldip2(+/-) vascular smooth muscle cells was dependent on ROS, and Poldip2(+/-) mice showed protection against experimental aortic aneurysm.

Conclusions:

Poldip2 knockdown leads to decreased H2O2 production, resulting in increased extracellular matrix deposition, enhanced vascular stiffness, and diminished agonist-mediated contraction.
Maintaining normal Poldip2 expression is essential for vascular integrity and proper physiological function.