Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2021 Apr 27;129(1):63–77. doi: 10.1161/CIRCRESAHA.120.318501

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© 2021 The Authors.

Circulation Research is published on behalf of the American Heart Association, Inc., by Wolters Kluwer Health, Inc. This is an open access article under the terms of the Creative Commons Attribution Non-Commercial-NoDerivs License, which permits use, distribution, and reproduction in any medium, provided that the original work is properly cited, the use is noncommercial, and no modifications or adaptations are made.

This article is made available via the PMC Open Access Subset for unrestricted re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the COVID-19 pandemic or until permissions are revoked in writing. Upon expiration of these permissions, PMC is granted a perpetual license to make this article available via PMC and Europe PMC, consistent with existing copyright protections.

PMC Copyright notice

Figure 5. — Endothelial cell (EC)–specific Prdm (positive regulatory domain-containing protein) 16 deficiency causes impaired EC-dependent relaxation upon hindlimb ischemia. A–C, Schematic representation (A) and quantification of phenylephrine (PE)-mediated absolute contraction (AC) in femoral artery (FA) segments of the ligated (L) and unligated (UL) side 3 d after FA ligation (FAL) in Prdm16^+/+ (n=7) or Prdm16^+/− (n=5–6) mice (B) and long-term EC-Prdm16^+/+ (n=3–5) or EC-Prdm16^−/⁻ (n=4–5) mice (C). D–F, Schematic representation (D) and quantification of relative EC-dependent relaxation upon administration of acetylcholine (ACh) in FA segments at d 3 after FAL in Prdm16^+/+ (n=7) or Prdm16^+/− (n=5–6) mice (E) and long-term EC-Prdm16^+/+ (n=3–5) or EC-Prdm16^−/− (n=4–5) mice (F). G–I, Schematic representation (G) and quantification of relative EC-independent relaxation upon administration of diethylamine NONOate (DEANO) in FA segments at d 3 after FAL in Prdm16^+/+ (n=7) or Prdm16^+/− (n=5–6) mice (H) and long-term EC-Prdm16^+/+ (n=3–5) or EC-Prdm16^−/− (n=4–5) mice (I). Data represent mean±SEM. *P<0.05: vs indicated condition (significance is only indicated in case of a differential genotypic response to FAL; Table III in the Data Supplement). M in (B, C, E, F, H, I) indicates molar.