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 Jan 14;11:1468. doi: 10.1038/s41598-020-80882-1

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

© The Author(s) 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

PMC Copyright notice

Mitochondrial ROS stabilize HIF-1α and drive HIF-1α-dependent proliferation in shunt LECs. (A) HIF-1α protein is significantly stabilized in sheared (s) control LECs compared with non-sheared (ns) controls; treatment of sheared control LECs with a mitochondrially targeted antioxidant mitoquinone (s + MQ) abrogates HIF-1α protein stabilization, *, P < 0.05, N = 3 control no shear compared with 3 control + shear; †, P < 0.05, N = 3 control + shear compared with 3 control + shear + MQ; (B) Treatment of shunt LECs with MQ abrogates HIF-1α expression but does not with triphenylphosphonium (TPP), a lipophilic cationic control; NB, each lane is a pooled sample of 3 distinct shunt LEC lines. (C) At 72hrs, treatment of shunt LECs with MQ (angled line bar) slows proliferation to the level observed in control LECs, P > 0.05, whether untreated, + MQ, or + TPP (white, speckled, and inverted caret bars, respectively); *, P < 0.05 compared to untreated shunt LECs (black bar). Treatment of shunt LECs with TPP (solid gray bar) does not change proliferation compared to untreated shunt LECs (black bar), and remains significantly faster than control LECs or shunt LECs treated with MQ, #, P < 0.05. N = 3 control, 3 shunt, for each condition: untreated, + TPP, and + MQ. NB, cell counts normalized to baseline 24 hr timepoint. (D) Knockdown of HIF-1α in shunt LECs (angled line bars) slows proliferation to levels observed in scramble treated controls (white bars), *, P < 0.05 comparing scramble treated control and shunt LECs, or scramble treated shunt LECs and siHIF-1α treated shunt LECs; N = 3 control + scr, 3 shunt + scr, 3 shunt + siHIF-1α. In panels A, C and D, error bars represent standard deviation. For panels A and B, full-length blots/gels are presented in Supplemental Fig. 6.