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. 2016 Feb 27;15:41. doi: 10.1186/s12944-016-0211-x

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© Kwon et al. 2016

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 3 — Prox1 plays a crucial role in the regulation of triglycerides in HepG2 cells. a HepG2 cells were transfected with siRNA against Prox1 mRNA (siProx1) or control siRNA (siCTR). After 48 h, cells were treated with or without rapamycin for additional 48 h. Phosphorylated mTOR (p-mTOR) was detected to confirm the inhibitory effect of rapamycin. mTOR and β-actin were measured as quantitative controls. b Total lipids were harvested from HepG2 cells manipulated as (a). siC and siP indicate control siRNA and siProx1, respectively. TG: triglycerides, Cho: cholesterol. c The amount of relative triglycerides compared with cholesterol was also increased by siProx1 as well as rapamycin and was statistically significant (p < 0.05). d HepG2 cells were transfected with a plasmid expressing human Prox1 or an empty plasmid. After 24 h, cells were treated with or without rapamycin for additional 48 h. R and D indicate rapamycin and DMSO, respectively. e TLC analysis using (d) samples. TG: triglycerides, Cho: cholesterol. f The relative analysis shows that the increase in triglycerides caused by rapamycin was significantly down-regulated by Prox1 over-expression (p < 0.05)