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Proceedings of the National Academy of Sciences of the United States of America logoLink to Proceedings of the National Academy of Sciences of the United States of America
. 2018 Apr 2;115(16):E3858–E3861. doi: 10.1073/pnas.1804573115

Correction for Li et al., Regulator of G protein signaling 5 protects against cardiac hypertrophy and fibrosis during biomechanical stress of pressure overload

PMCID: PMC5910882  PMID: 29610326

MEDICAL SCIENCES Correction for “Regulator of G protein signaling 5 protects against cardiac hypertrophy and fibrosis during biomechanical stress of pressure overload,” by Hongliang Li, Chengwei He, Jinhua Feng, Yan Zhang, Qizhu Tang, Zhouyan Bian, Xue Bai, Heng Zhou, Hong Jiang, Scott P. Heximer, Mu Qin, He Huang, Peter. P. Liu, and Congxin Huang, which was first published July 19, 2010; 10.1073/pnas.1008397107 (Proc Natl Acad Sci USA 107:13818–13823).

The authors wish to note the following: “The representative images in Fig. 1A, Fig. 4B, and Fig. S1C appeared incorrectly. Original data for the entire study was available and used to correct the figures. These errors do not affect any conclusions in the paper. We sincerely apologize for the mistake and inconvenience we may have caused.” The corrected Fig. 1, Fig. 4, and Fig. S1 appear below, with their respective legends. The SI has been updated online.

Fig. 1.

Fig. 1.

The effects of Rgs5 on cardiac hypertrophy. (A and B) Gross heart and WGA-FITC and HE staining of sham and AB mice at 4 wk after surgery in TG and WT mice (A) and in Rgs5−/− and Rgs5+/+ mice (B). Analysis of hypertrophic markers in TG and WT mice (C) and in Rgs5−/− and Rgs5+/+ mice (D). Total RNA was isolated from hearts of mice of the indicated groups, and expression of transcripts for ANP, BNP, and β-MHC induced by AB were determined by real-time PCR analysis. Data represent typical results of three to four different experiments as mean ± SEM (n = 4–11 mice per group). *P < 0.01 for WT/sham; #P < 0.01 for WT/AB after AB.

Fig. 4.

Fig. 4.

Inhibition of MEK-ERK1/2 signaling rescued abnormalities in Rgs5−/− mice. (A) U0126 blocked MEK1/2 and ERK1/2 phosphorylation mediated by AB in Rgs5−/− mice. (B) Effects of U0126 on histological changes at 2 wk after surgery. (C) The effects of U0126 on fibrosis. Left, PSR staining; Right, statistical results of fibrotic areas. (D) The effects of U0126 on hypertrophic and fibrotic markers expression induced by AB in Rgs5−/− mice. mRNA was determined by real-time PCR analysis. Data represent typical results of three to five different experiments as mean ± SEM (n = 4–12 mice/per group). *P < 0.01 for PBS/sham values; #P < 0.01 for PBS/AB after AB.

Fig. S1.

Fig. S1.

Characterization of human Rgs5 transgenic mice. (A) Representative Western blots of human Rgs5 protein in the heart tissue from four lines of TG and WT mice. (B) Representative Western blot of human Rgs5 protein from different tissue of TG mice as indicated (A, lung; B, muscle; C, brain; D, heart; E, kidney; F, spleen; G, liver; H, testis). (C and D) Representative Western blots and quantitative results of endogenous Rgs5 protein levels in the heart from WT and TG mice after AB at time points indicated (n = 7). *P < 0.01 for 0 d group.


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