Guo X, Kolpakov MA, Hooshdaran B, Schappell W, Wang T, Eguchi S, Elliott KJ, Tilley DG, Rao AK, Andrade-Gordon P, Bunce M, Madhu C, Houser SR, Sabri A
Cardiac Expression of Factor X Mediates Cardiac Hypertrophy and Fibrosis in Pressure Overload
J Am Coll Cardiol Basic Trans Science 2020;5:69–83.
In the above article, Figures 6 and 7 have been replaced due to the following errors:
In Figure 6, the original panel 6D was spliced. The splicing was not properly indicated in the figure, nor acknowledged in the text.
Correction: Panel 6D now shows full uncut gels for collagen III, TGF-β1, CTGF, and GAPDH.
Figure 6.
Interstitial Fibrosis, but not Perivascular Fibrosis, is Inhibited by Rivaroxaban Treatment Post-TAC
(A) Representative Masson trichrome staining shows exaggerated interstitial fibrosis in 3 weeks TAC versus sham mice, which was markedly suppressed by rivaroxaban treatment. Scale Bar: 100 μm. (B, C) Summary results for myocardial fibrosis area (B) and perivascular fibrosis area (C) (n = 5 each group). (D, E) (Top) Representative immunoblot analysis of sham and TAC hearts. (Bottom) Quantification of experiments represented as fold change compared to untreated sham normalized to GAPDH (n = 5 each group). (F) MMP2/9 activity in the left ventricle of sham and TAC mice treated with vehicle or rivaroxaban as determined by enzymatic activity assay. Results are expressed as RFU/min/mg protein (n = 5 for each group). Values are presented as mean ± SEM, ∗p < 0.05 vs. shams, †p < 0.05 vs. vehicle-treated TAC. Col. III = collagen type III; CTGF = connective tissue growth factor; MMP = matrix metalloprotease; TGF = transforming growth factor; TIMP = tissue inhibitor of metalloprotease; other abbreviations as in Figures 1 and 2.
In Figure 7, the gels in the original panel 7A were spliced. The splicing was not properly indicated in the figure, nor acknowledged in the text.
Correction: Panel 7A summarizes the results from 3 different Western blots. The revised panel 7A shows full uncut gels SM α-actin and GAPDH loading control lanes (upper panel) and for Col 1 and GAPDH (lower panel). The gels for TGF-B1 and GAPHD (middle panel) were cut to remove extraneous lanes. The areas of the gel that were cut are indicated with thin black lines, and the splicing is acknowledged in the text.
Also in Figure 7, the original Figure 7E mistakenly used the GAPD loading control lane from panel 7E.
Correction: Panel 7E now has the correct ERK loading control lane. The group data for panel 7E have been recalculated using the appropriate ERK loading control lane and are now shown in the right-hand side of panel 7E. The revised data analysis is similar to the original analysis of the group data and did not change the original interpretation of the findings in the original submission.
The figure legend for Figure 7 has also been changed. The correct figure legend should read as follows:
Figure 7.
FXa Induces Fibroblast Proliferation, Migration and Differentiation Through PAR-1
(A) This panel represents a composite of 3 different Western blots. Neonatal rat cardiac fibroblasts were pretreated with rivaroxaban (Riv., 0.5 μM) or vehicle for 15 min and then treated with FXa (100 nM) or thrombin (Thr., 1 U/ml) for 36 h and cell lysates were processed for immunoblot analysis. Left: Representative immunoblots for SM α-actin (upper panel), TGF-β1 (middle panel) and Col. I (lower panel). GAPDH was included as a loading control. The gel for TGF-β1 and the GAPDH loading control was spliced from the same gel exposure. The areas of the gel that were spliced are indicated with thin black lines. Right: Quantification of experiments represented as fold change compared to untreated control (Ctrl). (B) Migration scratch assay was performed to assess the rate of migration of cardiac fibroblasts untreated or treated with FXa or thrombin without or with rivaroxaban pretreatment. (C and D) A significant increase in the migration (C) and proliferation (D) rate was observed in FXa- and thrombin-treated fibroblasts compared with controls which was attenuated by rivaroxaban treatment. Scale bar: 200 μm. (E) Increased phosphorylation of Erk1/2 induced by FXa and Thrombin was lessened only by PAR1 antagonist SCH79797 (SHC), but not PAR2 antagonist GB83. (F and G) Improved migration and proliferation in FXa- and thrombin-treated cardiac fibroblasts were reduced by SCH79797, as counted from wound-scratch assays. Results are representative of 3 independent experiments. Data are mean ± SEM; ∗P < 0.05 vs. control; †P < 0.05 vs. treated fibroblasts.
The authors apologize for these errors.
The online version of the article has been corrected to reflect these changes.