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Correction: The Long Non-Coding HOTAIR Is Modulated by Cyclic Stretch and WNT/β-CATENIN in Human Aortic Valve Cells and Is a Novel Repressor of Calcification Genes

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In Figures 3 and 4 of the published article, several mu (µ) and beta (β) symbols are represented by empty squares. Please view the correct figures below.

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Figure 3. WNT/β-CATENIN signaling modulates HOTAIR, ALPL, and BMP2 levels.

A. AVICs exposed to cyclic stretch have 39% increased β-CATENINmRNA levels as compared to static controls. N  =  6. B. Cyclin D1 (CCND1) levels were examined in stretched AVICs since it is a known WNT/β-CATENIN target gene. Stretched AVICs have 91% increasedCCND1 expression as compared to static controls. N  =  4. C. Treatment with WNT agonist is sufficient to repress HOTAIR by 50% as compared to DMSO treated controls. N  =  3. D and E. AVICs treated with WNT agonist have increased ALPL and BMP2, 87% and 9.5 fold respectively. N  =  3. *<p0.05, %p<0.0005, ∧p<0.0001.

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Figure 4. Proposed mechanism by which stretch-mediated repression of HOTAIR is involved in aortic valve calcification.

Reference

  1. 1. Carrion K, Dyo J, Patel V, Sasik R, Mohamed SA, et al. (2014) The Long Non-Coding HOTAIR Is Modulated by Cyclic Stretch and WNT/β-CATENIN in Human Aortic Valve Cells and Is a Novel Repressor of Calcification Genes. PLoS ONE 9(5): e96577