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Song, et al.'s"Deep RNA Sequencing Reveals Novel Cardiac Transcriptomic Signatures for Physiological and Pathological Hypertrophy"

Figure 1

This figure provides an overview of quantities of genes that differ within and between different experimental groups of mice (notably between PAH and PHH models), and how these genes were differentially expressed. Information reported therein was obtained through high-throughput RNA sequencing of cardiac cells from three different mice in each model.

Part A of this figure provides a visual representation of the differentially expressed genes, within the cardiac tissue of each of four experimental groups of mice. Within sham mice, for example (upper left Venn diagram), different numbers of genes were expressed in different individuals (labeled Sham 1, 2 and 3, with corresponding circle color and numbers of genes expressed); the number of genes expressed in common to all of those individuals in shown in the middle of the corresponding Venn diagram where all circles overlap. This panel visualized the relatively high similarity of gene expression within experimental groups.

    Part B of figure 1 provides general comparisons of DEGs between experimental groups, summarizing the two most relevant group comparisons of sham versus TAC (PAH), and sedentary versus exercise (PHH; top and middle rows respectively).
    Boxes including "filtered gene sets" (filtered to include genes appearing at RPKM ≥ 2) note the numbers of genes expressed in both groups combined in the corresponding comparison. Differentially expressed genes between the two groups of a comparison, subdivided into up-regulated (Up) or down-regulated (Down) genes in in each comparison are noted in the third column. Notably, 70% of the DEGs were up-regulated in the PAH comparison while 73% of DEGs were down-regulated in the PHH comparison.
     Of these 2045 different DEGs in PAH and PHH models (accounting for overlap in genes expressed), a fraction (83) were regulated in the same fashion (e.g. up-regulated in both the PAH and PHH model). The genes of opposite regulation were of interest and explored further in the study, as those were taken as the most likely candidates for contributors to the differential tissue health in PAH versus PHH.

This figure provides only an overview of the information found in the study; further analyses of patterns among the expressed genes is necessary to identify meaningful interactions. This further analysis begins in Figure 2.

Introduction

Proceed to Figure 2

Table 1

Figure 3

Figure 4

References

Cha H, Kim JM, Oh JG, Jeong MH, Park CS, Park J, Jeong HJ, Park BK, Lee YH, Jeong D, Yang DK, Bernecker OY, Kim do H, Hajjar RJ, Park WJ. (2008). PICOT is a critical regulator of cardiac hypertrophy and cardiomyocyte contractility. Journal of Molecular and Cellular Cardiology, 45(6), 796-803.

Song, H. K., Hong, S. E., Kim, T., Kim D. H., et al. (2012). Deep RNA sequencing reveals novel cardiac transcriptomic signatures for physiological and pathological hypertrophy. PLoS One, 7, e35552.

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