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Heart Self-Repair May be Prompted with Regulatory RNAs

저자:   업로드:2017-08-23  조회수:

    New research has discovered a potential means to trigger damaged heart cells to self-heal. The discovery could lead to groundbreaking forms of treatment for heart diseases.


    Heart tissue is notoriously poor at self-repair, but it isn’t entirely helpless. It’s just super-slow because mature, developed hearts retain very few heart cells that hold regeneration potential. For example, in adult mouse or human heart, new cardiomyocytes (CMs) are generated at rates of about 1%, not enough to repair damage from cardiovascular disease. But what if those rates could be increased? To explore this possibility, scientists based at A*STAR's Genome Institute of Singapore (GIS) and the National University Health System (NUHS) looked at cardiac cell subpopulations and how they differed in gene expression.


    The scientists examined CMs from mouse and human hearts, from both failing and nonfailing adult hearts, using single nuclear RNA-sequencing. The scientists found that in cardiac subpopulations, the upregulation of cell cycle activators and inhibitors consequent to the stress-response varied. In particular, the scientists found that two long noncoding ribonucleic acids (ncRNAs) appear to regulate genes controlling the ability of heart cells to undergo repair or regeneration.




    Details of this work appeared in the journal Nature Communications, in an article entitled “Single Cardiomyocyte Nuclear Transcriptomes Reveal a lincRNA-Regulated De-Differentiation and Cell Cycle Stress-Response In Vivo.” The article describes how the GIS and NUHS scientists used weighted gene co-expression network analysis to explore whether heterogeneity of the stress-response gene expression changes among the larger majority of cell cycle-arrested CMs would uncover a subpopulation that could be motivated to re-enter cell cycle.


    “We noted distinct sub-populations of CMs and uncovered gene regulatory networks specific for each sub-population, displaying specific sub-group upregulation of cell cycle, and de-differentiation genes in the disease stress response,” wrote the article’s authors. “We further identified LINCMs [long intergenic noncoding RNA in nuclei of CMs] that occupy key nodal hubs in gene regulatory networks, and validated that knockdown of nodal LINCMs (namely, Gas5 and Sghrt) leads to corresponding changes in the expression of co-regulated network genes, including those known to control CM cell cycle.”


    Essentially, the scientists discovered that a unique subpopulation of heart cells in diseased hearts activates gene programs related to heart cell division, uncovering the gene expression heterogeneity of diseased heart cells for the firs

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