Lionheart LincRNA alleviates cardiac systolic dysfunction under pressure overload View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2020-08-13

AUTHORS

Yasuhide Kuwabara, Shuhei Tsuji, Masataka Nishiga, Masayasu Izuhara, Shinji Ito, Kazuya Nagao, Takahiro Horie, Shin Watanabe, Satoshi Koyama, Hisanori Kiryu, Yasuhiro Nakashima, Osamu Baba, Tetsushi Nakao, Tomohiro Nishino, Naoya Sowa, Yui Miyasaka, Takeshi Hatani, Yuya Ide, Fumiko Nakazeki, Masahiro Kimura, Yoshinori Yoshida, Tsukasa Inada, Takeshi Kimura, Koh Ono

ABSTRACT

Recent high-throughput approaches have revealed a vast number of transcripts with unknown functions. Many of these transcripts are long noncoding RNAs (lncRNAs), and intergenic region-derived lncRNAs are classified as long intergenic noncoding RNAs (lincRNAs). Although Myosin heavy chain 6 (Myh6) encoding primary contractile protein is down-regulated in stressed hearts, the underlying mechanisms are not fully clarified especially in terms of lincRNAs. Here, we screen upregulated lincRNAs in pressure overloaded hearts and identify a muscle-abundant lincRNA termed Lionheart. Compared with controls, deletion of the Lionheart in mice leads to decreased systolic function and a reduction in MYH6 protein levels following pressure overload. We reveal decreased MYH6 results from an interaction between Lionheart and Purine-rich element-binding protein A after pressure overload. Furthermore, human LIONHEART levels in left ventricular biopsy specimens positively correlate with cardiac systolic function. Our results demonstrate Lionheart plays a pivotal role in cardiac remodeling via regulation of MYH6. More... »

PAGES

434

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/s42003-020-01164-0

DOI

http://dx.doi.org/10.1038/s42003-020-01164-0

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1130064523

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/32792557


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