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Series GSE73597 Query DataSets for GSE73597
Status Public on Nov 01, 2015
Title miRNA-99 family diverges physiological cardiac hypertrophy to pathological cardiac hypertrophy
Organism Rattus norvegicus
Experiment type Non-coding RNA profiling by high throughput sequencing
Summary Purpose: The physiological cardiac hypertrophy is an adaptive condition that does not associate with myocyte cell death while pathological hypertrophy is a maladaptive condition associated with myocyte cell death. Alpha-2 macroglobulin (α-2M) an acute phase protein induces cardiac hypertrophy via the ERK1,2 and PI3K/Akt signaling. This study is aimed at exploring the miRNome of α-2M induced hypertrophied cardiomyocytes and to understand the role of miRNAs in determination of pathological and physiological hypertrophy.
Methods: Hypertrophy was induced in H9c2 cardiomyoblasts using alpha-2 macroglobulin. The induction of hypertrophy is confirmed by microscopy and gene expression studies. Subsequently, the total RNA was isolated and small RNA sequencing was executed in Illumina HiSeq 2000.
Results: Analysis of small RNA reads revealed the differential expression of a large set of miRNAs during hypertrophy. Among the differentially expressed candidates, miR-99 family (miR-99a, miR-99b and miR-100) showed significant downregulation upon α-2M treatment while isoproterenol treatment (pathological hypertrophy) upregulated their expression. The binding site for Egr1 transcription factor was identified in the promoter region of miR-99 family, and interestingly all miRNAs with Egr1 binding site proven by ChIP-Seq were downregulated during physiological hypertrophy
Conclusions: The results proved Egr-1 mediated regulation of miR-99 family determines the uniqueness of pathological and physiological hypertrophy. Upregulated miR-99 expression during pathological hypertrophy suggests that it can be a valuable diagnostic marker and potential therapeutic target for cardiac hypertrophy and heart failure.
 
Overall design Small RNA profiles of control and hypertrophied cardiomyocyte H9c2 cells were generated by deep sequencing using Illumina HiSeq 2000
 
Contributor(s) Ramasamy S, Velmurugan G
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Submission date Sep 30, 2015
Last update date May 15, 2019
Contact name Subbiah Ramasamy
E-mail(s) subbiahr@nrcbsmku.org
Phone +914522458220
Organization name Madurai Kamaraj University
Department Molecular Biology
Lab Cardiac Hypertrophy Laboratory
Street address Palkalainagar
City Madurai
State/province Tamilnadu
ZIP/Postal code 625021
Country India
 
Platforms (1)
GPL14844 Illumina HiSeq 2000 (Rattus norvegicus)
Samples (2)
GSM1898765 H9c2 Control cells
GSM1898766 H9c2 A2M treated cells
Relations
BioProject PRJNA297403
SRA SRP064340

Download family Format
SOFT formatted family file(s) SOFTHelp
MINiML formatted family file(s) MINiMLHelp
Series Matrix File(s) TXTHelp

Supplementary file Size Download File type/resource
GSE73597_RAW.tar 10.0 Kb (http)(custom) TAR (of TXT)
SRA Run SelectorHelp
Raw data are available in SRA
Processed data provided as supplementary file

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