RGD Reference Report - Induction by left ventricular overload and left ventricular failure of the human Jumonji gene (JARID2) encoding a protein that regulates transcription and reexpression of a protective fetal program. - Rat Genome Database

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Induction by left ventricular overload and left ventricular failure of the human Jumonji gene (JARID2) encoding a protein that regulates transcription and reexpression of a protective fetal program.

Authors: Bovill, E  Westaby, S  Reji, S  Sayeed, R  Crisp, A  Shaw, T 
Citation: Bovill E, etal., J Thorac Cardiovasc Surg. 2008 Sep;136(3):709-16. doi: 10.1016/j.jtcvs.2008.02.020. Epub 2008 Jun 9.
RGD ID: 9586018
Pubmed: PMID:18805276   (View Abstract at PubMed)
DOI: DOI:10.1016/j.jtcvs.2008.02.020   (Journal Full-text)

OBJECTIVE: We identified changes in Jumonji (JARID2) expression in failing human hearts and determined its effects on expressions of atrial natriuretic factor (ANF), myosin light chain 2a (MLC2A), and alpha myosin heavy chain (MHCA), genes associated with both human heart failure and the fetal gene program. METHODS: Left ventricular outflow tract cardiac biopsy samples were taken from 31 patients with aortic valvular stenosis. Hearts were grouped according to left ventricular size and function: nonfailing hearts (undilated with good function) and failing hearts (dilated with poor function). Protein levels were determined by Western blotting, and messenger RNA transcript levels by ratiometric reverse transcriptase-polymerase chain reaction. Luciferase assays in HL-2 cells were used to assess effects of Jarid2 on Anf, Mlc2a, and Mhca transcriptions. Chromatin immunoprecipitation was used to detect interaction of JARID2 with specific target-gene promoters. RESULTS: JARID2 and MHCA expressions were reduced in failing hearts, whereas MLC2A and ANF were increased. In HL-2 cell culture, Jarid2 suppressed Anf and Mlc2a but enhanced Mhca. Jarid2 expression was reduced by cyclic mechanical stress, with concomitant increased Anf and Mlc2a and decreased Mhca expressions, reproducing the expression profile found in decompensated human pressure overload. CONCLUSION: Jumonji expression is reduced by mechanical stress in human heart failure from aortic stenosis. JARID2 regulates ANF, MLC2A, and MHCA transcription and contributes to reexpression of the fetal gene program in decompensated aortic stenosis. JARID2 appears important in transcriptional regulation of fetal genes and may emerge as a diagnostic marker for left ventricular decompensation in aortic stenosis.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
aortic valve stenosis  IEP 9586018mRNA and protein:decreased expression:ventricle endocardium (human)RGD 
aortic valve stenosis  ISOJARID2 (Homo sapiens)9586018; 9586018mRNA and protein:decreased expression:ventricle endocardium (human)RGD 

Objects Annotated

Genes (Rattus norvegicus)
Jarid2  (jumonji and AT-rich interaction domain containing 2)

Genes (Mus musculus)
Jarid2  (jumonji and AT-rich interaction domain containing 2)

Genes (Homo sapiens)
JARID2  (jumonji and AT-rich interaction domain containing 2)


Additional Information