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Estrogen Mediated miRNA Expression Profiles During Cardiomyocyte Hypertrophy
Author(s) -
McCarty Candice Morgan,
Risner Gary,
Waikel Rebekah L.
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.509.2
MicroRNAs (miRNAs) are highly regulated during cardiac hypertrophy. Cardiomyocyte hypertrophy can be modeled in vitro by treating primary cardiomyocytes with known hypertrophy agents such as Phenylephrine (PE). In culture, cardiomyocytes retain sensitivity to estrogen (E2), which antagonizes the effects of PE on cardiomyocyte hypertrophy. We hypothesize that estrogen, at least in part, mediates its anti‐hypertrophy effects through miRNAs. To establish the profile of miRNA expression induced by the hypertrophic stimulator PE, cultured primary rat cardiomyocytes were treated with PE and total RNA isolated for miRNA analysis by Taqman RT‐PCR. The relative expression of selected miRNAs as compared to diluent control treated cardiomyocytes was determined. This provided a profile for the association of PE‐induced cardiomyocyte hypertrophy with the transcriptional regulation or stabilization of candidate miRNAs. Next, the effects of estrogen on the miRNAs pattern were determined in primary rat cardiomyocytes that had been exposed to PE as a hypertrophic stimulator. Cell surface area was used to document the effect of PE in inducing hypertrophy and the ability of E2 to inhibit this response. We observed alterations in the miRNA profile of cardiomyocytes exposed to PE +E2 as compared to those exposed only to PE, suggesting that estrogen is altering miRNA expression to inhibit cardiomyoctye hypertrophy.

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