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Abstract

A BIOMATHEMATICAL EQUATION FOR HEMODYNAMIC PRESSURE ALTERATION AND CARDIAC ARTERIAL ELASTIN EXPRESSION

Pratibha Kamble*

ABSTRACT

The hypothesis of studies is that acetyl salicylic acid (Aspirin, ASA) treatment can induce elastin gene. An increased lysine (K) residue would act as a source for NAD+ dependent histone deacetylase protein as it can deacetylate elastin at multiple lysine sites in cultured HL1 cardiomyocytes. A mathematical equation deduce the hemodynamic pressure state in normal and artherosclerotic model. Atrial Cardiomyocyts HL1 cells were cultured in Claycomb medium with 10% FBS, 100μmol/L norepinephrine and 4mmol/L L-glutamine (Invitrogen, Carlsbad, CA) in gelatin coated flasks. Cells were maintained at 37°C in an atmosphere containing 5% CO2. Cells were then incubated with either, 50 μM and 0.25 mM ASA for 48 h in the same medium. Respective controls were maintained with alcohol alone. At the end of the treatment, the medium was removed and the cells were washed with PBS and harvested in Trizol® for isolation of RNA. RT-PCR was performed for the analysis of gene expression. Our results in cultured HL1 cardiomyocytes showed ASA treatment induced elastin gene. We conclude from our results that ASA can increase elastin gene suggests that it can improve vascular stiffening and normalize hemodynamic pressure.

Keywords: Acetyl Salicylic acid, Elastin, Lysine.


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