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Expression of ventricular-type myosin light chain messenger RNA in spontaneously hypertensive rat atria
C Kumar1, C Saidapet, P Delaney
1Roche Institute of Molecular Biology, Roche Research Center, Nutley, New Jersey.
Abstract:
Using cloned DNA probes specific for two isoforms of cardiac myosin light chains (MLCs), nonphosphorylatable MLC1 and phosphorylatable, regulatory MLC2, we have observed that the MLC1 messenger RNA of ventricular type does not appear in detectable amounts in atrial cells of either normotensive Wistar-Kyoto rat strain (WKY) or spontaneously hypertensive rat strain (SHR). The messenger RNA of regulatory isoform of ventricular MLC2, on the other hand, is found in threefold excess in atria of SHR relative to that of age-matched WKY. The increased level of MLC2 messenger RNA is present even in 6-week-old SHR atria where there is no established overloading of the heart. Thus, it appears that the increased expression of the regulatory MLC2 gene in SHR atrial cells is a predetermined event, which, most likely, participates in functional adaptation of the myocardium in response to pressure overload and subsequent hypertrophy.
Insights
Cardiac myosin light chain 2 (MLC2) messenger RNA is overexpressed in the atria of spontaneously hypertensive rats (SHR) before pressure overload. This suggests a predetermined role for MLC2 in myocardial adaptation to hypertension.
Area of Science:
- Molecular biology
- Cardiovascular research
- Gene expression
Background:
- Cardiac myosin light chains (MLCs) are crucial for myocardial contractility.
- Two isoforms, MLC1 and MLC2, play distinct roles.
- MLC2 is a regulatory isoform involved in cardiac function.
Purpose of the Study:
- To investigate the expression of MLC1 and MLC2 messenger RNA (mRNA) in rat atrial cells.
- To compare MLC isoform mRNA levels between normotensive Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR).
- To determine if altered gene expression precedes cardiac hypertrophy in SHR.
Main Methods:
- Utilized cloned DNA probes specific for MLC1 and MLC2 isoforms.
- Analyzed mRNA levels in atrial cells of WKY and SHR rats.
- Compared gene expression in young (6-week-old) and adult SHR.
Main Results:
- Ventricular MLC1 mRNA was undetectable in atrial cells of both WKY and SHR.
- Ventricular MLC2 mRNA was found in threefold excess in SHR atria compared to WKY.
- Elevated MLC2 mRNA levels were observed in 6-week-old SHR, prior to significant cardiac overloading.
Conclusions:
- Increased expression of the regulatory MLC2 gene in SHR atrial cells appears to be a predetermined event.
- This predetermined upregulation of MLC2 likely contributes to the functional adaptation of the myocardium.
- MLC2 gene expression changes may play a role in response to pressure overload and subsequent hypertrophy in SHR.