PulseExploreJournal ClubDebatesTrendingResearchersJournals
Instagram
HomeExploreJournal ClubTrending
Synapse
⌘+K
Synapse
April 1, 1990Circulation Research40 citationsOpen Access

Differences in myosin isoform expression in the subepicardial and subendocardial myocardium during cardiac hypertrophy in the rat.

View Full Paper
LBLawrence B. BugaiskyPAPeter G. AndersonRHR S Hall

Key Result

Pressure overload-induced cardiac hypertrophy in rats significantly increased V3 myosin expression, which was higher in the subendocardial versus subepicardial myocardium at 8 weeks (46.6% vs 36.2%).

Structured PICO

P
Population
Young male rats (25-day-old)
I
Intervention
Ascending aorta constriction (0.024-inch diameter band) to induce progressive cardiac hypertrophy and congestive heart failure
C
Comparator
Subepicardial myocardium (internal comparison)
O
Outcome
Myosin isoform expression (percentage of V3 isoform) in the subendocardial and subepicardial myocardiumsurrogate

In a rat model of pressure overload-induced cardiac hypertrophy, V3 myosin expression increases significantly more in the subendocardial myocardium compared to the subepicardial myocardium.

Main Result

Absolute Event Rate: 46.6% vs 36.2%

p-value: p=≤0.05

Limitations

  • High degree of heterogeneity in myosin isoform expression throughout a given layer illustrates a potential danger in interpretation of gel results obtained from a single small tissue sample.
  • High degree of heterogeneity in myosin isoform expression in small adjacent samples, posing a danger for interpretation from single small tissue samples.

Abstract

We have investigated myosin isoform expression during progressive cardiac hypertrophy and the development of congestive heart failure in young male rats. Cardiac enlargement was produced by placing a constricting band (0.024-inch diameter) around the ascending aorta of 25-day-old animals, which resulted in progressively increased stenosis as the rat matured. A 57% and 77% cardiac hypertrophy was observed at 2 and 8 weeks, respectively, with signs of congestive failure at the latter time point. Myosin isoform expression was examined in the subendocardial and subepicardial myocardium of the left ventricle and the free wall of the right ventricle by use of native gel electrophoresis. The percentage of the V3 isoform increased dramatically in both ventricles. In the subendocardial myocardium of the left ventricle, expression of the V3 isoform increased (p less than or equal to 0.05) relative to the subepicardial myocardium at 2, 4, and 8 weeks (17.1% vs. 10.2%, 29.4% vs. 18%, and 46.6% vs. 36.2%). In addition to regional differences within a given transmural segment, we also observed a high degree of heterogeneity in myosin isoform expression throughout a given layer (particularly the subendocardial myocardium) when small (less than or equal to 10-15 mg) adjacent samples were examined. This variability illustrated a potential danger in interpretation of gel results obtained from a single small tissue sample. Thus, cardiac hypertrophy produced by pressure overload in 25-day-old rats resulted in significantly increased V3 myosin in both the left and right ventricles. Furthermore, within the hypertrophied left ventricle, the subendocardial myocardium contained a significantly greater percentage of V3 myosin than the subepicardial myocardium.(ABSTRACT TRUNCATED AT 250 WORDS)

Ask AI
Helpful
Bookmark
Share
View Full Paper

Cite This Study

Bugaisky et al. (1990) studied Cardiac hypertrophy and congestive heart failure. Ascending aorta constriction (pressure overload) vs. Subepicardial myocardium (regional comparison) was evaluated on Myosin V3 isoform expression percentage (p=≤0.05). Pressure overload-induced cardiac hypertrophy in rats significantly increased V3 myosin expression, which was higher in the subendocardial versus subepicardial myocardium at 8 weeks (46.6% vs 36.2%).

synapsesocial.com/papers/6a0ea99953f874f2b2229d40https://doi.org/10.1161/01.res.66.4.1127
Ask AI
Helpful
Bookmark
Share
View Full Paper