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Cardiomyocyte loss is not required for the progression of left ventricular hypertrophy induced by pressure overload in female mice
Author(s) -
Schipke Julia,
Grimm Clara,
Arnstein Georg,
Kockskämper Jens,
Sedej Simon,
Mühlfeld Christian
Publication year - 2016
Publication title -
journal of anatomy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 118
eISSN - 1469-7580
pISSN - 0021-8782
DOI - 10.1111/joa.12463
Subject(s) - pressure overload , heart failure , muscle hypertrophy , medicine , afterload , cardiology , volume overload , stereology , ejection fraction , constriction , left ventricular hypertrophy , endocrinology , blood pressure , cardiac hypertrophy
Left ventricular (LV) hypertrophy in response to hypertension and increased afterload frequently progresses to heart failure. It is under debate whether the loss of cardiomyocytes contributes to this transition. To address this question, female C57 BL /6 wild‐type mice were subjected to transverse aortic constriction ( TAC ) and developed compensated LV hypertrophy after 1 week, which progressed to heart failure characterized by reduced ejection fraction and pulmonary congestion 4 weeks post‐ TAC . Quantitative, design‐based stereology methods were used to estimate number and mean volume of LV cardiomyocytes. DNA strand breaks were visualized using the TUNEL method 6 weeks post‐ TAC to quantify the number of apoptotic cell nuclei. The volume of the LV myocardium as well as the cardiomyocyte mean volume increased progressively after TAC . In contrast, the number of LV cardiomyocytes remained constant 1 and 4 weeks post‐ TAC in comparison to sham‐operated mice. Moreover, there was no significant difference in the number of cardiomyocyte nuclei stained for DNA strand breaks at 6 weeks post‐ TAC . It was concluded that the loss of cardiomyocytes is not required for the transition from compensated hypertrophy to heart failure induced by TAC in the female murine heart.