Abstract
Atypically-shaped cardiomyocytes (ACMs) are beating heart cells identified in the cultures of cardiomyocyte-removed fractions obtained from adult mouse hearts. Since ACMs spontaneously develop into beating cells in the absence of hormones or chemicals, these cells are likely to be a type of cardiac progenitors rather than stem cells. “Native ACMs” are found as small interstitial cells among ventricular myocytes that co-express cellular prion protein (PrP) and cardiac troponin T (cTnT) in mouse and human heart tissues. However, the endogenous behavior of human ACMs is unclear. In the present study, we demonstrate that PrP+ cTnT+ cells are present in the human heart tissue with myocardial infarction (MI). These cells were mainly found in the border of necrotic cardiomyocytes caused by infarcts and also in the hibernating myocardium subjected to the chronic ischemia. The ratio of PrP+ cTnT+ cells to the total cells observed in the normal heart tissue section of mouse and human was estimated to range from 0.3–0.8%. Notably, living human PrP+ cTnT+ cells were identified in the cultures obtained at pathological autopsy despite exposure to lethal ischemic conditions for hours after death. These findings suggest that ACMs could survive in the ischemic human heart and develop into a sub-population of cardiac myocytes.
Highlights
The aim of the present study was to examine the morphological analysis whether native ACMs could survive in the ischemic human heart
These observations are similar to the reports that the distribution of Connexin 43 (Cx43) in cardiomyocytes are changed during the culture[19] and compensated and decompensated cardiac hypertrophy[20]
The present study demonstrates that native ACMs survive in the ischemic human heart where the ventricular myocytes died
Summary
The aim of the present study was to examine the morphological analysis whether native ACMs could survive in the ischemic human heart. The results show that PrP+ cTnT+ cells are present in the infarcted area of MI and in the hibernating area subjected to chronic ischemia of human heart tissue specimens. We demonstrate that the living human PrP+ cTnT+ cells, assumed to be ACMs, are identified in the cultures prepared from heart tissue dissected from the patients for the pathological autopsy approximately 2 h after death. The findings indicate that some of the ACMs in human heart could survive even after the adjacent ventricular myocytes die under pathophysiological conditions
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