Hyperplasia and hypertrophy of chicken cardiac myocytes during posthatching development

Abstract

For characterization of the growth pattern of cardiac myocytes during posthatching development, cardiac myocytes were enzymatically isolated from the ventricles of 1-, 15-, 29-, and 42-day-old chickens for measurement of myocyte nucleation, length, width, volume, and number, and for immunolabeling of cytoskeletal proteins. Ventricular myocyte number increased 156% from day 1 to day 42. Average cell volume increased more than 400%, and myocytes lengthened 125%, but cell width only increased 53% during this period. All myocytes were mononucleated at day 1. At day 15, 18% of myocytes became binucleated with < 1% of myocytes containing more than two nuclei. Interestingly, binucleated myocytes were able to divide with two nuclei going through mitosis at the same time. As demonstrated by staining with tubulin and alpha-actinin antibodies, two mitotic spindles and two cleavage furrows were formed in dividing binucleated myocytes. At day 42, binucleated myocytes increased to 44% with 11% of myocytes containing more than two nuclei. Sarcomeric alpha-actinin was partially disassembled in prometaphase and was reorganized into regular Z lines of sarcomeres in telophase. Desmin was disassembled in prophase and was reassembled during late telophase. These results suggest that chicken myocytes undergo hypertrophy and continue to proliferate during posthatching maturation, although it is currently believed that myocytes of all vertebrates withdraw from the cell cycle shortly after birth. We provide direct evidence for the first time of in vivo myocyte division in 6-wk-old chicken hearts.

Development of endothermy and concomitant increases in cardiac and skeletal muscle mitochondrial respiration in the precocial Pekin duck (Anas platyrhynchos domestica)

“…Associated changes at the cellular level in the heart also occur within the joey, with increases in mitochondria volume and muscle contractile machinery associated with leaving the pouch and obtaining endothermy (Snelling et al, 2015a). Through day 42 post-hatching in the chicken, ventricle size increases through both hyperplasia and hypertrophy after hatching (Li et al, 1997). It remains to be seen in the Pekin duck whether the increase in ventricle mass associated with the transition to endothermy is due to hypertrophic or hyperplasic growth of the hatchling heart.…”

Surgical removal of right-to-left cardiac shunt in the American alligator(Alligator mississippiensis) causes ventricular enlargement but does not alter apnoea or metabolism during diving

“…1996; Li et al, 1997;Sedmera et al, 2003). In addition, acute and chronic damage to the myocardium can induce hyperplastic growth of myocardial and connective tissues, as well as an increase in the number of nuclei in myocytes (Herget et al, 1997).…”

Engineered Early Embryonic Cardiac Tissue Increases Cardiomyocyte Proliferation by Cyclic Mechanical Stretch via p38-MAP Kinase Phosphorylation

“…1,2 The loss of cardiomyocyte (CM) proliferation in the postnatal myocardium is the major barrier to myocardial regeneration following injury in higher vertebrates. Current treatment options for heart failure include medical management, cardiac transplantation, mechanical circulatory left ventricular assist devices, and other experimental surgical approaches, which all have both short-and long-term limitations.…”

“…Several approaches to increase the number of CMs within injured myocardium have been attempted, including (1) activation and stimulation of host myocardial regeneration by transplanted cells via angiogenic and=or paracrine effects, 4,5 (2) direct transplantation of functional CMs or myogenic cells, [6][7][8] and (3) implantation of tissue constructs containing CMs. 9,10 In the latter two cases, the ideal donor CMs possess a high potential for division during cell preparation and potential for further proliferation following implantation to form a viable myocardial tissue within the surrounding injured recipient myocardium.…”

“…9,[13][14][15] Tissue-engineered cardiac tissue constructs provide the necessary 3D environment for efficient cell survival, functional integration, and sustained cardiac recovery. 9,10 We have recently developed a 3D engineered early embryonic cardiac tissue (EEECT) with similar cell proliferative activity and contractile properties to native developing 1 Cardiovascular Development Research Program, Children's Hospital of Pittsburgh of UPMC, Pittsburgh, Pennsylvania. Departments of 2 Bioengineering and 3 Pediatrics, University of Pittsburgh, Pittsburgh, Pennsylvania.…”