Proliferating cell nuclear antigen in developing and adult rat cardiac muscle cells.

The regulated expression of cyclins controls the cell cycle. Because cardiomyocytes in adult mammals withdraw permanently from the cell cycle and thus cannot regenerate after injury, we examined cyclin expression during development by comparing cyclin A-E mRNA levels in fetal and adult human hearts. Cyclin B mRNA was detectable in adult hearts, although at a level markedly lower than that in fetal hearts. Levels of cyclin C, D1, D2, D3, and E mRNA were essentially identical in the two groups. In contrast, cyclin A mRNA was undetectable in adult hearts whereas cyclin A mRNA and protein were readily detectable in fetal hearts and cardiomyocytes, respectively. We then measured cyclin A mRNA and protein levels in rat hearts at four stages of development (fetal and 2, 14, and 28 d). Cyclin A mRNA and protein levels decreased quickly after birth (to 37% at day 2) and became undetectable within 14 d, an observation consistent with reports that cardiomyocytes stop replicating in rats by the second to third postnatal week. This disappearance of cyclin A gene expression in human and rat hearts at the time cardiomyocytes become terminally differentiated suggests that cyclin A downregulation is important in the permanent withdrawal of cardiomyocytes from the cell cycle. (J. Clin. Invest. 1995. 95:2275-2280

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“…PCNA has been used before as a marker for cycling cells, including cardiomyocytes (46)(47)(48)(49)(50). Fig.…”

Section: Resultsmentioning

confidence: 99%

“…nisms that control proliferation and terminal differentiation in these two striated cell types may be quite distinct (5)(6)(7)53 (5,49,55).…”

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confidence: 99%

Disappearance of cyclin A correlates with permanent withdrawal of cardiomyocytes from the cell cycle in human and rat hearts.

et al. 1995

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“…In the young group, however, there was an increase during the evolution, which was close to the values presented by the young controls. The differentiated capacity of cell proliferation and hypertrophy in the hearts of young rats might be one of the mechanisms of contractility recovery of these animals 22 .…”

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“…Thus, the persistence of a low EF in infarcted adult rats probably occurred due to the inadequate compensatory hypertrophy of the non-infarcted areas and by the lower rate of cardiomyocyte replacement 16,22 .…”

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Avaliação ecocardiográfica evolutiva do infarto do miocárdio em ratos jovens e adultos

Pabis¹,

Miyague²,

Francisco³

et al. 2008

Arq. Bras. Cardiol.

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Localization of proliferating cell nuclear antigen in the developing and mature rat heart cell

et al. 1996

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Background The cardiac muscle cell ceases to divide shortly after birth; this cessation is followed by a limited period when DNA synthesis and karyokinesis occur without cytokinesis. The regulation of this process is not known. The purpose of this study is to explore the possible events that could lead to the cessation of cardiac muscle cell division. One protein requisite for DNA synthesis is proliferating cell nuclear antigen (PCNA). This protein is the auxiliary protein of DNA polymerase δ. Methods Rats of fetal age day 18 or days 0, 4, 8, 12, and 16 after birth were obtained. In addition, adult hearts were used for this study. Hearts from the fetal day‐18 rats and the day‐0 neonatal rats were digested. Cardiac myocytes were isolated and placed in culture for an analysis of DNA synthesis by using tridiated thymidine. Ventricular muscle tissue was isolated from hearts of all ages and frozen in liquid nitrogen for Northern and Western blot analyses. Results Tridiated thymidine analysis revealed that, although serum stimulation significantly increased the number of labeled fetal cardiac muscle cells, it did not have that effect on neonatal cardiac muscle cells in culture. Northern blot analysis revealed that the steady state levels of mRNA for PCNA remained constant from fetal day 18 through day 4 after birth. Steady state levels declined during the second postnatal week and then reached basal levels by day 16. PCNA message was still present in adult heart tissue. By using indirect immunofloursecence and Western blotting, PCNA protein could be located in the nucleus of cardiac muscle cells during the first 2 weeks after birth. At 16 days after birth, the protein was found in the cytoplasm in very low amounts but was not found in the nucleus. The protein was barely detectable by Western blotting in the cytoplasmic fraction from the adult myocardium. Conclusions The results of this study suggest that the PCNA message and protein product declined after birth, but both were present at low levels in the adult myocardium. However, the PCNA protein was not translocated to the nucleus in adult myocardial cells. The events involving PCNA correlated closely with the time period when cell division and then DNA synthesis ceased in these cells. © 1996 Wiley‐Liss, Inc.

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Proliferating cell nuclear antigen in developing and adult rat cardiac muscle cells.

Cited by 54 publications

References 46 publications

Disappearance of cyclin A correlates with permanent withdrawal of cardiomyocytes from the cell cycle in human and rat hearts.

Disappearance of cyclin A correlates with permanent withdrawal of cardiomyocytes from the cell cycle in human and rat hearts.

Avaliação ecocardiográfica evolutiva do infarto do miocárdio em ratos jovens e adultos

Localization of proliferating cell nuclear antigen in the developing and mature rat heart cell

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