Telomere shortening is an in vivo marker of myocyte replication and aging

被引：90

作者：

Kajstura, J ^{[1
]}

Pertoldi, B ^{[1
]}

Leri, A ^{[1
]}

Beltrami, CA ^{[1
]}

Deptala, A ^{[1
]}

Darzynkiewicz, Z ^{[1
]}

Anversa, P ^{[1
]}

机构：

[1] New York Med Coll, Dept Med, Valhalla, NY 10595 USA

来源：

AMERICAN JOURNAL OF PATHOLOGY | 2000年 / 156卷 / 03期

关键词：

D O I：

10.1016/S0002-9440(10)64949-8

中图分类号：

R36 [病理学];

学科分类号：

100104 ;

摘要：

To determine whether adult cardiac myocytes are capable of multiple divisions and whether this form of growth is restricted to a subpopulation of cells that retain this capacity with age, telomere lengths were measured in myocyte nuclei isolated from the left ventricle of fetal and neonatal Fischer 344 rats and rats at 4, 12, and 27 months after birth. Two independent methodologies were used for this analysis: laser scanning cytometer and confocal microscopy. In each case, fluorescence intensity of a peptide nucleic acid probe specific for telomeric sequence was evaluated. The two techniques yielded comparable results. Telomeric shortening increased with age in a subgroup of myocytes that constituted 16% of the entire cell population. In the remaining nondividing cells, progressive accumulation of a senescent associated nuclear protein, p16(INK4), was evidenced. In conclusion, a significant fraction of myocytes divides repeatedly from birth to senescence, counteracting the continuous death of cells in the aging mammalian rat heart.

引用

页码：813 / 819

页数：7

共 51 条

[31] The cardiac cell cycle, pocket proteins, and p300 [J].