Differential gene expression of human telomerase-associated protein hTERT and TEP1 in human hematopoietic cells

Citation
N. Uchida et al., Differential gene expression of human telomerase-associated protein hTERT and TEP1 in human hematopoietic cells, LEUK RES, 23(12), 1999, pp. 1127-1132
Citations number
31
Categorie Soggetti
Onconogenesis & Cancer Research
Journal title
LEUKEMIA RESEARCH
ISSN journal
01452126 → ACNP
Volume
23
Issue
12
Year of publication
1999
Pages
1127 - 1132
Database
ISI
SICI code
0145-2126(199912)23:12<1127:DGEOHT>2.0.ZU;2-0
Abstract
The maintenance of telomere length is crucial for the survival of cells. Re cently, genes for proteins that consist of human telomerase have been clone d and the results have indicated a close relationship between telomerase ac tivity and its gene expression. We studied the mRNA expression of the telom erase-associated genes, hTERT and TEP1, in hematopoietic cells in order to clarify the relation between them and telomerase activity using semiquantit ative RT-PCR. In polymorphonuclear cells and monocytes isolated from periph eral blood, which had no detectable telomerase activity, no hTERT mRNA expr ession was seen. On the other hand, lymphocytes and CD34-positive cells bot h demonstrated hTERT mRNA expression. TEP1 mRNA was detected in all samples , showing no differential expression. We then assessed hTERT and TEP1 mRNA expression in CD34-positive cells cultured in vitro with growth factors. Af ter 4 weeks of culture, all the cells showed myeloid differentiation and th e telomerase activity was downregulated. hTERT mRNA was expressed in CD34-p ositive cells, but was downregulated in 4-week-cultured cells. TEP1 showed no apparent differential expression. We conclude that hTERT mRNA expression is downregulated in accordance with telomerase downregulation during the c ourse of myeloid differentiation, which suggests that it plays a crucial Po le in the expression of enzyme activity, while TEP1 has a much smaller role to play, if any. (C) 1999 Elsevier Science Ltd. All rights reserved.