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The role of calcium/calmodulin-dependent protein kinase cascade on MIP-1alpha gene expression of ATL cells.

Abstract：

OBJECTIVE:Adult T-cell leukemia (ATL) is a mature CD4(+) T-cell malignancy caused by infection with human T-lymphotrophic virus type-1 and is associated with a marked hypercalcemia in many patients. Recently, it has been proposed that macrophage inflammatory protein-1alpha (MIP-1alpha) is the clinical hallmark of hypercalcemia in ATL. In this study, we investigated the effect of extracellular calcium on MIP-1alpha secretion in ATL cells and the role of Ca(2+)/calmodulin (CaM)-dependent protein kinase (CaM-K) cascade in transcriptional activation of MIP-1alpha. MATERIALS AND METHODS:MIP-1alpha protein levels in the culture supernatant collected from ATL cells were measured by enzyme-linked immunosorbent assay. Reporter plasmid containing the MIP-1alpha promoter was transfected to ATL cells, and the promoter activity was measured by luciferase assay. RESULTS:The addition of calcium to the culture medium enhanced the secretion of MIP-1alpha from ATL cells, which was inhibited by the CaM-KK inhibitor. The transfection of CaM-KIV stimulated MIP-1alpha promoter activity, and the upstream kinase CaM-KK enhanced the stimulatory effect of CaM-KIV on the promoter activity. Mutation in the cyclic adenosine 5' monophosphate response element (CRE) within the MIP-1alpha promoter significantly reduced the effect of CaM-KIV, and CRE mutant promoter activity was not significantly enhanced by the addition of calcium to the culture medium as compared to wild-type promoter activity. CONCLUSION:Hypercalcemia enhances MIP-1alpha secretion in ATL cells, and this mechanism requires the involvement of CaM-KK/CaM-KIV cascade through the CRE. These findings raise a possibility that the inhibitory effect of CaM-KK/CaM-KIV cascade may be a potential therapeutic target for ATL.

journal_name

Exp Hematol

journal_title

Experimental hematology

authors

Matsumoto K,Murao K,Imachi H,Nishiuchi T,Cao W,Yu X,Li J,Ahmed RA,Iwama H,Kobayashi R,Tokumitsu H,Ishida T

doi

10.1016/j.exphem.2007.11.013

subject

Has Abstract

pub_date

2008-04-01 00:00:00

pages

390-400

issue

4

eissn

0301-472X

issn

1873-2399

pii

S0301-472X(07)00688-1

journal_volume

36

pub_type

杂志文章

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