Both ERK and JNK are required for enhancement of MD-2 gene expression during differentiation of HL-60 cells

Biology of the Cell
Changlin LiZongliang Chang

Abstract

MD-2 is associated with the extracellular domain of TLR4 (Toll-like receptor 4) and augments TLR4-dependent LPS (lipopolysaccharide) responses in vitro. Our previous investigation found that PMA-induced HL-60 cell differentiation to macrophages is associated largely with TLR2 and CD14 and, to a much lesser extent, with TLR4. We studied the MD-2 expression during differentiation of HL-60 cells induced by PMA. The results showed that PMA, but not VitD(3) (1alpha,25-dihydroxy-vitamin D(3)), strongly induces MD-2 gene expression by HL-60 cells in a time- and dose-dependent manner. Treatment with an MEK [MAPK (mitogen-activated protein kinase)/ERK (extracellular-signal-regulated kinase) kinase] inhibitor (PD98059) and a JNK (c-Jun N-terminal kinase) inhibitor (SP600125) suppresses PMA-induced MD-2 gene expression, whereas impairment of p38 function by treatment with the inhibitor SB203580 has no effect on MD-2 mRNA. In order to reveal the possible molecular mechanism for such a regulation of MD-2 gene expression, we cloned and analysed the putative MD-2 gene promoter. Transient transfection of different deletion mutants demonstrated that the region -185/-171 (5'-TCCTTTACAGGAAGT-3') of the MD-2 gene promoter is closely related to gen...Continue Reading

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Nov 5, 2008·Proceedings of the National Academy of Sciences of the United States of America·James E StrongHeinz Feldmann
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