Retinoic acid-induced CD38 expression in HL-60 myeloblastic leukemia cells regulates cell differentiation or viability depending on expression levels
Retinoic acid-induced CD38 expression in HL-60 myeloblastic leukemia cells regulates cell differentiation or viability depending on expression levels
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DOI：
10.1002/jcb.20745
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发表时间：
2006-04-15
影响因子：
4
通讯作者：
Yen, A
中科院分区：
文献类型：
--
作者：
Lamkin, TJ;Chin, V;Yen, A
视黄酸诱导的HL-60人髓细胞白血病细胞中CD 38胞外酶受体的表达受RAR α和RXR调节，并根据每个细胞的表达水平增强或阻止细胞分化。RAR α激活引起CD 38表达，RXR激活也是如此，但不那么有效。通过MEK抑制来抑制MAPK信号传导减少了RAR和RXR两者的诱导表达。CD 38的表达增强了视黄酸诱导的髓样分化和GO细胞周期阻滞，但在较高的表达水平下，诱导的分化被阻断，而视黄酸诱导细胞活力丧失。在1，25-二羟维生素D3的情况下，诱导的单核细胞分化也增强了CD 38，而不是增强了更高的表达水平，但没有诱导的活力丧失。因此，CD 38的表达水平调节细胞对视黄酸的反应，促进细胞分化或丧失活力。因此，CD 38的细胞效应取决于其表达水平。
Retinoic acid-induced expression of the CD38 ectoenzyme receptor in HL-60 human myeloblastic leukemia cells is regulated by RAR alpha and RXR, and enhanced or prevented cell differentiation depending on the level of expression per cell. RARa activation Caused CD38 expression, as did RXR activation but not as effectively. Inhibition of MAPK signaling through MEK inhibition diminished the induced expression by both RARs and RXRs. Expression of CD38 enhanced retinoic acid-induced myeloid differentiation and GO cell cycle arrest, but at higher expression levels, induced differentiation was blocked and retinoic acid induced a loss of cell viability instead. In the case of 1,25-dihydroxyvitamin D3, induced monocytic differentiation was also enhanced by CD38 and not enhanced by higher expression levels, but without induced loss of viability. Expression levels of CD38 thus regulated the cellular response to retinoic acid, either propelling cell differentiation or loss of viability. The cellular effects of CD38 thus depend on its expression level.