Expression of granulocytic functions by leukemic promyelocytic HL-60 cells: differential induction by dimethylsulfoxide and retinoic acid

Matzner, Yaacov; Gavison, Rivka; Rachmilewitz, Eliezer A.; Fibach, Eitan

doi:10.1016/0045-6039(87)90481-7

Cited by 44 publications

(17 citation statements)

References 19 publications

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“…Human promyelocytic leukemia HL-60 cells can be differentiated by DMSO into neutrophil-like cells which are commonly used as a cell model to study mature human neutrophils in vitro [45,46]. In contrast to primary neutrophils, gene knockdown technique can be applied to the cultures of differentiating HL-60 cells, thus enabling generation of neutrophil-like dHL-60 cells with silenced expression of specific genes.…”

Section: Contrasting Effects Of Autophagy Suppression On Spontaneous mentioning

confidence: 99%

Differential effects of the autophagy inhibitors 3-methyladenine and chloroquine on spontaneous and TNF-α-induced neutrophil apoptosis

Pliyev

Menshikov

2012

Apoptosis

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Autophagy and apoptosis cooperate to modulate cell survival. Neutrophils are short-lived cells and apoptosis is considered to be the major mechanism of their death. In the present study, we addressed whether autophagy regulates neutrophil apoptosis and investigated the effects of autophagy inhibition on apoptosis of human neutrophils. We first showed that the established autophagy inhibitors 3-methyladenine (MA) and chloroquine (CQ) markedly accelerated spontaneous neutrophil apoptosis as was evidenced by phosphatidylserine exposure, DNA fragmentation and caspase-3 activation. Apoptosis induced by the autophagy inhibitors was completely abrogated by a pan-caspase inhibitor Q-VD-OPh. Unexpectedly, both MA and CQ significantly delayed neutrophil apoptosis induced by TNF-α, although the inhibitors did attenuate late pro-survival effect of the cytokine. The effect was specific for TNF-α because it was not observed in the presence of other inflammation-associated cytokines (IL-1β or IL-8). The autophagy inhibitors did not modulate surface expression of TNF-α receptors in the absence or presence of TNF-α. Both MA and CQ induced a marked down-regulation of a key anti-apoptotic protein Mcl-1 but did not affect significantly the levels of another anti-apoptotic protein Bcl-X(L). Finally, to confirm the effects of the pharmacological inhibition of autophagy by a genetic approach, we evaluated the consequences of siRNA-mediated autophagy suppression in neutrophil-like differentiated HL60 cells. Knockdown of ATG5 in the cells resulted in accelerated spontaneous apoptosis but attenuated TNF-α-induced apoptosis. Together, these data suggest that autophagy regulates neutrophil apoptosis in an inflammatory context-dependent manner and mediates the early pro-apoptotic effect of TNF-α in neutrophils.

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Section: Contrasting Effects Of Autophagy Suppression On Spontaneous mentioning

confidence: 99%

Differential effects of the autophagy inhibitors 3-methyladenine and chloroquine on spontaneous and TNF-α-induced neutrophil apoptosis

Pliyev

Menshikov

2012

Apoptosis

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“…The retinoid-responsive promyelocytic leukemia cell line HL-60 was used to determine whether the above antisera could specifically recognize endogenously expressed RAR-a and RAR-,B. In the absence of retinoids, these cells correspond predominantly to promyelocytes, whereas retinoids are known to induce their differentiation into granulocytes (12)(13)(14)(15).…”

Section: Preparation Of Rabbit Antibodies Directed Against Syntheticmentioning

confidence: 99%

Antibodies specific to the retinoic acid human nuclear receptors alpha and beta.

Gaub

Lutz

Ruberte

et al. 1989

Proc. Natl. Acad. Sci. U.S.A.

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Two cDNAs encoding two human receptors for retinoic acid (RA), RAR-alpha and RAR-beta, have been characterized recently. Synthetic peptides corresponding to the cDNA-deduced amino acid sequences unique to RAR-alpha and RAR-beta were used to generate anti-RAR-alpha antiserum (SP171) and anti-RAR-beta antisera (SP172 and SP248). The specificity of these antisera was confirmed both by immunocytochemical detection of these receptors in COS-1 cells transfected with RAR-alpha and RAR-beta expression vectors and by immunoblot analyses performed with whole extracts of these cells. We also demonstrate that these antisera recognize RAR-alpha and RAR-beta endogenously expressed in the RA-responsive human promyelocytic leukemia cell line HL-60.

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“…The differentiated HL-60 cells posses multiple granulocytic characteristics, including expression and repression of key proteins and surface markers as well as the morphology and the ability to generate ROS [28][29][30][31][32]. However, ATRA differentiated HL-60 cells also possess monocytic functional characteristics as the cells are able to secrete a considerable amount of IL-8 [33,34].…”

Section: Introductionmentioning

confidence: 99%

Immunomodulatory effects of testosterone evaluated in all-trans retinoic acid differentiated HL-60 cells, granulocytes, and monocytes

Boje

Moesby

Timm

et al. 2012

International Immunopharmacology

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Expression of granulocytic functions by leukemic promyelocytic HL-60 cells: differential induction by dimethylsulfoxide and retinoic acid

Cited by 44 publications

References 19 publications

Differential effects of the autophagy inhibitors 3-methyladenine and chloroquine on spontaneous and TNF-α-induced neutrophil apoptosis

Differential effects of the autophagy inhibitors 3-methyladenine and chloroquine on spontaneous and TNF-α-induced neutrophil apoptosis

Antibodies specific to the retinoic acid human nuclear receptors alpha and beta.

Immunomodulatory effects of testosterone evaluated in all-trans retinoic acid differentiated HL-60 cells, granulocytes, and monocytes

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