All-trans-retinoic acid and Erk1/2 signaling synergistically regulate the expression of CD300B in human monocytic cells

Yong Wu, Qiuyan Chen, Tongkun Pai, A. Catharine Ross

Research output: Contribution to journalArticle

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Abstract

The regulation of the cell-surface receptors that constitute the gene cluster, CD300, also known as the Myeloid Activating/Inhibitory Receptor (MAIR) family, is poorly understood. In the present study, we tested the hypothesis that all-trans-RA (RA), a bioactive form of vitamin A long recognized for its role in regulation of immune cell activities, may be a potent regulator of the expression of human CD300B. In monocytic THP-1 cells, RA (20. nM) alone significantly increased CD300B mRNA within 2. h and up to 20-fold after 24. h; however, CD300B protein determined by flow cytometry and confocal microscopy showed little change. A search for coactivating molecules revealed that phorbol myristyl acetate (PMA), a mimetic of diacylglycerol, alone increased CD300B mRNA by less than 5-fold; however, the combination of at-RA and PMA increased CD300B mRNA nearly 60-fold. Moreover, CD300B protein was increased. CD300B molecules were mainly located on the plasma membrane and in the endosomal compartment, sharing a distribution/recycling pattern similar to transferrin receptor CD71. The induction of CD300B mRNA by PMA required signaling through the MEK/ERK branch of the MAP kinase pathway, as PD98059, a MEK1/2 inhibitor, abrogated this response, while SB203580, an inhibitor of the p38 pathway, had no effect. Our data suggest a model in which RA alone induces a CD300B mRNA response in which transcripts accumulate but remain untranslated and therefore " sterile," whereas RA combined with signals from the ERK1/2 pathway results in both increased CD300B transcription and protein expression on the cell surface and in endocytic vesicles.

Original languageEnglish (US)
Pages (from-to)68-78
Number of pages11
JournalCellular Immunology
Volume268
Issue number2
DOIs
StatePublished - Mar 29 2011

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Tretinoin
Messenger RNA
Acetates
Transport Vesicles
Proteins
Transferrin Receptors
MAP Kinase Signaling System
Diglycerides
Mitogen-Activated Protein Kinase Kinases
Extracellular Signal-Regulated MAP Kinases
Recycling
Cell Surface Receptors
Multigene Family
Vitamin A
Confocal Microscopy
Flow Cytometry
Cell Membrane
phorbol

All Science Journal Classification (ASJC) codes

  • Immunology

Cite this

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title = "All-trans-retinoic acid and Erk1/2 signaling synergistically regulate the expression of CD300B in human monocytic cells",
abstract = "The regulation of the cell-surface receptors that constitute the gene cluster, CD300, also known as the Myeloid Activating/Inhibitory Receptor (MAIR) family, is poorly understood. In the present study, we tested the hypothesis that all-trans-RA (RA), a bioactive form of vitamin A long recognized for its role in regulation of immune cell activities, may be a potent regulator of the expression of human CD300B. In monocytic THP-1 cells, RA (20. nM) alone significantly increased CD300B mRNA within 2. h and up to 20-fold after 24. h; however, CD300B protein determined by flow cytometry and confocal microscopy showed little change. A search for coactivating molecules revealed that phorbol myristyl acetate (PMA), a mimetic of diacylglycerol, alone increased CD300B mRNA by less than 5-fold; however, the combination of at-RA and PMA increased CD300B mRNA nearly 60-fold. Moreover, CD300B protein was increased. CD300B molecules were mainly located on the plasma membrane and in the endosomal compartment, sharing a distribution/recycling pattern similar to transferrin receptor CD71. The induction of CD300B mRNA by PMA required signaling through the MEK/ERK branch of the MAP kinase pathway, as PD98059, a MEK1/2 inhibitor, abrogated this response, while SB203580, an inhibitor of the p38 pathway, had no effect. Our data suggest a model in which RA alone induces a CD300B mRNA response in which transcripts accumulate but remain untranslated and therefore {"} sterile,{"} whereas RA combined with signals from the ERK1/2 pathway results in both increased CD300B transcription and protein expression on the cell surface and in endocytic vesicles.",
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All-trans-retinoic acid and Erk1/2 signaling synergistically regulate the expression of CD300B in human monocytic cells. / Wu, Yong; Chen, Qiuyan; Pai, Tongkun; Ross, A. Catharine.

In: Cellular Immunology, Vol. 268, No. 2, 29.03.2011, p. 68-78.

Research output: Contribution to journalArticle

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AU - Ross, A. Catharine

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AB - The regulation of the cell-surface receptors that constitute the gene cluster, CD300, also known as the Myeloid Activating/Inhibitory Receptor (MAIR) family, is poorly understood. In the present study, we tested the hypothesis that all-trans-RA (RA), a bioactive form of vitamin A long recognized for its role in regulation of immune cell activities, may be a potent regulator of the expression of human CD300B. In monocytic THP-1 cells, RA (20. nM) alone significantly increased CD300B mRNA within 2. h and up to 20-fold after 24. h; however, CD300B protein determined by flow cytometry and confocal microscopy showed little change. A search for coactivating molecules revealed that phorbol myristyl acetate (PMA), a mimetic of diacylglycerol, alone increased CD300B mRNA by less than 5-fold; however, the combination of at-RA and PMA increased CD300B mRNA nearly 60-fold. Moreover, CD300B protein was increased. CD300B molecules were mainly located on the plasma membrane and in the endosomal compartment, sharing a distribution/recycling pattern similar to transferrin receptor CD71. The induction of CD300B mRNA by PMA required signaling through the MEK/ERK branch of the MAP kinase pathway, as PD98059, a MEK1/2 inhibitor, abrogated this response, while SB203580, an inhibitor of the p38 pathway, had no effect. Our data suggest a model in which RA alone induces a CD300B mRNA response in which transcripts accumulate but remain untranslated and therefore " sterile," whereas RA combined with signals from the ERK1/2 pathway results in both increased CD300B transcription and protein expression on the cell surface and in endocytic vesicles.

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