Differentiation of human monocytes in vitro with granulocyte–macrophage colony-stimulating factor and macrophage colony-stimulating factor produces distinct changes in cGMP phosphodiesterase expression

Bender, Andrew T.; Ostenson, Cari L.; Giordano, Daniela; Beavo, Joseph A.

doi:10.1016/j.cellsig.2003.08.009

Cited by 61 publications

(65 citation statements)

References 46 publications

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“…Our results conclusively show that PDE1B2 is a major regulator of ANF-stimulated cGMP in the macrophage cell type studied. This is consistent with an earlier finding of higher up-regulation of the ANF receptor GC-A in primary macrophages that up-regulate PDE1B2 upon differentiation from a monocyte (11). Our experiments with the Ca ϩ2 ionophore ionomycin indicate that PDE1B2 is functionally activated in intact cells by changes in Ca ϩ2 levels.…”

Section: Discussionsupporting

confidence: 92%

“…Eleven different PDE gene families have been described and characterized based on their sequences and regulatory properties (6)(7)(8). Recent work has described changes in the expression of several PDE isoforms in monocytes and monocyte-derived cells upon cytokine stimulation (9)(10)(11). Thus, each monocyte-derived cell type has a unique system for regulating cyclic nucleotide levels.…”

mentioning

confidence: 99%

“…Thus, each monocyte-derived cell type has a unique system for regulating cyclic nucleotide levels. For instance, differentiation of a monocyte into a peritoneal-like macrophage with the cytokine macrophage colony-stimulating factor (M-CSF) induces PDE2A expression, whereas differentiation to an alveolar-like macrophage with granulocyte-macrophage colony-stimulating factor (GM-CSF) up-regulates PDE1B2 instead of PDE2A (11). However, addition of IL-4 in the presence of GM-CSF changes the differentiation to a dendritic cell and suppresses PDE1B2 up-regulation (10,12).…”

mentioning

confidence: 99%

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PDE1B2 regulates cGMP and a subset of the phenotypic characteristics acquired upon macrophage differentiation from a monocyte

Bender

Beavo

2006

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

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Monocyte-to-macrophage differentiation with the cytokine granulocyte-macrophage colony-stimulating factor induces expression of the cyclic nucleotide phosphodiesterase PDE1B2. However, what role PDE1B2 plays in macrophage biology has not been elucidated. We have addressed this question by inhibiting PDE1B2 induction by using RNA interference. Using a retrovirus-based system, we created HL-60 stable cell lines that express a short-hairpin RNA targeting PDE1B2. HL-60 cells treated with phorbol-12-myristate-13-acetate differentiate to a macrophage-like phenotype and upregulate PDE1B2. However, expression of PDE1B2 short hairpin RNA effectively suppresses PDE1B2 mRNA, protein, and activity up-regulation. Using the HL-60 PDE1B2 knockdown cells and agonists for either adenylyl or guanylyl cyclase, it was found that PDE1B2 predominantly regulates cGMP and plays a lesser role in cAMP regulation in response to cyclase agonists. Furthermore, in intact HL-60 cells, PDE1B2 activity can be regulated by changes in Ca ؉2 levels. Inhibiting PDE1B2 up-regulation does not prevent HL-60 cell differentiation, because several markers of macrophage differentiation are unaffected. However, suppression of PDE1B2 expression alters some aspects of the macrophage-like phenotype, because cell spreading, phagocytic ability, and CD11b expression are augmented. The cAMP analog 8-Bromo-cAMP reverses the changes caused by PDE1B2 knockdown. Also, PDE1B2 knockdown cells have lower basal levels of cAMP and alterations in the phosphorylation state of several probable PKA substrate proteins. Thus, the effects of PDE1B2 on differentiation may ultimately be mediated through decreased cAMP. In conclusion, PDE1B2 regulates a subset of phenotypic changes that occur upon phorbol-12-myristate-13-acetate-induced differentiation and likely also plays a role in differentiated macrophages by regulating agonist-stimulated cGMP levels.cyclic AMP ͉ cyclic GMP ͉ phosphodiesterase

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Section: Discussionsupporting

confidence: 92%

mentioning

confidence: 99%

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confidence: 99%

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PDE1B2 regulates cGMP and a subset of the phenotypic characteristics acquired upon macrophage differentiation from a monocyte

Bender

Beavo

2006

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

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“…In addition, Ctcf-deficient macrophages expressed, e.g., higher levels of the chemokine receptor CX3CR1 (,33), which is known to regulate intestinal macrophage homeostasis 37 and phosphodiesterase Pde2a (,33), which is induced during macrophage colony-stimulating factor differentiation of macrophages. 38 …”

Section: Deletion Of Ctcf Gene In the Macrophage Subpopulationsmentioning

confidence: 99%

The DNA-binding factor Ctcf critically controls gene expression in macrophages

et al. 2013

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“…Macrophages were cultured in duplicate in the complete medium alone or with daily additions for 7 days of human recombinant VEGF at 50 ng/ml and bFGF at 10 ng/ml (PeproTech, Rocky Hill, NJ, USA): the time and dosage schedule were chosen on the basis of previous experiments resulting in a maximum expression of EC antigens after a 7-day stimulation. The human monocyte THP-1 cell line (American Type Culture Collection, Rockville, MD, USA), used as control, was cultured and differentiated into macrophages with phorbol myristate acetate as described (Bender et al, 2004).…”

Section: Patientsmentioning

confidence: 99%

Vasculogenic mimicry by bone marrow macrophages in patients with multiple myeloma

et al. 2007

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Differentiation of human monocytes in vitro with granulocyte–macrophage colony-stimulating factor and macrophage colony-stimulating factor produces distinct changes in cGMP phosphodiesterase expression

Cited by 61 publications

References 46 publications

PDE1B2 regulates cGMP and a subset of the phenotypic characteristics acquired upon macrophage differentiation from a monocyte

PDE1B2 regulates cGMP and a subset of the phenotypic characteristics acquired upon macrophage differentiation from a monocyte

The DNA-binding factor Ctcf critically controls gene expression in macrophages

Vasculogenic mimicry by bone marrow macrophages in patients with multiple myeloma

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