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The zinc finger transcription factor ZBP-89 is a repressor of the human β2-integrin CD11b gene
Abstract
Integrin CD11b is a differentiation marker of the myelomonocytic lineage and an important mediator of inflammation. Expression of theCD11b gene is transcriptionally induced as myeloid precursors differentiate into mature cells, then drops as monocytes further differentiate into macrophages. Previous studies have identified elements and factors involved in the transcriptional activation of the CD11b gene during myeloid differentiation, but no data exist regarding potential down-regulatory factors, especially in the later stages of differentiation. Using 2 copies of a GC-rich element (−141 to −110) in the CD11bpromoter, we probed a cDNA expression library for interacting proteins. Three clones were identified among 9.1 million screened, all encoding the DNA-binding domain of the zinc finger factor ZBP-89. Overexpression of ZBP-89 in the monocyte precursor cell line U937 reducedCD11b promoter-driven luciferase activity when U937 cells were induced to differentiate into monocytelike cells using phorbol esters. To identify the differentiation stage at which ZBP-89 repression of the CD11b gene is exerted, the protein level of ZBP-89 was correlated with that of CD11b mRNA in differentiating U937 as well as in normal human monocytes undergoing in vitro differentiation into macrophages. A clear inverse relationship was observed in the latter but not the former state, suggesting that ZBP-89 represses CD11b gene expression during the further differentiation of monocytes into macrophages.
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“Collectively, RhoH activity in the myeloid cell is critical in promoting macrophage terminal differentiation by the repression of the interlinked Cdc42 and Wnt intracellular signalling pathways and inflammatory effector proteins, CD11b and CD93.”
From The Role of RhoH in TCR Signalling and Its Involvement in Diseases (2021) · cites this paper as [66]
In the citing paper
“These monocytes and myeloblasts were treated with phorbol ester for 48 h and terminal differentiation into macrophages confirmed by their acquisition of a strong adhesive phenotype, morphological spreading, and characteristic down‐regulation of CD11b and CD93 protein expression (Figure 4A, B, Supplemental Figure S1) [54, 55].”
From Bimodal expression of RHOH during myelomonocytic differentiation: Implications for the expansion of AML differentiation therapy (2021) · cites this paper as [54]
In the citing paper
“The down‐regulation of CD11b and CD93 protein expression are individual hallmarks of the differentiation of monocytes into macrophages (Figure 4A, B) [54, 55].”
From Bimodal expression of RHOH during myelomonocytic differentiation: Implications for the expansion of AML differentiation therapy (2021) · cites this paper as [54]
In the citing paper
“In addition, RHOH induction is demonstrated to cause the down‐regulation of CD11b and CD93 protein expression characteristic of monocytes terminally differentiating into macrophages (Figure 4C) [54, 55].”
From Bimodal expression of RHOH during myelomonocytic differentiation: Implications for the expansion of AML differentiation therapy (2021) · cites this paper as [54]
In the citing paper
“Thus this terminal phase of monocytic differentiation is characterized by repression of inflammatory effector proteins such as the β2 integrin CD11b and CD93 [54, 55].”
From Bimodal expression of RHOH during myelomonocytic differentiation: Implications for the expansion of AML differentiation therapy (2021) · cites this paper as [54]
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Citations
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The proto-oncogene PU.1 regulates expression of the myeloid-specific CD11b promoter
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The Role of RhoH in TCR Signalling and Its Involvement in Diseases
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Leupold, J. H., Asangani, I. A., Mudduluru, G., & Allgayer, H. (2012) · Bioscience Reports · doi:10.1042/bsr20110045 · Cited by 23
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Self-citation
Metadata
- Authors
- Park, H., Shelley, C. S., & Arnaout, M. A.
- Affiliations
- From the Leukocyte Biology and Inflammation Program, Renal Unit, Massachusetts General Hospital, Harvard Medical School, Boston, MA.
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 2003-02-01
- Volume
- 101
- Issue
- 3
- Pages
- 894-902
- ISSN
- 1528-0020
- 0006-4971
- Cited by
- 26
- References
- 3
- Language
- en
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