Expression of transcription factor zinc-binding protein-89 (ZBP-89) is inhibited by inflammatory cytokines

Borghaei, Ruth C.; Chambers, Mariah

doi:10.2147/plmi.s6249

Cited by 6 publications

(1 citation statement)

References 35 publications

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“…As a transcriptional factor, this gene is capable of influencing a lot on their tightly regulated genes. According to previous reports, ZNF148 mRNA and protein expression are significantly inhibited in human primary gingival fibroblasts by IL‐1β [16]. An exciting finding demonstrated that ZNF148 could bind to the MMP3 promoter at a polymorphic (5A/6A) site together with NF‐κB and further affect MMP3 protein levels.…”

Section: Discussionmentioning

confidence: 89%

Loss of microRNA‐147 function alleviates synovial inflammation through ZNF148 in rheumatoid and experimental arthritis

Jiang

et al. 2021

Eur J Immunol

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MicroRNA‐147 (miR‐147) had been previously found induced in synoviocytes by inflammatory stimuli derived from T cells in experimental arthritis. This study was designed to verify whether loss of its function might alleviate inflammatory events in joints of experimental and rheumatoid arthritis (RA). Dark Agouti (DA) rats were injected intradermally with pristane to induce arthritis, and rno‐miR‐147 antagomir was locally administrated into individual ankle compared with negative control or rno‐miR‐155‐5p antagomir (potential positive control). Arthritis onset, macroscopic severity, and pathological changes were monitored. While in vitro, gain or loss function of hsa‐miR‐147b‐3p/hsa‐miR‐155‐5p and ZNF148 was achieved in human synovial fibroblast cell line SW982 and RA synovial fibroblasts (RASF). The expression of miRNAs and mRNAs was detected by using RT‐quantitative PCR, and protein expression was detected by using Western blotting. Anti‐miR‐147 therapy could alleviate the severity, especially for the synovitis and joint destruction in experimental arthritis. Gain of hsa‐miR‐147b‐3p/hsa‐miR‐155‐5p function in TNF‐α stimulated SW982 and RASF cells could upregulate, in contrast, loss of hsa‐miR‐147b‐3p/hsa‐miR‐155‐5p function could downregulate the gene expression of TNF‐α, IL‐6, MMP3, and MMP13. Hence, such alteration could participate in synovial inflammation and joint destruction. RNAi of ZNF148, a miR‐147's target, increased gene expression of TNF‐α, IL‐6, MMP3, and MMP13 in SW982 and RASF cells. Also, mRNA sequencing data showed that hsa‐miR‐147b‐3p mimic and ZNF148 siRNA commonly regulated the gene expression of CCL3 and DEPTOR as well as some arthritis and inflammation‐related pathways. Taken together, miR‐147b‐3p contributes to synovial inflammation through repressing ZNF148 in RA and experimental arthritis.

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Section: Discussionmentioning

confidence: 89%

Loss of microRNA‐147 function alleviates synovial inflammation through ZNF148 in rheumatoid and experimental arthritis

Jiang

et al. 2021

Eur J Immunol

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Zinc-binding protein-89 (ZBP-89) cooperates with NF-κB to regulate expression of matrix metalloproteinases (MMPs) in response to inflammatory cytokines

Borghaei

Gorski

Seutter

et al. 2016

Biochemical and Biophysical Research Communications

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Promoter cloning and characterization of the human programmed cell death protein 4 (pdcd4) gene: evidence for ZBP-89 and Sp-binding motifs as essential Pdcd4 regulators

et al. 2012

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Pdcd4 (programmed cell death protein 4) is an important novel tumour suppressor inhibiting transformation, translation, invasion and intravasation, and its expression is down-regulated in several cancers. However, little is known about the transcriptional regulation and the promoter of this important tumour suppressor. So far the following is the first comprehensive study to describe the regulation of Pdcd4 transcription by ZBP-89 (zinc-finger-binding protein 89), besides characterizing the gene promoter. We identified the transcriptional start sites of the human pdcd4 promoter, a functional CCAAT-box, and the basal promoter region. Within this basal region, computer-based analysis revealed several potential binding sites for ZBPs, especially for Sp (specificity protein) family members and ZBP-89. We identified four Sp1/Sp3/Sp4-binding elements to be indispensable for basal promoter activity. However, overexpression of Sp1 and Sp3 was not sufficient to enhance Pdcd4 protein expression. Analysis in different solid cancer cell lines showed a significant correlation between pdcd4 and zbp-89 mRNA amounts. In contrast with Sp transcription factors, overexpression of ZBP-89 led to an enhanced expression of Pdcd4 mRNA and protein. Additionally, specific knockdown of ZBP-89 resulted in a decreased pdcd4 gene expression. Reporter gene analysis showed a significant up-regulation of basal promoter activity by co-transfection with ZBP-89, which could be abolished by mithramycin treatment. Predicted binding of ZBP-89 to the basal promoter was confirmed by EMSA (electrophoretic mobility-shift assay) data and supershift analysis for ZBP-89. Taken together, data for the first time implicate ZBP-89 as a regulator of Pdcd4 by binding to the basal promoter either alone or by interacting with Sp family members.

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Expression of transcription factor zinc-binding protein-89 (ZBP-89) is inhibited by inflammatory cytokines

Cited by 6 publications

References 35 publications

Loss of microRNA‐147 function alleviates synovial inflammation through ZNF148 in rheumatoid and experimental arthritis

Loss of microRNA‐147 function alleviates synovial inflammation through ZNF148 in rheumatoid and experimental arthritis

Zinc-binding protein-89 (ZBP-89) cooperates with NF-κB to regulate expression of matrix metalloproteinases (MMPs) in response to inflammatory cytokines

Promoter cloning and characterization of the human programmed cell death protein 4 (pdcd4) gene: evidence for ZBP-89 and Sp-binding motifs as essential Pdcd4 regulators

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