Class A Scavenger Receptor Exacerbates Osteoclastogenesis by an Interleukin-6-Mediated Mechanism through ERK and JNK Signaling Pathways

Guo, Shuyu; Ni, Yuanyuan; Ben, Jingjing; Xia, Yang; Zhou, Tingting; Wang, Dongyue; Ni, Jinliang; Bai, Hui; Wang, Lin; Ma, Junqing; Chen, Qi

doi:10.7150/ijbs.14654

Cited by 23 publications

(14 citation statements)

References 42 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The skulls were dissected free of soft tissue, and fixed in 70% ethanol overnight. The slice thickness for micro-CT scans was 18 μm at 50 kV and 456 μA 24 . Images were reconstructed and analyzed by NRecon v1.6 and CTAn v1.13.8.1 software (Bruker, Germany).…”

Section: Methodsmentioning

confidence: 99%

“…SCAPs were used to evaluate stem cell surface markers on flow cytometric (FCM) analysis. Briefly, cell suspensions were collected and incubated in the dark for 1 h at 4 °C with CD29 APC, CD90 PE CY7, CD34-PE and CD45-FITC antibodies (BD Biosciences, San Jose, USA) 24 . Cells were washed twice in PBS and the expression profiles analyzed by flow cytometry following staining 29 .…”

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Role of GATA binding protein 4 (GATA4) in the regulation of tooth development via GNAI3

Guo

Zhang

Zhou

et al. 2017

Sci Rep

Self Cite

View full text Add to dashboard Cite

Transcription factor GATA4 regulates cardiac and osteoblast differentiation. However, its role in tooth development is not clear. Therefore, we generated Wnt1-Cre;GATA4 fl/fl mice, with conditional inactivation of the GATA4 gene in the dental papilla mesenchymal cells. Phenotypic analysis showed short root deformity along with reduced expressions of odonto/osteogenic markers. Proliferation (but not apoptosis) of cells around the apical area of the root was attenuated. In vitro, we knocked down GATA4 expression in stem cells of dental apical papilla (SCAPs). Proliferation, migration and odonto/ osteogenic differentiation of SCAPs were affected in the shGATA4 group. Overexpression of GATA4 in SCAPs increased mineralization. Based on our previous iTRAQ results, guanine nucleotide binding proteins 3 (GNAI3) is one of the distinct proteins after GATA4 deletion. G protein signaling is involved in bone development, remodeling, and disease. In this study, both GATA4 deletion in the mouse root and knock-down in human SCAPs decreased the expression of GNAI3. Dual-luciferase and ChIP assay confirmed the direct binding of GATA4 to the GNAI3 promoter, both in vitro and in vivo. GNAI3 knockdown significantly decreased the odonto/osteogenic differentiation ability of SCAPs. We thus establish the role of GATA4 as a novel regulator of root development and elucidate its downstream molecular events.Development of tooth root occurs after crown formation and the process involves reciprocal epithelio-mesenchymal interactions 1, 2 . The hard tissue of tooth is comprised of enamel, dentin, and cementum. Dental epithelial cells are the precursors of ameloblasts which in turn form the enamel. Odontoblasts differentiate from dental papilla mesenchymal cells and form the dentin. Dental follicle cells are genuine precursors of cementoblasts which in turn differentiate into cementoblasts. Both odontoblasts and cementoblasts are derived from neural crest cells (NCCs).GATA binding protein 4 (GATA4) is a zinc finger-containing transcription factor, and is reported to play a vital function in cardiac and intestinal development 3, 4 . GATA4 also regulates the expression of the angiogenic marker vascular endothelial growth factor (VEGF), and VEGF was reported to promote embryonic jaw extension 5,6 . According to our own previous microarray results (unpublished data), GATA4 expression in the embryonic mouse maxillofacial tissues at embryo day 13.5 (E13.5) was significantly higher than that at E18.5. This result suggests a vital role of GATA4 in the development of the maxillofacial tissues. Besides, several studies have indicated a role of GATA4 in the regulation of osteoblasts 7,8 . The development of both bone and tooth has several common features. Both MSCs from bone marrows and SCAPs were as potent in osteo/dentinogenic differentiation 9 . This aroused our interest in studying the effect of GATA4 in tooth development. So far, the involvement of GATA4 in tooth development has never been reported. One of the reasons is that global knockout of GATA...

show abstract

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Role of GATA binding protein 4 (GATA4) in the regulation of tooth development via GNAI3

Guo

Zhang

Zhou

et al. 2017

Sci Rep

Self Cite

View full text Add to dashboard Cite

show abstract

“…Genetically modified mice were sacrificed at various time points and fixed in freshly prepared 4% paraformaldehyde (PFA) overnight at 4°C. The slice thickness for micro-CT scans was 18 μm at 50 kV and 456 μA 13. Images were reconstructed and analysed using NRecon v1.6 and CTAn v1.13.8.1 software (Bruker, Germany).…”

Section: Methodsmentioning

confidence: 99%

GATA Binding Protein 4 Regulates Tooth Root Dentin Development via FBP1

et al. 2020

Self Cite

View full text Add to dashboard Cite

Tooth development is a complex process that is regulated precisely by several signalling pathways and transcription factors. GATA-binding protein 4 (GATA4) is a DNA binding transcription factor, and our previous study showed that GATA4 is a novel regulator of root development. However, it remains unclear whether GATA4 is necessary for odontoblast differentiation and dentin formation. Here, we evaluated the phenotypic changes of Wnt1-Cre;GATA4fl/fl mice. The mutant mice showed defective dentin and short root deformity. The odontoblasts lost polarity instead of exhibiting a shorter height and flattened morphology. Moreover, the expression of several molecules, such as DSPP, COL-1, DCN, and PCNA, were downregulated during mutant tooth development. In vivo, we injected lentivirus to overexpress GATA4 in mice root. The dentin formation and the expression of odonto/osteogenic markers (DSPP, COL-1, DCN) were enhanced in the GATA4 overexpression group. During the in vitro study, the ability of proliferation, migration and odonto/osteogenic differentiation was declined by GATA4 knockdown approach in human dental pulp stem cells (DPSCs). The expression of odonto/osteogenic markers (DSPP, BMP4, RUNX2, OSX, OPN, OCN) was reduced in the shGATA4 group, while overexpressing GATA4 in DPSCs promoted mineralization. Furthermore, an immunoprecipitation-mass spectrometry procedure was used to confirm the interaction between GATA4 and Fructose-1, 6-bisphosphatase 1 (FBP1). We used gain and lose-of-function to delineated the role of GATA4 in regulating FBP1 expression. Knocking down GATA4 in DPSCs resulted in decreased glucose consumption and lactate production. We used small hairpin RNA targeting FBP1 to reduce the expression of FBP1 in DPSCs, which significantly increased glucose consumption and lactate production. Together, the results suggested that GATA4 is important for root formation and odontoblast polarity, as it promotes the growth and differentiation of dental mesenchymal cells around the root and affects the glucose metabolism of DPSCs via the negative regulation of FBP1.

show abstract

“…Scanning was performed with a micro-CT scanner (Skyscan, Kontich, Belgium). Slice thickness was 18 μm at 50 kV and 456 μA [ 31 ]. Finally, images were reconstructed and analyzed using NRecon v1.6 and CTAn v1.13.8.1 software.…”

Section: Methodsmentioning

confidence: 99%

GATA4 as a novel regulator involved in the development of the neural crest and craniofacial skeleton via Barx1

et al. 2018

Self Cite

View full text Add to dashboard Cite

The role of GATA-binding protein 4 (GATA4) in neural crest cells (NCCs) is poorly defined. Here we showed that mouse NCCs lacking GATA4 exhibited developmental defects in craniofacial bone, teeth, and heart. The defects likely occurred due to decreased cell proliferation at the developmental stage. The in vitro results were consistent with the mouse model. The isobaric tags for relative and absolute quantitation assay revealed that BARX1 is one of the differentially expressed proteins after GATA4 knockdown in NCCs. On the basis of the results of dual-luciferase, electro-mobility shift, and chromatin immunoprecipitation assays, Barx1 expression is directly regulated by GATA4 in NCCs. In zebrafish, gata4 knockdown affects the development of NCCs derivatives. However, the phenotype in zebrafish could be partly rescued by co-injection of gata4 morpholino oligomers and barx1 mRNA. This study identified new downstream targets of GATA4 in NCCs and uncovered additional evidence of the complex regulatory functions of GATA4 in NCC development.

show abstract

Class A Scavenger Receptor Exacerbates Osteoclastogenesis by an Interleukin-6-Mediated Mechanism through ERK and JNK Signaling Pathways

Cited by 23 publications

References 42 publications

Role of GATA binding protein 4 (GATA4) in the regulation of tooth development via GNAI3

Role of GATA binding protein 4 (GATA4) in the regulation of tooth development via GNAI3

GATA Binding Protein 4 Regulates Tooth Root Dentin Development via FBP1

GATA4 as a novel regulator involved in the development of the neural crest and craniofacial skeleton via Barx1

Contact Info

Product

Resources

About