Dynamic expression of miR-206-3p during mouse skin development is independent of keratinocyte differentiation

Yuan, Ming; Zhou, Hong; Wu, Weijiang; Hu, Lichao; Chen, Hongbing

doi:10.3892/mmr.2015.4456

Cited by 8 publications

(6 citation statements)

References 31 publications

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“…In this study, we demonstrated that miR-206-3p was significantly downregulated in shGATA4 OMSCs and their supernatant-derived exosomes. miR-206-3p is widely acknowledged as a characteristic, positive regulator of muscle differentiation 27 and is also expressed at remarkable levels in brown adipocytes 28 . Studies also indicated the potential role of miR-206-3p in the pathogenesis and pathology of osteoporosis 21 , 22 .…”

Section: Discussionmentioning

confidence: 99%

GATA4-driven miR-206-3p signatures control orofacial bone development by regulating osteogenic and osteoclastic activity

Guo¹,

Gu²,

Ma³

et al. 2021

Theranostics

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Growth disorders in the orofacial bone development process may lead to orofacial deformities. The balance between bone matrix formation by mesenchymal lineage osteoblasts and bone resorption by osteoclasts is vital for orofacial bone development. Although the mechanisms of orofacial mesenchymal stem cells (OMSCs) in orofacial bone development have been studied intensively, the communication between OMSCs and osteoclasts remains largely unclear. Methods: We used a neural crest cell-specific knockout mouse model to investigate orofacial bone development in GATA-binding protein 4 (GATA4) morphants. We investigated the underlying mechanisms of OMSCs-derived exosomes (OMExos) on osteoclastogenesis and bone resorption activity in vitro . miRNAs were extracted from OMExos, and differences in miRNA abundances were determined using an Affymetrix miRNA array. Luciferase reporter assays were used to validate the binding between GATA4 and miR-206-3p in OMSCs and to confirm the putative binding of miR-206-3p and its target genes in OMSCs and osteoclasts. The regulatory mechanism of the GATA4-miR-206-3p axis in OMSC osteogenic differentiation and osteoclastogenesis was examined in vitro and in vivo . Results: Wnt1-Cre;Gata4 fl/fl mice (cKO) not only presented inhibited bone formation but also showed active bone resorption. Osteoclasts cocultured in vitro with cKO OMSCs presented an increased capacity for osteoclastogenesis, which was exosome-dependent. Affymetrix miRNA array analysis showed that miR-206-3p was downregulated in exosomes from shGATA4 OMSCs. Moreover, the transcriptional activity of miR-206-3p was directly regulated by GATA4 in OMSCs. We further demonstrated that miR-206-3p played a key role in the regulation of orofacial bone development by directly targeting bone morphogenetic protein-3 (Bmp3) and nuclear factor of activated T -cells, cytoplasmic 1 (NFATc1). OMExos and agomiR-206-3p enhanced bone mass in Wnt1-cre;Gata4 fl/fl mice by augmenting trabecular bone structure and decreasing osteoclast numbers. Conclusion: Our findings confirm that miR-206-3p is an important downstream factor of GATA4 that regulates the functions of OMSCs and osteoclasts. These results demonstrate the efficiency of OMExos and microRNA agomirs in promoting bone regeneration, which provide an ideal therapeutic tool for orofacial bone deformities in the future.

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Section: Discussionmentioning

confidence: 99%

GATA4-driven miR-206-3p signatures control orofacial bone development by regulating osteogenic and osteoclastic activity

Guo¹,

Gu²,

Ma³

et al. 2021

Theranostics

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“…A list of microRNAs found to degrade BDNF mRNA transcripts in oncology research is as follows: miR-10a, miR-22, miR-204, miR-107, miR-382, miR-496, miR-497, miR-584, miR-744, miR-26a-1, and miR-26a-2 subtypes [24,28,58,60,72,75,78,88,93,94,96,102,112,125,126,128,132,133,137,190]. The evidence that miR-206 is able to suppress BDNF synthesis in diverse tissues such as the cardiac muscles, the skeletal muscles, and the endothelial tissue elucidates a role for microRNAs in tissue-tissue communication, although their actions might be locally regulated [30,43,45,48,61,92,102,115,120,139,142,169,171,177,191]. Some microRNAs are released from cells by membrane-derived vesicles, lipoproteins, and other ribonucleoprotein complexes and travel through the blood stream reaching recipient cells in distant tissues [192], providing communication between disparate cell types and diverse biological mechanisms and homeostatic pathways.…”

Section: Bdnf By Micrornasmentioning

confidence: 98%

BDNF Modulation by microRNAs: An Update on the Experimental Evidence

De Assis,

Murawska-Ciałowicz

2024

Cells

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MicroRNAs can interfere with protein function by suppressing their messenger RNA translation or the synthesis of its related factors. The function of brain-derived neurotrophic factor (BDNF) is essential to the proper formation and function of the nervous system and is seen to be regulated by many microRNAs. However, understanding how microRNAs influence BDNF actions within cells requires a wider comprehension of their integrative regulatory mechanisms. Aim: In this literature review, we have synthesized the evidence of microRNA regulation on BDNF in cells and tissues, and provided an analytical discussion about direct and indirect mechanisms that appeared to be involved in BDNF regulation by microRNAs. Methods: Searches were conducted on PubMed.gov using the terms “BDNF” AND “MicroRNA” and “brain-derived neurotrophic factor” AND “MicroRNA”, updated on 1 September 2023. Papers without open access were requested from the authors. One hundred and seventy-one papers were included for review and discussion. Results and Discussion: The local regulation of BDNF by microRNAs involves a complex interaction between a series of microRNAs with target proteins that can either inhibit or enhance BDNF expression, at the core of cell metabolism. Therefore, understanding this homeostatic balance provides resources for the future development of vector-delivery-based therapies for the neuroprotective effects of BDNF.

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“…Y. Peng et al, 2016;Xia et al, 2016;Xiang et al, 2016;Yan et al, 2015;Xiao yu Zhang et al, 2018). The evidences that miR-206 is able to suppress BDNF synthesis in diverse tissues such as the cardiac muscles, the skeletal muscles and the endothelial tissue elucidate a role for microRNAs in a tissue-tissue communication, although their actions might be locally regulated (Guan et al, 2021; S. T. Lee et al, 2012;Mu et al, 2015;Solomon et al, 2019;Tapocik et al, 2014;Tian et al, 2014;Xie et al, 2017;Xing et al, 2018;X. Yang et al, 2014;.…”

Section: Bdnf By Micrornasmentioning

confidence: 99%

BDNF Modulation by microRNAs: An Update on the Experimental Evidence

de Assis,

Murawska-cialowicz

2024

Preprint

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MicroRNAs can interfere with a protein function by suppressing their messenger RNA translation or the synthesis of its related factors. The function of brain-derived neurotrophic factor (BDNF) is essential to the proper formation and function of the nervous system and is seen to be regulated by many microRNAs. However, understanding how microRNAs influence BDNF actions within cells requires a wider comprehension of their integrative regulatory mechanisms. Aim: In this literature review, we have synthesized the evidence of microRNA regulation on BDNF in cells and tissues, and provided an analytical discussion about direct and indirect mechanisms that appeared involved in BDNF regulation by microRNAs. Methods: Searches were conducted on PubMed.gov using the terms “BDNF” AND “MicroRNA” and “brain-derived neurotrophic factor” AND “MicroRNA”, updated on September 1st, 2023. Papers without open access were requested from the authors. One hundred and seventy-one papers were included for review and discussion. Results and Discussion: The local regulation of BDNF by microRNAs involves a complex interaction between a series of microRNAs with target proteins that can either inhibit or enhance BDNF expression, at the core of cell metabolism. Therefore, understanding this homeostatic balance provides resources for the future development of vector-delivery-based therapies for the neuroprotective effects of BDNF.

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Dynamic expression of miR-206-3p during mouse skin development is independent of keratinocyte differentiation

Cited by 8 publications

References 31 publications

GATA4-driven miR-206-3p signatures control orofacial bone development by regulating osteogenic and osteoclastic activity

GATA4-driven miR-206-3p signatures control orofacial bone development by regulating osteogenic and osteoclastic activity

BDNF Modulation by microRNAs: An Update on the Experimental Evidence

BDNF Modulation by microRNAs: An Update on the Experimental Evidence

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