Expression of Concern: MiRNA‐218 regulates osteoclast differentiation and inflammation response in periodontitis rats through Mmp9

Guo, Jie; Zeng, Xuemin; Miao, Jie; Liu, Chunpeng; Wei, Fulan; Liu, Dongxu; Zheng, Zhong; Ting, Kang; Wang, Chunling; Liu, Yi

doi:10.1111/cmi.12979

Cited by 53 publications

(35 citation statements)

References 38 publications

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“…Related study confirmed that miR‐218 suppressed the progression of cervical cancer via the LYN/NF‐κB signalling pathway (Xu, et al , 2018). In addition, miR‐218 plays an important role in regulating the osteoclast differentiation and inflammation response in rats with periodontitis (Guo, et al , 2019) and the development of human natural killer cells (Victor, et al , 2018). Here, miR‐218 suppressed the activation of NF‐κB and the LPS‐induced secretion of TNF‐α, IL‐1β and IL‐6.…”

Section: Discussionmentioning

confidence: 99%

Exosome‐derived uterine miR‐218 isolated from cows with endometritis regulates the release of cytokines and chemokines

Wang

Xiao

Xie

et al. 2020

Microbial Biotechnology

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Summary As an inflammation of the endometrium, endometritis can affect fertility and lead to serious economic losses in the dairy industry. Widely found in various tissues and body fluids, exosomes and exosome micro (mi)RNAs have been shown to play an important regulatory role in the immune responses. As one of differentially expressed exosome miRNAs, miR‐218 is involved in the pathogenesis of bovine endometritis. The mechanisms of miR‐218 in regulating the release of cytokines and chemokines in endometritis, however, are poorly understood. Exosomes were isolated from bovine uterine cavity fluid and verified by transmission electron microscopy. An in vitro lipopolysaccharide‐treated cell model for bovine endometritis was then established to evaluate the correlation between exosome‐derived miR‐218 and the immune responses. We demonstrated that exosomes could be used to deliver miR‐218 from endometrial epithelial cells (EECs) into the uterine microenvironment and adjacent recipient cells to modulate local immune responses. miR‐218 packaged in the exosomes secreted from EECs acts as an inhibitor by blocking immune factors such as interleukin (IL)‐6, IL‐1β, tumour necrosis factor‐α, the chemokines macrophage inflammatory genes (MIP)‐1α and MIP‐1β to maintain the immune balance in the uterus. However, uterine inflammation altered the immunoregulatory mechanism of exosome miR‐218. MiR‐218 is a potential biomarker for the detection of endometritis. Our findings also revealed a new mechanism for the development of endometritis in cows.

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Section: Discussionmentioning

confidence: 99%

Exosome‐derived uterine miR‐218 isolated from cows with endometritis regulates the release of cytokines and chemokines

Wang

Xiao

Xie

et al. 2020

Microbial Biotechnology

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“…MicroRNAs (miRNAs), small noncoding RNAs rarely translated into peptides or protein, are of great importance in multiple biological processes and various kinds of disease . Several studies have proved that miRNAs could be critical regulators in bone remodeling and inflammatory response such as periodontitis . The aberrant miRNA expression reacting to pathologic products, in turn, affects periodontitis .…”

Section: Introductionmentioning

confidence: 99%

“…6,7 Several studies have proved that miRNAs could be critical regulators in bone remodeling and inflammatory response such as periodontitis. [8][9][10] The aberrant miRNA expression reacting to pathologic products, in turn, affects periodontitis. [9][10][11] In our previous studies, it has been shown that microRNA-335-5p (miR-335-5p) could promote osteoblast differentiation and bone regeneration in vitro and in miR-335-5p transgenic (335-Tg) mice via inhibiting DKK1, a Wnt pathway antagonist, which have been well-characterized.…”

Section: Introductionmentioning

confidence: 99%

“…[8][9][10] The aberrant miRNA expression reacting to pathologic products, in turn, affects periodontitis. [9][10][11] In our previous studies, it has been shown that microRNA-335-5p (miR-335-5p) could promote osteoblast differentiation and bone regeneration in vitro and in miR-335-5p transgenic (335-Tg) mice via inhibiting DKK1, a Wnt pathway antagonist, which have been well-characterized. [3][4][5] Besides, several studies have reported the inhibitive effects of miR-335-5p on bone-related disorders.…”

Section: Introductionmentioning

confidence: 99%

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Potential roles of miR‐335‐5p on pathogenesis of experimental periodontitis

Lian

Liu

et al. 2019

J of Periodontal Research

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Background and Objective Periodontitis is a prevalent oral disease responsible for tooth loss. MicroRNAs have been proven crucial in bone disorders over the past decades. Promotive effect on osteogenic activities by microRNA‐335‐5p (miR‐335‐5p) has been well demonstrated, but its role involved in the pathogenesis of periodontitis remains elusive. In this study, we established experimental periodontitis (EP) on transgenic mice overexpressing miR‐335‐5p (335‐Tg) to investigate the novel effects of miR‐335‐5p on periodontal inflammation and bone loss. Methods Experimental periodontitis was established via ligation. The expression of inflammatory and osteoclastic genes was examined by quantitative real‐time PCR (qPCR). Morphology of alveolar bone was analyzed by microcomputed tomography (μCT). Hematoxylin and eosin (H&E), tartrate‐resistant acid phosphatase (TRAP), and Toll‐like receptor 4 (TLR4) immunohistochemistry (IHC) staining were conducted for histological analysis. Results The expression of miR‐335‐5p decreased significantly in the periodontal tissues of EP. Compared to the WT‐EP group, μCT analysis showed less bone loss in the 335‐Tg‐EP group accompanying with a decreased number of TRAP‐positive osteoclasts. H&E and IHC staining exhibited attenuated inflammation and TLR4 expression in the 335‐Tg‐EP group. Furthermore, reduced expressions of IL‐1β, IL‐6, TNF‐α, and TLR4 were also detected in the 335‐Tg‐EP group. Overexpression of miR‐335‐5p in vivo weakened the periodontal bone destruction and inflammation compared with the WT‐EP group. Conclusions Our data exhibit novel roles of miR‐335‐5p in preventing bone loss and inflammation in experimental periodontitis.

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“…Last, miR-218-5p has been stated to promote osteogenic differentiation of MSCs in mice (41) and increase bone formation by targeting WNT pathway inhibitors, (42) all the while also negatively regulating osteoclastogenesis through RANKL, Mmp9, and NF-κB. (43,44) Of note, we have recently published findings of elevated serum Dickkopf-1 (DKK1; dickkopf WNT signaling pathway inhibitor 1) concentrations in these same PLS3 mutation-positive subjects. (45) DKK1 is an osteocyte-derived inhibitor of the WNT pathway in bone.…”

Section: Discussionmentioning

confidence: 87%

Unique, Gender-Dependent Serum microRNA Profile in PLS3 Gene-Related Osteoporosis

Mäkitie

Hackl

Weigl³

et al. 2020

Journal of Bone and Mineral Research

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Plastin 3 (PLS3), encoded by PLS3, is a newly recognized regulator of bone metabolism, and mutations in the encoding gene result in severe childhood-onset osteoporosis. Because it is an X chromosomal gene, PLS3 mutation-positive males are typically more severely affected whereas females portray normal to increased skeletal fragility. Despite the severe skeletal pathology, conventional metabolic bone markers tend to be normal and are thus insufficient for diagnosing or monitoring patients. Our study aimed to explore serum microRNA (miRNA) concentrations in subjects with defective PLS3 function to identify novel markers that could differentiate subjects according to mutation status and give insight into the molecular mechanisms by which PLS3 regulates skeletal health. We analyzed fasting serum samples for a custom-designed panel comprising 192 miRNAs in 15 mutation-positive (five males, age range 8-76 years, median 41 years) and 14 mutation-negative (six males, age range 8-69 years, median 40 years) subjects from four Finnish families with different PLS3 mutations. We identified a unique miRNA expression profile in the mutation-positive subjects with seven significantly upregulated or downregulated miRNAs (miR-93-3p, miR-532-3p, miR-133a-3p, miR-301b-3p, miR-181c-5p, miR-203a-3p, and miR-590-3p; p values, range .004-.044). Surprisingly, gender subgroup analysis revealed the difference to be even more distinct in female mutation-positive subjects (congruent p values, range .007-.086) than in males (p values, range .127-.843) in comparison to corresponding mutation-negative subjects. Although the seven identified miRNAs have all been linked to bone metabolism and two of them (miR-181c-5p and miR-203a-3p) have bioinformatically predicted targets in the PLS3 3 0 untranslated region (3 0-UTR), none have previously been reported to associate with PLS3. Our results indicate that PLS3 mutations are reflected in altered serum miRNA levels and suggest there is crosstalk between PLS3 and these miRNAs in bone metabolism. These provide new understanding of the pathomechanisms by which mutations in PLS3 lead to skeletal disease and may provide novel avenues for exploring miRNAs as biomarkers in PLS3 osteoporosis or as target molecules in future therapeutic applications.

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Expression of Concern: MiRNA‐218 regulates osteoclast differentiation and inflammation response in periodontitis rats through Mmp9

Cited by 53 publications

References 38 publications

Exosome‐derived uterine miR‐218 isolated from cows with endometritis regulates the release of cytokines and chemokines

Exosome‐derived uterine miR‐218 isolated from cows with endometritis regulates the release of cytokines and chemokines

Potential roles of miR‐335‐5p on pathogenesis of experimental periodontitis

Unique, Gender-Dependent Serum microRNA Profile in PLS3 Gene-Related Osteoporosis

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