RETRACTED ARTICLE: Mirt2 functions in synergy with miR-377 to participate in inflammatory pathophysiology of Sjögren's syndrome

Xin, Miaomiao; Liang, Hongda; Wang, Hongyue; Di, Wen; Wang, Liqin; Zhao, Lei; Sun, Mingshu; Wang, Jibo

doi:10.1080/21691401.2019.1626413

Cited by 14 publications

(14 citation statements)

References 29 publications

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“…High levels of miR-155-5p have also been reported in inflammatory lesion models, such as cerebral ischemia-reperfusion injury (45). As previously reported, an inflammatory lesion model was established in SGECs by treatment with IFN-γ, where IFN-γ-treatment increased apoptosis and IL-6 and TNF-α mRNA expression (30).…”

Section: Discussionmentioning

confidence: 75%

“…In total, five mice were randomly selected from the 30 mice and the salivary glands were collected from the parotid, submandibular and sublingual glands. In accordance with previous research, SGECs were extracted from the salivary glands of five mice and pooled (30). Briefly, the salivary glands were washed 2-3 times with PBS.…”

Section: Methodsmentioning

confidence: 99%

“…Negative control (NC)/miR-155-5p agomir (25 nmol/l; Shanghai GenePharma Co., Ltd.) or NC/miR-155-5p antagomir (25 nmol/l; Shanghai GenePharma Co., Ltd.) were transfected into SGECs for 24 h at 37˚C using Lipofectamine ® 3000 reagent (5 µl; Invitrogen; Thermo Fisher Scientific, Inc.). SGECs were treated with IFN-γ (10 ng/ml, Sino Biological https://www.sinobiological.com/) for 12 h at 37˚C to induce inflammation as previously described (30). For drug inhibition, SGECs were transfected with miR-155-5p agomir/agomir NC for 24 h at 37˚C, followed by treatment with IFN-γ (10 ng/ml) and pyrrolidine dithiocarbamate (PDTC, 100 uM; Shanghai Aladdin Biochemical Technology Co., Ltd.) for 12 h. For rescue experiments, ARRB2 overexpression vector (pcDNA3.1;…”

Section: Methodsmentioning

confidence: 99%

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Protective effects of miR‑155‑5p silencing on IFN‑γ‑induced apoptosis and inflammation in salivary gland epithelial cells

et al. 2021

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Previous studies have demonstrated that microRNAs (miRNAs/miRs) serve a vital role in the pathogenesis of Sjögren's syndrome (SS). The present study aimed to investigate the role of miR-155-5p in SS and determine its underlying molecular mechanism. An inflammatory lesion model was established by stimulating salivary gland epithelial cells (SGECs) with interferon-γ (IFN-γ). The apoptosis of SGECs was measured by using flow cytometry. Levels of proinflammatory factors were detected by reverse transcription-quantitative PCR and ELISA, respectively. Immunofluorescence was used for p65 staining. Dual-luciferase reporter assay was performed to verify the interaction between miR-155-5p and arrestin β2 (ARRB2). The protein levels in the NF-κB signaling pathway were assessed by western blotting. The results of the present study demonstrated that treatment with IFN-γ increased miR-155-5p expression, in addition to inducing apoptosis and inflammation in SGECs. Furthermore, overexpression of miR-155-5p promoted IFN-γ-induced apoptosis and inflammation in SGECs. Overexpression of miR-155-5p also increased Bax protein expression, enzyme activities of caspase 3 and caspase 9, release of inflammatory cytokines interleukin-6 and tumor necrosis factor-α, and decreased Bcl-2 protein expression in IFN-γ-treated SGECs. By contrast, all of the effects aforementioned were reversed following miR-155-5p knockdown. These results demonstrated that miR-155-5p activated the NF-κB signaling pathway, where treatment with the NF-κB inhibitor, pyrrolidine dithiocarbamate, reversed the effects of miR-155-5p overexpression on the inflammatory factors in IFN-γ-induced SGECs. miR-155-5p was demonstrated to target ARRB2 and negatively regulated its expression levels, such that overexpression of ARRB2 reversed the effects of miR-155-5p overexpression on the inflammatory response, apoptosis and the NF-κB signaling pathway in IFN-γ-treated SGECs. Collectively, results from the present study suggest that miR-155-5p may activate the NF-κB signaling pathway by negatively regulating ARRB2 to promote salivary gland damage during SS pathogenesis. This suggests that miR-155-5p may serve to be a potential target for the treatment of SS.

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Section: Discussionmentioning

confidence: 75%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Protective effects of miR‑155‑5p silencing on IFN‑γ‑induced apoptosis and inflammation in salivary gland epithelial cells

et al. 2021

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“…Subsequently, Xin et al (5) demonstrated that lncRNA myocardial infarction associated transcript 2 (Mirt2) reduces apoptosis and inflammatory levels in interferon (IFN)-γ-induced inflammation in salivary gland epithelial cells. It is hypothesized that Mirt2 might block NF-κB, and Janus kinase (JAK)/STAT3 signaling by increasing miR-377 expression levels.…”

Section: Role Of Lncrnas In Oral Inflammatory Disordersmentioning

confidence: 99%

“…Numerous factors, including non-coding (nc)RNAs, leukocytes, cytokines and complement components, are involved in this process (2,3). Long non-coding (lnc)RNAs affect oral inflammation by sponging microRNAs (miRNA/miR) (4) or activating downstream target miRNAs (5). Research on competing endogenous (ce)RNA mechanisms, in which lncRNAs sponge specific miRNAs to suppress their target genes, has increased in numbers in over the last 2 years (6).…”

Section: Introductionmentioning

confidence: 99%

Long non‑coding RNAs are novel players in oral inflammatory disorders, potentially premalignant oral epithelial lesions and oral squamous cell carcinoma (Review)

Zhang

Qiu

et al. 2020

Int J Mol Med

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In recent years, a large number of studies have shown that the abnormal expression of long non-coding (lnc)RNAs can lead to a variety of different diseases, including inflammatory disorders, cardiovascular disease, nervous system diseases, and cancers. Recent research has demonstrated the biological characteristics of lncRNAs and the important functions of lncRNAs in oral inflammation, precancerous lesions and cancers. The present review aims to explore and discuss the potential roles of candidate lncRNAs in oral diseases by summarizing multiple lncRNA profiles in diseased and healthy oral tissues to determine the altered lncRNA signatures. In addition, to highlight the exact regulatory mechanism of lncRNAs in oral inflammatory disorders, potentially premalignant oral epithelial lesions and oral squamous cell carcinoma. The detection of lncRNAs in oral samples has the potential to be used as a diagnostic and an early detection tool for oral diseases. Furthermore, lncRNAs are promising future therapeutic targets in oral diseases, and research in this field may expand in the future.

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Quercetin ameliorates salivary gland apoptosis and inflammation in primary Sjögren's syndrome through regulation of the leptin/OB‐R signaling

Chang

Kong

Guo

et al. 2022

Drug Development Research

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Dry mouth is the main manifestation of Sjögren syndrome (SS). Quercetin has been reported to alleviate radiation‐induced salivary gland damage, yet the effect of quercetin on SS‐caused salivary gland damage remains unclear. This study aimed to investigate the effects of quercetin on SS‐induced salivary gland damage and the mechanism underlying its therapeutic potential in SS. Here, NOD/Ltj mice were used to spontaneously mimic SS‐induced salivary gland inflammation in vivo and salivary gland epithelial cells (SGECs) were stimulated by interferon‐γ (IFN‐γ) to mimic cell inflammation in vitro. Results showed that quercetin significantly reduced loss of saliva flow, salivary gland damage, cell apoptosis, and inflammatory response in NOD/Ltj mice. Quercetin treatment also significantly reduced the increased serum leptin (LP) levels in NOD/Ltj mice. Furthermore, quercetin blocked the increases in the expression of obesity receptor (OB‐R) and its downstream Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) signaling in the salivary glands. In vitro experiments confirmed that quercetin could protect SGECs from IFN‐γ‐induced cell apoptosis and inflammation through the LP/OB‐R‐activated JAK2/STAT3 signaling. Hence, quercetin might protect against SS‐induced salivary gland damage by relieving cell apoptosis and inflammation by inhibiting the LP/OB‐R signaling, providing a new perspective for treating SS‐induced dry mouth.

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RETRACTED ARTICLE: Mirt2 functions in synergy with miR-377 to participate in inflammatory pathophysiology of Sjögren's syndrome

Cited by 14 publications

References 29 publications

Protective effects of miR‑155‑5p silencing on IFN‑γ‑induced apoptosis and inflammation in salivary gland epithelial cells

Protective effects of miR‑155‑5p silencing on IFN‑γ‑induced apoptosis and inflammation in salivary gland epithelial cells

Long non‑coding RNAs are novel players in oral inflammatory disorders, potentially premalignant oral epithelial lesions and oral squamous cell carcinoma (Review)

Quercetin ameliorates salivary gland apoptosis and inflammation in primary Sjögren's syndrome through regulation of the leptin/OB‐R signaling

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