Long noncoding RNA H19 regulates the therapeutic efficacy of mesenchymal stem cells in rats with severe acute pancreatitis by sponging miR-138-5p and miR-141-3p

Song, Guodong; Zhou, Jia; Song, Ruimei; Liu, Dalu; Yu, Wennian; Xie, Wangcheng; Ma, Zhilong; Gong, Jian; Meng, Hui; Yang, Tianshe; Zhang, Song

doi:10.1186/s13287-020-01940-z

Cited by 24 publications

(15 citation statements)

References 46 publications

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“…Li et al demonstrated that miR-141-3p is important for osteogenic differentiation of stem cells from the apical papillae (SCAPs) [ 28 ]; miR-141-3p inhibits the proliferation of SCAPs and accelerates cellular senescence by downregulating the expression of YAP [ 28 ]. Recently, it has been found that knockdown of miR-141-3p can promote the proliferation level of mesenchymal stem cells by upregulating the expression of β -catenin, C-Myc, and cyclin D1 [ 29 ]. Despite these findings, the effect of miR-141-3p on the osteogenic differentiation ability of hPDLSCs under an inflammatory microenvironment has not been elucidated.…”

Section: Discussionmentioning

confidence: 99%

miR-141-3p Regulates EZH2 to Attenuate Porphyromonas gingivalis Lipopolysaccharide-Caused Inflammation and Inhibition of Osteogenic Differentiation in Human Periodontal Ligament Stem Cells

Zhu

Xiong

2022

Computational and Mathematical Methods in Medicine

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Objective. miR-141-3p has been demonstrated to be both anti-inflammatory and osteoprotective. This study is aimed at investigating the effect of miR-141-3p on osteogenic differentiation of human periodontal ligament stem cells (hPDLSCs) stimulated by Porphyromonas gingivalis lipopolysaccharide (PgLPS) and its mechanism. Methods. PgLPS was used to induce an inflammatory environment, and overexpression of miR-141-3p was done to assess its effect on hPDLSCs in an inflammatory environment. The level of miR-141-3p and EZH2 in hPDLSCs from each treatment group was detected via qRT-PCR, and the inflammatory factors IL-6 and IL-8 in the supernatant of each group were detected by ELISA. ALP staining and alizarin red staining were used to assess the effect of miR-141-3p on the osteogenic differentiation ability of hPDLSCs, and also, western blot was used to detect expression of osteogenic differentiation-related proteins. Further, dual-luciferase reporter assay examined whether miR-141-3p targeted EZH2. Results. PgLPS led to a significant decrease of miR-141-3p in hPDLSCs. Overexpression of miR-141-3p could enhance ALP activity and alizarin red staining intensity and increase Runx2, OPN and OCN protein expression levels in PgLPS-treated hPDLSCs. Additionally, miR-141-3p could reduce IL-6 and IL-8. miR-141-3p could target and negatively regulate EZH2, and overexpression of EZH2 reversed the promoting effect of miR-141-3p on osteogenic differentiation. Conclusion. miR-141-3p can attenuate PgLPS-induced inhibition of osteogenic differentiation and inflammation in hPDLSCs by negatively regulating EZH2.

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Section: Discussionmentioning

confidence: 99%

miR-141-3p Regulates EZH2 to Attenuate Porphyromonas gingivalis Lipopolysaccharide-Caused Inflammation and Inhibition of Osteogenic Differentiation in Human Periodontal Ligament Stem Cells

Zhu

Xiong

2022

Computational and Mathematical Methods in Medicine

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“…lncRNAs are involved in the progression of AP (1,42). The current study demonstrated that TUG1 expression was upregulated in AR42J cells cotreated with caerulein and LPS, suggesting that TUG1 may act as a promoter of AP.…”

Section: Discussionmentioning

confidence: 99%

“…Acute pancreatitis (AP) is a type of inflammatory disease, which results from the dysregulation of pancreatic enzymes in the pancreas (1,2). AP is very common, has a considerably high mortality rate and can cause systemic complications (3).…”

Section: Introductionmentioning

confidence: 99%

Emodin inhibits the progression of acute pancreatitis via regulation of lncRNA TUG1 and exosomal lncRNA TUG1

Wen

Tang

et al. 2021

Mol Med Rep

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Acute pancreatitis (AP) is one of the most frequent gastrointestinal diseases and has no specific treatment. It has been shown that dysfunction of pancreatic acinar cells can lead to AP progression. Emodin is a natural product, which can alleviate the symptoms of AP. However, the mechanism by which emodin regulates the function of pancreatic acinar cells remains unclear. Thus, the present study aimed to investigate the mechanism by which emodin modulates the function of pancreatic acinar cells. To mimic AP in vitro, pancreatic acinar cells were cotreated with caerulein and lipopolysaccharide (LPS). Exosomes were isolated using the ExoQuick precipitation kit. Western blot analysis, Nanosight Tracking analysis and transmission electron microscopy were performed to detect the efficiency of exosome separation. Gene expression was detected by reverse transcription-quantitative PCR. The levels of IL-1β and TNF-α were detected by ELISA. The data indicated that emodin significantly decreased the levels of IL-1β and TNF-α in the supernatant samples derived from AR42J cells cotreated with caerulein and LPS. In addition, emodin significantly promoted the proliferation of AR42J cells cotreated with caerulein and LPS, and inhibited apoptosis, while the effect of emodin was reversed by long non-coding (lnc)RNA taurine upregulated 1 (TUG1) overexpression. The expression level of TUG1 in AR42J cells or exosomes derived from AR42J cells was significantly increased following treatment of the cells with LPS and caerulein, while this effect was notably reversed by emodin treatment. In addition, exosomes derived from caerulein and LPS cotreated AR42J cells inhibited the differentiation and anti-inflammatory function of regulatory T cells, while treatment of the cells with emodin significantly decreased this effect. In conclusion, the data indicated that emodin inhibited the induction of inflammation in AR42J cells by regulating the expression of cellular and exosomal lncRNA. Therefore, emodin may be used as a potential agent for the treatment of AP.

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“…However, no data have been presented to verify the effect of NAFLD-derived lncRNA MALAT1 on the regulation of AP. It is reported that lncRNAs are involved in the progression of acute pancreatitis [ 15 , 16 ], but the influence of NAFLD-derived MALAT1 in acute pancreatitis remains blurry.…”

Section: Introductionmentioning

confidence: 99%

Nonalcoholic Fatty Liver Hepatocyte-Derived lncRNA MALAT1 Aggravates Pancreatic Cell Inflammation via the Inhibition of Autophagy by Upregulating YAP

Liu

Yao

Liu

et al. 2022

Computational Intelligence and Neuroscience

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Background. Acute pancreatitis (AP) is one of the most common gastrointestinal disorders, which causes death with a high mortality rate of about 30%. The study aims to identify whether the nonalcoholic fatty liver disease (NAFLD)-derived lncRNA MALAT1 participates in the inflammation of pancreatic cell and its potential mechanism. Methods. The NAFLD cell model was constructed by treating HepG2 cells with FFA. The in vitro model of acute pancreatitis (AP) was established by the administration of caerulein on AR42J cells. MALAT1 and si-MALAT1 were transfected into pancreatic cells, and then exosomes were collected from the NAFLD cell model and then were cocultured with AR42J cells. Transmission electron microscopy was used to observe the morphology of exosomes. Oil Red O staining was applied to reveal the lipid deposition. The triglyceride, IL-6, and TNF-α levels were detected using ELISA. The MALAT1 level in exosomes was detected by qRT-PCR. The CD9, CD63, CD81, and CYP2E1, LC3II, and LC3I levels were detected by western blot. Results. MALAT1 was upregulated in NAFLD-derived exosomes and increased the levels of IL-6 and TNF-α in pancreatic cells. NAFLD-derived exosomes inhibited YAP phosphorylation, decreased the levels of IL-6 and TNF-α, and reduced the ratio of LC3II/LC3I protein in pancreatic cells. Silencing MALAT1 significantly returned the inhibitory effect of NAFLD on hippo-YAP pathway. YAP1 signal transduction inhibitor CA3 reversed the decrease of LC3II/LC3I expression and the increase of IL-6 and TNF-α levels induced by MALAT1 in the AP cell model. Conclusions. NAFLD-derived MALAT1 exacerbates pancreatic cell inflammation via inhibiting autophagy by upregulating YAP.

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Long noncoding RNA H19 regulates the therapeutic efficacy of mesenchymal stem cells in rats with severe acute pancreatitis by sponging miR-138-5p and miR-141-3p

Cited by 24 publications

References 46 publications

miR-141-3p Regulates EZH2 to Attenuate Porphyromonas gingivalis Lipopolysaccharide-Caused Inflammation and Inhibition of Osteogenic Differentiation in Human Periodontal Ligament Stem Cells

miR-141-3p Regulates EZH2 to Attenuate Porphyromonas gingivalis Lipopolysaccharide-Caused Inflammation and Inhibition of Osteogenic Differentiation in Human Periodontal Ligament Stem Cells

Emodin inhibits the progression of acute pancreatitis via regulation of lncRNA TUG1 and exosomal lncRNA TUG1

Nonalcoholic Fatty Liver Hepatocyte-Derived lncRNA MALAT1 Aggravates Pancreatic Cell Inflammation via the Inhibition of Autophagy by Upregulating YAP

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