Activation of <scp>PI3K/Akt/mTOR</scp> signaling pathway triggered by <scp>PTEN</scp> downregulation in the pathogenesis of <scp>C</scp>rohn's disease

Long, Shuo; He, Yao; Chen, Min Hu; Cao, Kang; Chen, Yu Jun; Chen, Bai Li; Mao, Ren; Zhang, Sheng Hong; Zhu, Zhaoqin; Zeng, Zhi; Hu, Pin Jin

doi:10.1111/1751-2980.12095

Cited by 23 publications

(13 citation statements)

References 19 publications

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“…Research indicates that UCMSCs can upregulate the expression of PTEN, which leads to the decline of the migration ability of tumor cells and thus inhibits their biological activity (Ali, 2000). This mechanism is also supported by our research members' findings, that is, that UCMSCs induce the apoptosis of hepatic stellate cells by upregulating the expression of PTEN (Long et al, 2013).…”

Section: Introductionsupporting

confidence: 80%

Effect of human umbilical cord mesenchymal stem cells on endometriotic cell proliferation and apoptosis

Ln¹,

Lin²,

Bn³

et al. 2015

Genet. Mol. Res.

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ABSTRACT. The objective of this study was to observe the effects of human umbilical cord mesenchymal stem cells (UCMSCs) on the proliferation and apoptosis of endometriotic cells. Endometriotic cells and UCMSCs were primarily cultured in vitro. In the experimental group, a UCMSC and endometriotic cell non-contact co-culture system was established. The control group consisted of 1 x 10 5 endometriotic cells cultured alone. The proliferation and apoptosis of endometriotic cells were respectively detected using the MTT method and flow cytometry. The mRNA expression level of the tensin homologue gene (PTEN) in endometriotic cells was detected by reverse transcriptionpolymerase chain reaction amplification. Compared with the control group, the proliferation of endometriotic cells in the experimental group was clearly inhibited (P < 0.05) and time-dependent (P < 0.05). In addition, the number of apoptotic cells were significantly increased (P < 0.05), and the amount of cells, which entered S phase from G1 phase, decreased significantly. Furthermore, the mRNA expression level of the PTEN gene in the experimental group was significantly higher than in the control group (P < 0.05). These results suggest that UCMSCs might inhibit the proliferation of human endometriotic cells in vitro and promote their apoptosis by upregulating the expression of PTEN.

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Section: Introductionsupporting

confidence: 80%

Effect of human umbilical cord mesenchymal stem cells on endometriotic cell proliferation and apoptosis

Ln¹,

Lin²,

Bn³

et al. 2015

Genet. Mol. Res.

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“…The PI3K-Akt signaling pathway is activated by variety of pathogens leading to accentuate diseases 36 . For example, activation of this signaling pathway promotes actin rearrangement, leading to the host inflammatory response that persists in IBD 37 . Additionally, cell destruction caused by viruses can expose cryptic receptors to promote bacteria adhesion and it is well known, that some symbiotic gut microbiota and invasive intestinal pathogens invade epithelial cells, and cause extensive intestinal damage [38][39][40] .…”

Section: Discussionmentioning

confidence: 99%

Differential expression and correlation analysis of miRNA–mRNA profiles in swine testicular cells infected with porcine epidemic diarrhea virus

Zhang

Chang

Zhang

et al. 2021

Sci Rep

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The variant virulent porcine epidemic diarrhea virus (PEDV) strain (YN15) can cause severe porcine epidemic diarrhea (PED); however, the attenuated vaccine-like PEDV strain (YN144) can induce immunity in piglets. To investigate the differences in pathogenesis and epigenetic mechanisms between the two strains, differential expression and correlation analyses of the microRNA (miRNA) and mRNA in swine testicular (ST) cells infected with YN15, YN144, and mock were performed on three comparison groups (YN15 vs Control, YN144 vs Control, and YN15 vs YN144). The mRNA and miRNA expression profiles were obtained using next-generation sequencing (NGS), and the differentially expressed (DE) (p-value < 0.05) mRNA and miRNA were obtained using DESeq R package. mRNAs targeted by DE miRNAs were predicted using the miRanda algortithm. 8039, 8631 and 3310 DE mRNAs, and 36, 36, and 22 DE miRNAs were identified in the three comparison groups, respectively. 14,140, 15,367 and 3771 DE miRNA–mRNA (targeted by DE miRNAs) interaction pairs with negatively correlated expression patterns were identified, and interaction networks were constructed using Cytoscape. Six DE miRNAs and six DE mRNAs were randomly selected to verify the sequencing data by real-time relative quantitative reverse transcription polymerase chain reaction (qRT-PCR). Based on bioinformatics analysis, we discovered the differences were mostly involved in host immune responses and viral pathogenicity, including NF-κB signaling pathway and bacterial invasion of epithelial cells, etc. This is the first comprehensive comparison of DE miRNA–mRNA pairs in YN15 and YN144 infection in vitro, which could provide novel strategies for the prevention and control of PED.

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“…The mechanism of microRNA-21 has been investigated in Caco-2 cells, and may involve an effect on paracellular permeability via the PTEN level and Akt phosphorylation [33]. Moreover, activation of PI3K/Akt pathway has been demonstrated to inhibit the differentiation of T cells towards regulatory T cells [37] and previously a decreased PTEN expression level was observed in intestinal mucosal lymphocytes in CD patients, compared to controls [38]. …”

Section: Discussionmentioning

confidence: 99%

Genetic variation and expression levels of tight junction genes identifies association between MAGI3 and inflammatory bowel disease

2017

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BackgroundInflammatory bowel disease (IBD) is associated with increased intestinal permeability, which involves paracellular passage regulated through tight junctions (TJ). The aim of the study was to investigate single nucleotide polymorphisms (SNP) located in genes encoding interacting TJ proteins and corresponding expressions, in relation to IBD.MethodsAllelic associations between TJ-related genes (F11R, MAGI1, MAGI2, MAGI3, PARD3, PTEN, and TJP1) and IBD, Crohn’s disease (CD), or ulcerative colitis (UC) were investigated. PTPN22 was included since it’s located in the same genetic region as MAGI3. Gene expression levels were investigated in relation to genotype, inflammatory status, phenotype, and medical treatment.ResultsThe two strongest allelic associations were observed between IBD and SNPs in MAGI2 (rs6962966) and MAGI3 (rs1343126). Another MAGI3 SNP marker (rs6689879) contributed to increased ileal MAGI3 expression level in non-IBD controls. Furthermore, association between inflammation and decreased expression levels of MAGI3, PTEN, and TJP1 in colonic IBD as well as UC mucosa, and between inflammation and increased expression of PTPN22 in colonic IBD mucosa, was observed.ConclusionsOur findings lend support to a genetic basis for modulation of intestinal epithelial barrier in IBD, and we have identified MAGI3 as a new candidate gene for IBD.Electronic supplementary materialThe online version of this article (doi:10.1186/s12876-017-0620-y) contains supplementary material, which is available to authorized users.

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Activation of PI3K/Akt/mTOR signaling pathway triggered by PTEN downregulation in the pathogenesis of Crohn's disease

Abstract: The PI3K/Akt/mTOR signaling pathway was activated in CD. The activation of the PI3K/Akt/mTOR pathway caused by PTEN downregulation may be involved in the pathogenesis of CD.

Cited by 23 publications

References 19 publications

Effect of human umbilical cord mesenchymal stem cells on endometriotic cell proliferation and apoptosis

Effect of human umbilical cord mesenchymal stem cells on endometriotic cell proliferation and apoptosis

Differential expression and correlation analysis of miRNA–mRNA profiles in swine testicular cells infected with porcine epidemic diarrhea virus

Genetic variation and expression levels of tight junction genes identifies association between MAGI3 and inflammatory bowel disease

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