Overexpression of GATA4 enhances the antiapoptotic effect of exosomes secreted from cardiac colony-forming unit fibroblasts via miRNA221-mediated targeting of the PTEN/PI3K/AKT signaling pathway

Hao, Chunshu; Lu, Zhengri; Zhao, Yuanyuan; Chen, Zhong; Shen, Chengxing; Ma, Genshan; Chen, Lijuan

doi:10.1186/s13287-020-01759-8

Cited by 19 publications

(18 citation statements)

References 51 publications

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“…Contrary to the function of PI3K, PTEN reduces the activation of AKT and prevents all downstream signaling events regulated by AKT 54 . Evidence has confirmed the involvement of the PTEN/PI3K/AKT signaling pathway in the pathogenesis of many heart diseases, including coronary heart disease, chronic cardiac failure, and myocardial infarction (MI) 55 . Significantly, the PI3K/AKT pathway also plays a decisive role in the mechanism of heavy metal toxicity.…”

Section: Discussionmentioning

confidence: 99%

“…54 Evidence has confirmed the involvement of the PTEN/PI3K/AKT signaling pathway in the pathogenesis of many heart diseases, including coronary heart disease, chronic cardiac failure, and myocardial infarction (MI). 55 Significantly, the PI3K/AKT pathway also plays a decisive role in the mechanism of heavy metal toxicity. Studies have confirmed that Cd exposure inhibited PI3K/AKT signaling pathway to induce cell apoptosis.…”

Section: Western Blotting Analysismentioning

confidence: 99%

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Selenium protects against cadmium‐induced cardiac injury by attenuating programmed cell death viaPI3K/AKT/PTENsignaling

Feng

Yang

et al. 2022

Environmental Toxicology

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Cadmium (Cd) is an environmental pollutant that has an enormous influence on agricultural production, but selenium (Se) can alleviate its toxicity. The present study aimed to illustrate the effects of Se on Cd-induced heart injury. All 40 rabbits were randomly divided into four groups: control group, Se [0.5 mg kg À1 Ábody weight (BW)] group, Cd (1 mg kg À1 ÁBW) group, and Se + Cd group. After 30 days of feeding, morphological changes, the levels of oxidative stress and myocardial enzyme, the content of cardiac troponin T, programmed cell death (pyroptosis, autophagy and apoptosis), and PI3K/AKT/PTEN transduction capacity were observed. The results showed that Cd destroyed the physiological balance of trace elements and caused myocardial damage, increased the cardiac oxidative damage and led to programmed cell death.Coadministration of Se prominently ameliorated histological lesions and improved cardiac function of hearts in Cd-induced rabbits. Furthermore, Se exerted detoxification and oxidation resistance, maintained trace element homeostasis, and alleviated the changes of mRNA and protein levels of pyroptosis-, autophagy-and apoptosiscontrolling factors and PI3K/AKT/PTEN signal molecules caused by Cd. In conclusion, Se might protect against Cd-induced pyroptosis, autophagy and apoptosis by interfering with PI3K/AKT/PTEN signaling in heart.

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Section: Discussionmentioning

confidence: 99%

Section: Western Blotting Analysismentioning

confidence: 99%

Selenium protects against cadmium‐induced cardiac injury by attenuating programmed cell death viaPI3K/AKT/PTENsignaling

Feng

Yang

et al. 2022

Environmental Toxicology

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“…PTEN, a homolog of phosphatase and tension protein missing from chromosome 10, is an effective tumor suppressor that regulates cell growth and survival [ 25 , 26 ]. For instance, miR-221 has been reported to curb PTEN expression and activate phosphatidylinositol 3 kinase (PI3K)/AKT, thus repressing the apoptosis of cardiomyocytes (CMs) [ 27 ]. In addition, Per2 facilitates NHAC-kn inflammation in osteoarthritis by heightening the PTEN level and dampening the PI3K/Akt expression [ 28 ].…”

Section: Discussionmentioning

confidence: 99%

miR-19b-3p relieves intervertebral disc degeneration through modulating PTEN/PI3K/Akt/mTOR signaling pathway

Zhao

2021

Aging

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Emerging studies have revealed that non-coding RNAs contribute to regulating intervertebral disc degeneration (IVDD). Here, we intended to probe into the function of miR-19b-3p in IVDD evolvement. The miR-19b-3p level in the intervertebral disc (IVD) tissues of IVDD patients and IL-1β/TNF-α/hydrogen peroxide-treated human nucleus pulposus cells (HNPCs) was determined by quantitative real-time polymerase chain reaction (qRT-PCR). Also, qRT-PCR was conducted to examine the profiles of MMP-3, MMP-9, MMP-13, ADAMTS-4 and ADAMTS-5. The PTEN/PI3K/Akt/mTOR pathway was examined by Western blot (WB). The miR-19b-3p overexpression assay was carried out, and HNPC proliferation and apoptosis were compared by the cell counting kit-8 (CCK-8) assay and flow cytometry (FCM). In addition, the mechanism of action of miR-19b-3p was clarified using the PTEN inhibitor (VO-Ohpic triphosphate) or the mTOR inhibitor (Rapamycin) on the basis of IL-1β intervention and miR-19b-3p mimics transfection. Our results testified that miR-19b-3p expression was curbed in IVD tissues of the IVDD patients (vs. normal IVD tissues) and IL-1β-, TNF-α, or hydrogen peroxide-treated HNPCs. Up-regulating miR-19b-3p enhanced HNPC proliferation and hampered its apoptosis. Moreover, miR-19b-3p dampened the PTEN profile and activated the PI3K/Akt/mTOR pathway. Interestingly, attenuating PTEN reduced IL-1β-, TNF-α-, or hydrogen peroxide-mediated HNPC apoptosis and up-regulated PI3K/Akt/mTOR, while inhibiting the mTOR pathway offset the protective function of miR-19b-3p . Further mechanism studies illustrated that miR-19b-3p targeted the 3’untranslated region (UTR) of PTEN and abated the PTEN level. This research confirmed that miR-19b-3p suppressed HNPC apoptosis in the in-vitro model of IVDD by regulating PTEN/PI3K/Akt/mTOR pathway.

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“…Ectopic expression of EZH2 in prostate cells can induce the transcriptional repression of a specific cohort of genes involved in prostate cancer [ 47 ]. GATA4 overexpression was shown to enhance the protective effect of cCFU-F-derived exosomes on myocardial ischemic injuries [ 48 ]. KCNC2 with tumor-specific alternative splicing is associated with the development of glioma [ 49 ].…”

Section: Discussionmentioning

confidence: 99%

Identifying the Predictive Role of Oxidative Stress Genes in the Prognosis of Glioma Patients

Wang

Liu

et al. 2021

Med Sci Monit

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Background Gliomas are primary aggressive brain tumors with poor prognoses. Oxidative stress plays a crucial role in the tumorigenesis and drug resistance of gliomas. The aim of the present study was to use integrated bioinformatics analyses to evaluate the prognostic value of oxidative stress-related genes (OSRGs) in glioma. Material/Methods Disease- and prognosis-associated OSRGs were identified using microarray and clinical data from the Chinese Glioma Genome Atlas database. Functional enrichment, gene-gene interaction, protein-protein interaction, and survival analyses were performed in screened OSRGs. The protein expression was validated by the Human Protein Atlas database. A risk score model was constructed and verified through Cox regression, receiver operating characteristic curve, principal component, and stratified analyses. The Cancer Genome Atlas (TCGA) database was used for external validation. A nomogram was constructed to facilitate the clinical application. Results Twenty-one disease-associated and 14 prognosis-associated OSRGs were identified. Enrichment analyses indicated that these signature OSRGs were involved in tumorigenesis and drug resistance of glioma. The risk score model demonstrated a significant difference in overall survival between the high- and low-risk groups. The area under the curve and hazard ratio (1.296) revealed the independent prognostic value of the model. The model exhibited good predictive efficacy in the TCGA cohort. A clinical nomogram was constructed to calculate survival rates in glioma patients at 1, 3, and 5 years. Conclusions Our comprehensive study indicated that OSRGs were valuable for prognosis prediction in glioma, which provides a novel insight into the relationship between oxidative stress and glioma and a potential therapeutic strategy for glioma patients.

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Overexpression of GATA4 enhances the antiapoptotic effect of exosomes secreted from cardiac colony-forming unit fibroblasts via miRNA221-mediated targeting of the PTEN/PI3K/AKT signaling pathway

Cited by 19 publications

References 51 publications

Selenium protects against cadmium‐induced cardiac injury by attenuating programmed cell death viaPI3K/AKT/PTENsignaling

Selenium protects against cadmium‐induced cardiac injury by attenuating programmed cell death viaPI3K/AKT/PTENsignaling

miR-19b-3p relieves intervertebral disc degeneration through modulating PTEN/PI3K/Akt/mTOR signaling pathway

Identifying the Predictive Role of Oxidative Stress Genes in the Prognosis of Glioma Patients

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