Epigallocatechin-3-gallate inhibits inflammation and epithelial‑mesenchymal transition through the PI3K/AKT pathway via upregulation of PTEN in asthma

Yang, Nan; Zhang, Han; Cai, Xuxu; Shang, Yunxiao

doi:10.3892/ijmm.2017.3292

Cited by 44 publications

(40 citation statements)

References 48 publications

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“…Recently, numerous studies have investigated the protective effects of EGCG against asthma and other lung diseases such as COPD and lung pneumonia. EGCG may suppress inflammation and inflammatory cell infiltration into the lungs of asthmatic mice, and may also inhibit epithelial-mesenchymal transition EMT via the PI3K/Akt signaling pathway through upregulating the expression of phosphatase and tensin homolog (PTEN), both in vivo and in vitro [81].…”

Section: Other Dietary Constituents and Lung Infectionsmentioning

confidence: 99%

Functional Role of Dietary Intervention to Improve the Outcome of COVID-19: A Hypothesis of Work

Messina

Polito

Monda

et al. 2020

IJMS

158

150

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Background: On the 31 December 2019, the World Health Organization (WHO) was informed of a cluster of cases of pneumonia of unknown origin detected in Wuhan City, Hubei Province, China. The infection spread first in China and then in the rest of the world, and on the 11th of March, the WHO declared that COVID-19 was a pandemic. Taking into consideration the mortality rate of COVID-19, about 5-7%, and the percentage of positive patients admitted to intensive care units being 9-11%, it should be mandatory to consider and take all necessary measures to contain the COVID-19 infection. Moreover, given the recent evidence in different hospitals suggesting IL-6 and TNF-α inhibitor drugs as a possible therapy for COVID-19, we aimed to highlight that a dietary intervention could be useful to prevent the infection and/or to ameliorate the outcomes during therapy. Considering that the COVID-19 infection can generate a mild or highly acute respiratory syndrome with a consequent release of pro-inflammatory cytokines, including IL-6 and TNF-α, a dietary regimen modification in order to improve the levels of adiponectin could be very useful both to prevent the infection and to take care of patients, improving their outcomes.

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Section: Other Dietary Constituents and Lung Infectionsmentioning

confidence: 99%

Functional Role of Dietary Intervention to Improve the Outcome of COVID-19: A Hypothesis of Work

Messina

Polito

Monda

et al. 2020

IJMS

158

150

View full text Add to dashboard Cite

show abstract

“…Accordingly, these data identified PTEN as an endogenous defender against inflammation-mediated cellular damage in nasal epithelial cells. Previous studies have also illustrated the beneficial role of PTEN in acute kidney injury (28), diabetes (71), cardiomyopathy (72) and chronic fatty liver disease (73). Therefore, an approach to reverse PTEN activity could be considered as adjuvant therapy to enhance anti-inflammatory treatments in patients with chronic nasal and sinus inflammation, but this needs to be investigated further.…”

Section: Discussionmentioning

confidence: 97%

“…PTEN functions as a tumor suppressor involving in the regulation of the cell growth and differentiation (27). Previous studies have demonstrated that PTEN upregulation provides a survival advantage to nasal epithelial cells in asthma (28). Furthermore, pharmacological PTEN inhibition amplifies acute kidney injury (29,30), regulates inflammation-induced migration of myelocytes in zebrafish (31), and impacts nuclear factor-κB inflammatory pathways (32).…”

Section: Pten Enhances Nasal Epithelial Cell Resistance To Tnfα-inducmentioning

confidence: 99%

PTEN enhances nasal epithelial cell resistance to TNFα‑induced inflammatory injury by limiting mitophagy via repression of the TLR4‑JNK‑Bnip3 pathway

Xiang

Shouchuan

2018

Mol Med Report

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Nasal epithelial cell inflammatory injury is associated with chronic obstructive pulmonary disease development. However, the mechanism by which inflammation triggers nasal epithelial cell damage remains unclear. In the present study, tumor necrosis factor (TNF)α was used to induce an inflammatory injury and explore the underlying pathogenesis for nasal epithelial cell apoptosis in vitro, with a focus on mitochondrial homeostasis. Then, cellular apoptosis was detected via a terminal deoxynucleotidyl‑transferase‑mediated dUTP nick end labeling assay and western blotting. Mitochondrial function was evaluated via JC‑1 staining, mPTP opening measurement and western blotting. The results demonstrated that TNFα treatment induced nasal epithelial cell apoptosis, proliferation arrest and migration inhibition via downregulating phosphatase and tensin homolog (PTEN) levels. Increased PTEN expression was associated with reduce Toll‑like receptor (TLR)4‑c‑Jun kinase (JNK)‑Bcl2‑interacting protein 3 (Bnip3) pathway signaling, leading to reductions in mitophagy activity. Excessive mitophagy resulted in ATP deficiencies, mitochondrial dysfunction, caspase‑9 activation and cellular apoptosis. By contrast, PTEN overexpression in nasal epithelial cells alleviated the mitochondrial damage and cellular apoptosis via inhibiting the TLR4‑JNK‑Bnip3 pathway, favoring the survival of nasal epithelial cells under inflammatory injury. Therefore, this data uncovered a potential molecular basis for nasal epithelial cell apoptosis in response to inflammatory injury, and PTEN was identified as the endogenous defender of nasal epithelial cell survival via controlling lethal mitophagy by inhibiting the TLR4‑JNK‑Bnip3 pathway, suggesting that this pathway may be a potential target for clinically treating chronic nasal and sinus inflammatory injury.

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“…At present, it mainly focuses on inflammation, immune response changes and airway remodeling caused by abnormal subepithelial myofibroblasts and chronic inflammation. Studies have shown that abnormalities in multiple signaling pathways in lung tissue involve the development and progression of asthma, such as the PI3K/Akt, MAPK, ERK, JAK and c-Jun (El-Hashim et al, 2017;Li et al, 2015;Southworth et al, 2018;Wagh et al, 2017;Yang et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

“…Particularly, many studies have shown that activation of the PI3K/Akt pathway plays an important role in the development of asthma by activating oxidative stress and inflammatory responses (Wagh et al, 2017;Yang et al, 2018). The serine/threonine kinase Akt, also known as PKB (protein kinase B), is activated by lipid products of phosphatidylinositol 3kinase (PI3K).…”

Section: Introductionmentioning

confidence: 99%

Methylated Vnn1 at promoter regions induces asthma occurrence via the PI3K/Akt/NFκB-mediated inflammation in the IUGR mice

et al. 2020

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statementVascular noninflammatory molecule 1 (Vannin-1) is elevated in the intrauterine growth retardation (IUGR) asthmatic mice, leading to activation of the PI3K/Akt/NFκB pathway responsible for bronchial oxidative stress and hyperresponsiveness. AbstractIntrauterine growth retardation (IUGR) has high risk of developing bronchial asthma in childhood, whereas the underlying mechanisms remain unclear. This study aimed to disclose the role of vascular noninflammatory molecule 1 (vannin-1, encoded by the Vnn1 gene) and its downstream signaling in the IUGR asthmatic mice induced by ovalbumin. More significant histological alterations and increase of vannin-1 expressions were revealed in IUGR asthmatic mice, accompanied by elevated methylation of Vnn1 promoter regions. In IUGR asthmatic mice, we also found i) a direct binding of HNF4α and PGC1α to Vnn1 promoter by CHIP assay; ii) a direct interaction of HNF4α with PGC1α; iii) upregulation of phospho-PI3K p85/p55 and phospho-Akt Ser473 and downregulation of phospho-PTENT yr366 ; iv) increase in nuclear NFκB p65 and decrease in cytosolic IκB-α. In primary cultured bronchial epithelial cells derived from the IUGR asthmatic mice, knockdown of Vnn1 prevented upregulation of phospho-Akt Ser473 and increase of reactive oxygen species (ROS) and TGF-β production. Taken together, we demonstrate that elevated vannin-1 activates the PI3K/Akt/NFκB signaling pathway, leading to ROS and inflammation reactions responsible for asthma occurrence in IUGR. We also disclose that interaction of PGC1α and HNF4α promotes methylation of Vnn1 promoter regions and then upregulates vannin-1 expression.Biology Open • Accepted manuscript by guest on August 5, 2020 http://bio.biologists.org/ Downloaded from

show abstract

Epigallocatechin-3-gallate inhibits inflammation and epithelial‑mesenchymal transition through the PI3K/AKT pathway via upregulation of PTEN in asthma

Cited by 44 publications

References 48 publications

Functional Role of Dietary Intervention to Improve the Outcome of COVID-19: A Hypothesis of Work

Functional Role of Dietary Intervention to Improve the Outcome of COVID-19: A Hypothesis of Work

PTEN enhances nasal epithelial cell resistance to TNFα‑induced inflammatory injury by limiting mitophagy via repression of the TLR4‑JNK‑Bnip3 pathway

Methylated Vnn1 at promoter regions induces asthma occurrence via the PI3K/Akt/NFκB-mediated inflammation in the IUGR mice

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