TXNIP knockdown alleviates hepatocyte ischemia reperfusion injury through preventing p38/JNK pathway activation

Zhang, Yong; Miao, Liangsheng; Cai, Yingmin; He, Jiaxuan; Zhang, Zhenni; Wu, Gang; Zheng, Juan

doi:10.1016/j.bbrc.2018.05.185

Cited by 14 publications

(12 citation statements)

References 33 publications

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“…In a previous study, Lekva T et al has reported the high TXNIP mRNA level in Cushing's syndrome [20]. TXNIP has also been documented to be overexpressed in hepatocyte ischemia reperfusion injury [21]. What's more, we also discovered that MEG3 specifically bound to miR-214 to modulate TXNIP expression, and reduced MEG3 expression caused a rise in miR-214 expression which could declined TXNIP expression.…”

Section: Discussionsupporting

confidence: 59%

Long non-coding RNA MEG3 silencing and microRNA-214 restoration elevate osteoprotegerin expression to ameliorate osteoporosis by limiting TXNIP

Ding¹,

Gu²,

Yang³

et al. 2019

Preprint

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BackgroundLong non-coding RNAs (LncRNAs) have been found to regulate innumerable diseases, yet the role of lncRNA MEG3 in osteoporosis (OP) has rarely been discussed. Here, we intend to probe into the mechanism of MEG3 on OP development by modulating microRNA-214 (miR-214) and thioredoxin-interacting protein (TXNIP)MethodsRat models of OP were established. MEG3, miR-214, and TXNIP mRNA expression in rat femoral tissues was detected, along with TXNIP, PCNA, cyclin D1, OCN, RUNX2, Osteolix, OPG, and PANKL protein expression. Ca, P and ALP contents in rat blood samples were also determined. Primary osteoblasts were isolated and cultured. Viability, COL-I, COL-II and COL-Χ contents, ALP content and activity, and mineralized nodule area of rat osteoblasts in each group were further detected.ResultsMEG3 and TXNIP were overexpressed while miR-214 was underexpressed in femoral tissues of OP rats. MEG3 silencing and miR-214 overexpression increased BMD, BV/TV, Tb.N, Tb.Th, the number of osteoblasts, collagen area and OPG expression, and downregulated PANKL of femoral tissues in OP rats. MEG3 silencing and miR-214 overexpression elevated Ca and P contents and reduced ALP content in OP rats’ blood, elevated viability, differentiation ability, COL-I and COL-Χ contents and ALP activity, and abated COL-II content of osteoblasts. MEG3 specifically bound to miR-214 to regulate TXNIP.ConclusionCollectively, we demonstrated that MEG3 silencing and miR-214 overexpression promote proliferation and differentiation of osteoblasts in OP by downregulating TXNIP, which further improves OP.

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Section: Discussionsupporting

confidence: 59%

Long non-coding RNA MEG3 silencing and microRNA-214 restoration elevate osteoprotegerin expression to ameliorate osteoporosis by limiting TXNIP

Ding¹,

Gu²,

Yang³

et al. 2019

Preprint

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“…We have also found that the overexpressed miR‐20b‐3p could decelerate the retinal cell apoptosis in retina of DR rats by targeting TXNIP. In accordance with this result, Zhang et al have provided evidence that the inhibition of XTNIP could ameliorate the oxygen–glucose deprivation and reoxygenation‐induced cell apoptosis in hepatic ischemia and reperfusion injury …”

Section: Discussionmentioning

confidence: 56%

Elevated microRNA‐20b‐3p and reduced thioredoxin‐interacting protein ameliorate diabetic retinopathy progression by suppressing the NLRP3 inflammasomes

Wang

et al. 2020

IUBMB Life

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Over the years, microRNA‐20b‐3p (miR‐20b‐3p) has been found to play an essential role in human diseases; we aimed to investigate the effect of miR‐20b‐3p on the progression of diabetic retinopathy (DR). The DR rat models were established by streptozotocin injection and treated with miR‐20b‐3p mimics, silenced, or overexpressed thioredoxin‐interacting protein (TXNIP). Afterward, the expression of miR‐20b‐3p and TXNIP, visual function, inflammatory factors, microvascular injury, vascular permeability, cell apoptosis, and angiogenesis in rats' retinal tissues were assessed. The target relation between miR‐20b‐3p and TXNIP was confirmed by dual luciferase reporter gene assay. MiR‐20b‐3p was poorly expressed while TXNIP was highly expressed in DR rats' retinal tissues. Elevated miR‐20b‐3p and inhibited TXNIP promoted the visual function, and restricted the inflammatory reaction, microvascular injury, vascular permeability, cell apoptosis, and angiogenesis in DR rats, thereby decelerating the development of DR. Furthermore, TXNIP was targeted by miR‐20b‐3p. We have found in this study that elevated miR‐20b‐3p could repress the levels of inflammatory factors by inhibiting TXNIP, thus attenuating the pathology of retina in DR rats, which provided new candidates for DR treatment.

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“…MAPK pathways have important roles in cell proliferation, differentiation, apoptosis and inflammation ( 52 , 53 ). Studies have indicated that extracellular signals are transferred between cells via the MAPK pathway in order to induce various cellular responses ( 54 , 55 ).…”

Section: Discussionmentioning

confidence: 99%

Theaflavins attenuate ethanol‑induced oxidative stress and cell apoptosis in gastric mucosa epithelial cells via downregulation of the mitogen‑activated protein kinase pathway

2018

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Ethanol-induced diseases of the gastric mucosa are the most common and refractory diseases of gastrointestinal system in clinic, and are mediated by oxidative stress and apoptosis pathways. Theaflavins (TFs) are considered to be antioxidants. The present study aimed to determine the molecular mechanism underlying the ability of TFs to attenuate ethanol-induced oxidative stress and apoptosis in GES-1 gastric mucosa epithelial cells. A Cell Counting Kit-8 (CCK-8) assay was performed to investigate the cell viability of GES-1 cells following administration of ethanol (0.5 mol/l) and subsequent treatment with TFs (20, 40 and 80 µg/ml) for specific time intervals. A carboxyfluorescein diacetate succinimidyl ester assay was used to measure proliferation and further investigate the results of the CCK-8 assay. Flow cytometry was performed to measure reactive oxygen species (ROS) levels and the apoptosis rates of GES-1 cells. Furthermore, levels of oxidative stress-associated factors, including malondialdehyde, superoxide dismutase and glutathione, were investigated using commercial kits. Reverse transcription-quantitative polymerase chain reaction and western blot assays were performed to determine the expression levels of apoptosis-associated factors, as well as the phosphorylation levels of extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and p38 kinase (p38). The results of the present study demonstrated that treatment with ethanol inhibited GES-1 cell proliferation, and enhanced ROS levels and apoptosis rates, potentially via downregulation of B-cell lymphoma-2 (Bcl-2) expression and upregulation of Bcl-2-associated X and caspase-3 expression levels, as well as enhancing the phosphorylation levels of ERK, JNK and p38. However, treatment with TFs was revealed to attenuate the effects of ethanol administration on GES-1 cells in a dose-dependent manner. In conclusion, TFs may attenuate ethanol-induced oxidative stress and apoptosis in gastric mucosa epithelial cells via downregulation of various mitogen-activated protein kinase pathways.

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TXNIP knockdown alleviates hepatocyte ischemia reperfusion injury through preventing p38/JNK pathway activation

Cited by 14 publications

References 33 publications

Long non-coding RNA MEG3 silencing and microRNA-214 restoration elevate osteoprotegerin expression to ameliorate osteoporosis by limiting TXNIP

Long non-coding RNA MEG3 silencing and microRNA-214 restoration elevate osteoprotegerin expression to ameliorate osteoporosis by limiting TXNIP

Elevated microRNA‐20b‐3p and reduced thioredoxin‐interacting protein ameliorate diabetic retinopathy progression by suppressing the NLRP3 inflammasomes

Theaflavins attenuate ethanol‑induced oxidative stress and cell apoptosis in gastric mucosa epithelial cells via downregulation of the mitogen‑activated protein kinase pathway

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