Suppression of microRNA‑27a protects against liver ischemia/reperfusion injury by targeting PPARγ and inhibiting endoplasmic reticulum stress

Chi, Xiaobin; Jiang, Yi; Chen, Yongbiao; Yang, Fang; Cai, Qiucheng; Fan, Pingsheng; Lv, Lizhi; Zhang, Xiaojin

doi:10.3892/mmr.2019.10645

Cited by 8 publications

(7 citation statements)

References 45 publications

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“…They can affect apoptosis, autophagy, inflammation, oxidation, etc . By bioinformatic analysis and a dual-luciferase reporter assay, PPARγ was identified as a target gene of miR-27a ( Chi et al, 2019 ). For the molecular mechanism of PPARγ signaling, microRNA, or other noncoding RNA (circular RNA, long noncoding RNA, etc .…”

Section: Summary and Perspectivementioning

confidence: 99%

PPARγ in Ischemia-Reperfusion Injury: Overview of the Biology and Therapy

et al. 2021

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Ischemia-reperfusion injury (IRI) is a complex pathophysiological process that is often characterized as a blood circulation disorder caused due to various factors (such as traumatic shock, surgery, organ transplantation, burn, and thrombus). Severe metabolic dysregulation and tissue structure destruction are observed upon restoration of blood flow to the ischemic tissue. Theoretically, IRI can occur in various tissues and organs, including the kidney, liver, myocardium, and brain, among others. The advances made in research regarding restoring tissue perfusion in ischemic areas have been inadequate with regard to decreasing the mortality and infarct size associated with IRI. Hence, the clinical treatment of patients with severe IRI remains a thorny issue. Peroxisome proliferator-activated receptor γ (PPARγ) is a member of a superfamily of nuclear transcription factors activated by agonists and is a promising therapeutic target for ameliorating IRI. Therefore, this review focuses on the role of PPARγ in IRI. The protective effects of PPARγ, such as attenuating oxidative stress, inhibiting inflammatory responses, and antagonizing apoptosis, are described, envisaging certain therapeutic perspectives.

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Section: Summary and Perspectivementioning

confidence: 99%

PPARγ in Ischemia-Reperfusion Injury: Overview of the Biology and Therapy

et al. 2021

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“…However, modulation of ATAD3a expression has little effect on the activation of caspases, which demonstrated that the regulation of apoptosis by ATAD3a occurs in a caspase-independent manner. It has been documented that miR-27a plays an important role in the regulation of apoptosis [42][43][44]. miR-27a can regulate cell apoptosis by targeting Fas-associated protein with death domain (FADD) [42], SMAD5 [43], PPAR gamma [44], etc.…”

Section: Discussionmentioning

confidence: 99%

miRNA‐27a Transcription Activated by c‐Fos Regulates Myocardial Ischemia‐Reperfusion Injury by Targeting ATAD3a

Bao

Qiao

et al. 2021

Oxidative Medicine and Cellular Longevity

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MicroRNA-27a (miR-27a) has been implicated in myocardial ischemia-reperfusion injury (MIRI), but the underlying mechanism is not well understood. This study is aimed at determining the role of miR-27a in MIRI and at investigating upstream molecules that regulate miR-27a expression and its downstream target genes. miR-27a expression was significantly upregulated in myocardia exposed to ischemia/reperfusion (I/R) and cardiomyocytes exposed to hypoxia/reoxygenation (H/R). c-Fos could regulate miR-27a expression by binding to its promoter region. Moreover, overexpression of miR-27a led to a decrease in cell viability, an increase in LDH and CK-MB secretion, and an increase in apoptosis rates. In contrast, suppression of miR-27a expression resulted in the opposite effects. ATPase family AAA-domain-containing protein 3A (ATAD3a) was identified as a target of miR-27a. miR-27a regulated the translocation of apoptosis-inducing factor (AIF) from the mitochondria to the nucleus and H/R-induced apoptosis via the regulation of ATAD3a. It was found that inhibiting miR-27a in vivo by injecting a miR-27a sponge could ameliorate MIRI in an isolated rat heart model. In conclusion, our study demonstrated that c-Fos functions as an upstream regulator of miR-27a and that miR-27a regulates the translocation of AIF from the mitochondria to the nucleus by targeting ATAD3a, thereby contributing to MIRI. These findings provide new insight into the role of the c-Fos/miR-27a/ATAD3a axis in MIRI.

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“…endoplasmic reticulum stress (erS) is considered a driving force of acute renal failure (arF) induced by i/r (9). increasing evidence indicates that persistent activation of erS and subsequent elevation of apoptotic cascades are key to the pathogenesis of renal i/r injury (10)(11)(12)(13). additionally, a previous study confirmed that apoptosis occurs in the early phase of ischemia and can be worsened by reperfusion (13).…”

Section: Introductionmentioning

confidence: 98%

Nobiletin alleviates ischemia/reperfusion injury in the kidney by activating PI3K/AKT pathway

et al. 2020

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recent studies have demonstrated that nobiletin (NOB) displays anti-oxidative and anti-apoptotic efficacies against multiple pathological insults. However, the potential effects of noB on the injury caused by ischemia and reperfusion (i/r) in the kidney remain undetermined. in the present study, i/r injury was elicited by right kidney removal and left renal pedicel clamping for 45 min, followed by reperfusion for 24 h. noB was added at the start of reperfusion. Histological examination, detection of biomarkers in plasma, and measurement of apoptosis induced by endoplasmic reticulum stress (erS) were used to evaluate renal injury. additionally, the Pi3K/aKT inhibitor lY294002 was also used in mechanistic experiments. NOB pre-treatment significantly reduced renal damage caused by i/r injury, as indicated by decreased serum levels of creatine, blood urea nitrogen and tubular injury scores. Furthermore, noB inhibited elevated erS-associated apoptosis, as evidenced by reduced apoptotic rates and erS-related signaling molecules (such as, c/eBP homologous protein, caspase-12 and glucose-regulated protein of 78 kda). noB increased phosphorylation of proteins in the Pi3K/aKT pathway. The inhibition of Pi3K/aKT signaling with pharmacological inhibitors could reverse the beneficial effects of NOB during renal i/r insult. in conclusion, noB pre-treatment may alleviate i/r injury in the kidney by inhibiting reactive oxygen species production and erS-induced apoptosis, partly through the Pi3K/aKT signaling pathway.

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Suppression of microRNA‑27a protects against liver ischemia/reperfusion injury by targeting PPARγ and inhibiting endoplasmic reticulum stress

Cited by 8 publications

References 45 publications

PPARγ in Ischemia-Reperfusion Injury: Overview of the Biology and Therapy

PPARγ in Ischemia-Reperfusion Injury: Overview of the Biology and Therapy

miRNA‐27a Transcription Activated by c‐Fos Regulates Myocardial Ischemia‐Reperfusion Injury by Targeting ATAD3a

Nobiletin alleviates ischemia/reperfusion injury in the kidney by activating PI3K/AKT pathway

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