MicroRNA-29a/b/c targets iNOS and is involved in protective remote ischemic preconditioning in an ischemia-reperfusion rat model of non-alcoholic fatty liver disease

Duan, Yunfei; Sun, Donglin; Chen, Jing; Zhu, Feng; An, Yong

doi:10.3892/ol.2017.5623

Cited by 15 publications

(10 citation statements)

References 38 publications

(47 reference statements)

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“…Written informed consent for chemotherapy treatment was obtained from all patients with confirmed diagnosis of TNBC detected by inpatient biopsy. All patients were tested for liver function(serum enzymology test) ( 33 ), electrocardiogram and echocardiography to evaluate their tolerance to chemotherapy. Oral dexamethasone tablets were given 3 days prior to NAC.…”

Section: Methodsmentioning

confidence: 99%

Association between the methylation status of PCDH17 and the efficacy of neoadjuvant chemotherapy in triple-negative breast cancer

Kong

Liang

et al. 2020

Oncol Lett

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The present study aimed to assess whether the methylation status of the protocadherin 17 gene ( PCDH17 ) in triple-negative breast cancer (TNBC) tissues was associated with the efficacy of neoadjuvant chemotherapy (NAC). The present study included 280 patients diagnosed with TNBC using core needle biopsy. Tumor pathological diagnosis was determined via hematoxylin and eosin staining. Immunohistochemical staining was used to determine estrogen receptor, progesterone receptor, human epidermal growth factor receptor-2 and Ki-67 status. PCDH17 methylation status was analyzed using methylation-specific PCR. χ 2 tests were performed to analyze differences between PCDH17 methylation status and TNBC clinicopathological features. Univariate and multivariate logistic regressions were used to analyze whether PCDH17 methylation status predicted a curative effect of NAC. The multivariate analysis included factors with P<0.2 from the univariate analysis and those that were clinically associated with NAC. A total of 228 patients were positive for PCDH17 methylation, while the remainder 52 were negative. Additionally, 107 patients achieved pathological complete response (pCR) after NAC. The pCR rate was 67.3% among the 52 patients negative for PCDH17 methylation and 31.6% among the 228 patients positive for PCDH17 methylation. Patients who were negative for PCDH17 methylation and had high Ki67 expression exhibited significantly higher pCR rates than their counterparts. The present results demonstrate that PCDH17 methylation status may predict the response to NAC in patients with TNBC. Therefore, this epigenetic characteristic may serve as an indicator of treatment efficacy.

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Section: Methodsmentioning

confidence: 99%

Association between the methylation status of PCDH17 and the efficacy of neoadjuvant chemotherapy in triple-negative breast cancer

Kong

Liang

et al. 2020

Oncol Lett

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“…117 The role of miRNA-24's in RIP's antinecrotic effect remains unclear, as RIP can increase as well as decrease its production. 121 When RIP was produced using I/R of the hind limb, it caused a decrease in the miRNA-29a/b/c level in skeletal muscles. This miRNA inhibits the expression of an inducible NO synthase (iNOS).…”

Section: Exosomes and Micrornasmentioning

confidence: 99%

“…This miRNA inhibits the expression of an inducible NO synthase (iNOS). 121 The authors proposed that a decrease in the miRNA-29a/b/c level in the blood plasma promotes iNOS expression in remote organs which provides the protective effect. Thus, exosomes that contain various proteins as well as mRNA and miRNA may well comprise an important humoral component of the cardioprotective effect of RIP.…”

Section: Exosomes and Micrornasmentioning

confidence: 99%

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A Review of Humoral Factors in Remote Preconditioning of the Heart

Tsibulnikov

Маслов

Gorbunov

et al. 2019

J Cardiovasc Pharmacol Ther

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A humoral mechanism of cardioprotection by remote ischemic preconditioning (RIP) has been clearly demonstrated in various models of ischemia–reperfusion including upper and lower extremities, liver, and the mesenteric and renal arteries. A wide range of humoral factors for RIP have been proposed including hydrophobic peptides, opioid peptides, adenosine, prostanoids, endovanilloids, endocannabinoids, calcitonin gene-related peptide, leukotrienes, noradrenaline, adrenomedullin, erythropoietin, apolipoprotein, A-I glucagon-like peptide-1, interleukin 10, stromal cell-derived factor 1, and microRNAs. Virtually, all of the components of ischemic preconditioning’s signaling pathway such as nitric oxide synthase, protein kinase C, redox signaling, PI3-kinase/Akt, glycogen synthase kinase β, ERK1/2, mitoKATP channels, Connexin 43, and STAT were all found to play a role. The signaling pattern also depends on which remote vascular bed was subjected to ischemia and on the time between applying the rip and myocardial ischemia occurs. Because there is convincing evidence for many seemingly diverse humoral components in RIP, the most likely explanation is that the overall mechanism is complex like that seen in ischemic preconditioning where multiple components are both in series and in parallel and interact with each other. Inhibition of any single component in the right circumstance may block the resulting protective effect, and selectively activating that component may trigger the protection. Identifying the humoral factors responsible for RIP might be useful in developing drugs that confer RIP’s protection in a more comfortable and reliable manner.

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“…RIPC (4 min ischemia/4 min reperfusion) induced eNOS activation, leading to NO production to preserve sinusoidal structure and blood flow [61]. In addition, RIPC (5 min ischemia/5 min reperfusion) regulated the expressions of iNOS and eNOS and the expressions of miR-34a, miR-122, and miR-27b injury related miRs in fatty livers, thus attenuating I/R injury [62,63]. RIPC (10 min ischemia/10 min reperfusion) also induced the up-regulation of HO-1, induced autophagy, and then reduced the damaged mitochondria to inhibit apoptosis and eventually protect hepatic cells from I/R injury [64,65].…”

Section: Ripc In Warm Ischemia Without Liver Resectionmentioning

confidence: 99%

Ischemic Preconditioning Directly or Remotely Applied on the Liver to Reduce Ischemia-Reperfusion Injury in Resections and Transplantation

Cornide‐Petronio¹,

Jiménez‐Castro²,

Gracia‐Sancho³

et al. 2019

Liver Disease and Surgery [Working Title]

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Ischemia-reperfusion (I/R) injury is an important cause of liver damage occurring during surgical procedures. In liver resection, I/R causes post-operative transaminasemia and liver function failure. In liver transplantation, I/R causes graft dysfunction, ranging from biochemical abnormalities to primary non-function of the transplanted organ. Ischemic preconditioning is a surgical strategy to reduce the severity of I/R and improve post-operative outcomes by prior exposure to a brief period of vascular occlusion directly to the target organ or remotely to a distant vascular bed. This chapter aims to discuss the different ischemic preconditioning strategies in both liver resection surgery and liver transplantation. In addition, we will describe the differences of such surgical strategies in both steatotic and nonsteatotic livers in both preclinical experiments and clinical practice. Such information may be useful to guide the design of the effective ischemic preconditioning methods in the surgery of hepatic resections and liver transplantation.

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MicroRNA-29a/b/c targets iNOS and is involved in protective remote ischemic preconditioning in an ischemia-reperfusion rat model of non-alcoholic fatty liver disease

Cited by 15 publications

References 38 publications

Association between the methylation status of PCDH17 and the efficacy of neoadjuvant chemotherapy in triple-negative breast cancer

Association between the methylation status of PCDH17 and the efficacy of neoadjuvant chemotherapy in triple-negative breast cancer

A Review of Humoral Factors in Remote Preconditioning of the Heart

Ischemic Preconditioning Directly or Remotely Applied on the Liver to Reduce Ischemia-Reperfusion Injury in Resections and Transplantation

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