Remote Ischemic Perconditioning Modulates Apelin Expression After Renal Ischemia-Reperfusion Injury

Gholampour, Firouzeh; Bagheri, Atefeh; Barati, Anis; Masoudi, Raheleh; Owji, Seyed Mohammad

doi:10.1016/j.jss.2019.09.063

Cited by 7 publications

(3 citation statements)

References 39 publications

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“…Brain tissue ischaemia could cause local cerebral ischaemic injury. RIPerC refers to repetitive and intermittent blood flow blocking stimulation of the limbs, through nerve conduction, body fluids, and systemic inflammatory responses, to modulate the endogenous protective mechanism of motivation [5,10,26]. Thereby, it induces the tolerance of the heart, brain, liver, kidney, lung, and other organs to ischaemia and hypoxia, and improves the ability of remote vital organs to resist ischaemia and hypoxia damage.…”

Section: Discussionmentioning

confidence: 99%

“…RIPerC refers to the implementation of RIC after cerebral ischaemia and before reperfusion. It is worth noting that there have been many studies on the application of RIPerC to ischaemic animal models, and it was initially found that RIPerC can significantly reduce the infarct volume of the ischaemic animal model organs [5,27]. However, the mechanism by which RIPerC interferes with ischaemic stroke to reduce cerebral infarction volume and improve neurological function has not yet been reported.…”

Section: Introductionmentioning

confidence: 99%

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Remote ischaemic perconditioning reduces the infarct volume and improves the neurological function of acute ischaemic stroke partially through the miR-153-5p/TLR4/p65/IkBa signalling pathway

Zha¹,

Miao²,

Rong³

et al. 2021

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Remote ischemic perconditioning (RIPerC) could improve neuronal damage and inhibit inflammation and apoptosis.We conducted an in-depth exploration of the protective mechanism of RIPerC in cerebral ischaemia injury. In this study, a middle cerebral artery occlusion (MCAO) mouse model was built. According to whether to undergo RIPerC treatment and the duration of cerebral infarction, mice were divided into 5 groups: Sham group, MCAO 3.0 h group, MCAO 4.5 h group, MCAO 3.0 h + RIPerC group, and MCAO 4.5 h + RIPerC group. Overexpressed or silenced miR-153-5p was transfected into the cells to analyse the effects of oxygen-glucose deprivation (OGD) treatment on Neuro-2a cell viability, apoptosis, and related gene expressions by performing quantitative real-time polymerase chain reaction (qRT-PCR), MTT assay, flow cytometry, and Western blot. Bioinformatics analysis, qRT-PCR, dual-luciferase experiment, and RNA immunoprecipitation (RIP) were used to screen and verify the miRNA and downstream mRNA-targeted Toll-like receptor 4 (TLR4). The rescue test further verified the effects of the above target genes and miR-153-5p on the apoptosis of OGD-injured cells, apoptosis-related proteins, and the p65/IκBα pathway. The plasma levels of miR-153-5p in 68 patients with ischaemic stroke were detected within 6 hours of onset, and the patients were followed up for 3 months. We found that, in in vivo studies, RIPerC treatment inhibits cerebral infarction volume and neurological damage, and promotes the expression of miR-153-5p in the MCAO animal model. The expression of miR-153-5p in OGD cells was inhibited, and its upregulation protected Neuro-2a cells. TLR4 was predicted to be the target gene of miR-153-5p and could offset the effect of miR-153-5p mimic on OGD cell protection after up-regulating TLR4. TLR4 overexpression promoted the activation of OGD on the p65/IκBα pathway. Compared with the high plasma miR-153-5p group, the 3-month overall survival rate of patients with ischaemic stroke in the low plasma miR-153-5p group was significantly lower (χ 2 = 5.095, p = 0.024). In conclusion, RIPerC intervention inhibits the damage caused by cerebral ischaemia partially through the miR-153-5p/TLR4/p65/IκBα signalling pathway.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Remote ischaemic perconditioning reduces the infarct volume and improves the neurological function of acute ischaemic stroke partially through the miR-153-5p/TLR4/p65/IkBa signalling pathway

Zha¹,

Miao²,

Rong³

et al. 2021

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“…Moreover, AKI is strongly associated with adverse outcomes including the development of CKD, kidney failure and death, although the mechanisms are poorly defined 150 . Studies in models of AKI suggest early upregulation of the apelin system that is followed by downregulation as injury progresses 151,152 . This dynamic change is similar to that seen in heart failure.…”

Section: Acute Kidney Injurymentioning

confidence: 99%

The therapeutic potential of apelin in kidney disease

et al. 2021

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Chronic kidney disease (CKD) is an increasingly common public health concern with a global prevalence of ~10% 1 . This disease now ranks as the 12th leading cause of death worldwide 1 . CKD results from a heterogeneous group of conditions that lead to a progressive and irreversible impairment in kidney function. It is defined as a reduction in estimated glomerular filtration rate (eGFR) to <60 ml/min/1.73 m 2 and/or the presence of markers of kidney damage on at least two occasions at least 3 months apart 2 .CKD is independently associated with cardiovascular disease 3 . As eGFR decreases, the risks of major cardiovascular events, cardiovascular mortality and all-cause mortality increase 4 . Importantly, patients with stage 1-3 CKD (eGFR >30 ml/min/1.73 m 2 ) are more likely to die from cardiovascular disease than they are to reach kidney failure 4,5 and around 50% of patients with kidney failure die from cardiovascular causes 6 . Not only are cardio vascular events more common in patients with CKD, but outcomes following such events are worse than in the general population 7 . Almost 8% of global cardiovascular deaths in 2017 were attributable to CKD 1 .Hypertension is both a cause and a consequence of CKD. As kidney function declines, blood pressure rises, and more than 85% of patients with CKD are hypertensive 8 . Thus, reducing blood pressure in CKD is a key therapeutic strategy that not only slows the progression to kidney failure but also reduces cardiovascular risk 9 . However, more than 30% of patients with CKD require four or more antihypertensive agents to achieve adequate blood pressure control and up to 50% never reach their target blood pressure 8 . Uncontrolled hypertension promotes the development of left ventricular hypertrophy (LVH). The prevalence of LVH increases as kidney function declines and it is present in ~50% of patients with an eGFR of <25 ml/min/1.73 m 2 (ref. 10 ). Alongside hypertension and LVH, arterial stiffness, endothelial dysfunction and proteinuria are characteristic features of CKD and important independent predictors of cardiovascular disease 4,[11][12][13][14] .Current evidence-based management of CKD is limited to blockers of the renin-angiotensin-aldosterone system (RAAS) that slow CKD progression 4,8 . Sodiumglucose co-transporter 2 (SGLT2) inhibitors, which were originally developed for the treatment of type 2 diabetes mellitus (T2DM), have also now been shown to improve kidney and cardiovascular end points in patients with and without T2DM 15,16 . However, an urgent unmet need remains for novel treatments 17 . The ideal therapy would provide direct renoprotection and reduce proteinuria, while also offering broad cardiovascular protection. The apelin system has exciting therapeutic potential in this regard. In this Review, we focus on current

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Bioactive peptide apelin rescues acute kidney injury by protecting the function of renal tubular mitochondria

et al. 2021

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Remote Ischemic Perconditioning Modulates Apelin Expression After Renal Ischemia-Reperfusion Injury

Cited by 7 publications

References 39 publications

Remote ischaemic perconditioning reduces the infarct volume and improves the neurological function of acute ischaemic stroke partially through the miR-153-5p/TLR4/p65/IkBa signalling pathway

Remote ischaemic perconditioning reduces the infarct volume and improves the neurological function of acute ischaemic stroke partially through the miR-153-5p/TLR4/p65/IkBa signalling pathway

The therapeutic potential of apelin in kidney disease

Bioactive peptide apelin rescues acute kidney injury by protecting the function of renal tubular mitochondria

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