scholarly journals Emerging Role of microRNAs in Stroke Protection Elicited by Remote Postconditioning

2021 ◽  
Vol 12 ◽  
Author(s):  
Giuseppe Pignataro
Keyword(s):  
Vital Role ◽  
Brain Protection ◽  
Remote Ischemic Conditioning ◽  
Ischemic Brain ◽  
Ischemic Conditioning ◽  
Theranostic Agents ◽  
Sparing Effect ◽  
Therapeutic Tools ◽  
Remote Postconditioning

Remote ischemic conditioning (RIC) represents an innovative and attractive neuroprotective approach in brain ischemia. The purpose of this intervention is to activate endogenous tolerance mechanisms by inflicting a subliminal ischemia injury to the limbs, or to another “remote” region, leading to a protective systemic response against ischemic brain injury. Among the multiple candidates that have been proposed as putative mediators of the protective effect generated by the subthreshold peripheral ischemic insult, it has been hypothesized that microRNAs may play a vital role in the infarct-sparing effect of RIC. The effect of miRNAs can be exploited at different levels: (1) as transducers of protective messages to the brain or (2) as effectors of brain protection. The purpose of the present review is to summarize the most recent evidence supporting the involvement of microRNAs in brain protection elicited by remote conditioning, highlighting potential and pitfalls in their exploitation as diagnostic and therapeutic tools. The understanding of these processes could help provide light on the molecular pathways involved in brain protection for the future development of miRNA-based theranostic agents in stroke.

scholarly journals Remote ischemic conditioning enhances oxygen supply to ischemic brain tissue in a mouse model of stroke: Role of elevated 2,3-biphosphoglycerate in erythrocytes

2020 ◽  
pp. 0271678X2095226
Author(s):  
Lin Wang ◽  
Changhong Ren ◽  
Yang Li ◽  
Chen Gao ◽  
Ning Li ◽  
...  
Keyword(s):  
Mouse Model ◽  
Brain Tissue ◽  
Oxygen Supply ◽  
Dissociation Curve ◽  
Tissue Oxygen ◽  
Remote Ischemic Conditioning ◽  
Ischemic Brain ◽  
Ischemic Conditioning ◽  
Oxygen Dissociation ◽  
Ischemic Brain Tissue

Oxygen supply for ischemic brain tissue during stroke is critical to neuroprotection. Remote ischemic conditioning (RIC) treatment is effective for stroke. However, it is not known whether RIC can improve brain tissue oxygen supply. In current study, we employed a mouse model of stroke created by middle cerebral artery occlusion (MCAO) to investigate the effect of RIC on oxygen supply to the ischemic brain tissue using a hypoxyprobe system. Erythrocyte oxygen-carrying capacity and tissue oxygen exchange were assessed by measuring oxygenated hemoglobin and oxygen dissociation curve. We found that RIC significantly mitigated hypoxic signals and decreased neural cell death, thereby preserving neurological functions. The tissue oxygen exchange was markedly enhanced, along with the elevated hemoglobin P50 and right-shifted oxygen dissociation curve. Intriguingly, RIC markedly elevated 2,3-biphosphoglycerate (2,3-BPG) levels in erythrocyte, and the erythrocyte 2,3-BPG levels were highly negatively correlated with the hypoxia in the ischemic brain tissue. Further, adoptive transfusion of 2,3-BPG-rich erythrocytes prepared from RIC-treated mice significantly enhanced the oxygen supply to the ischemic tissue in MCAO mouse model. Collectively, RIC protects against ischemic stroke through improving oxygen supply to the ischemic brain tissue where the enhanced tissue oxygen delivery and exchange by RIC-induced 2,3-BPG-rich erythrocytes may play a role.

Abstract WP295: Remote Limb Ischemic Conditioning in Murine Focal Cerebral Ischemia

Stroke ◽  
2017 ◽  
Vol 48 (suppl_1) ◽  
Author(s):  
Kazuo Kitagawa ◽  
Moeko Saitoh ◽  
Kentaro Ishizuka
Keyword(s):  
Cerebral Ischemia ◽  
Focal Cerebral Ischemia ◽  
Infarct Volume ◽  
Limb Ischemia ◽  
Brain Protection ◽  
Remote Ischemic Conditioning ◽  
Ischemic Conditioning ◽  
Transient Focal Cerebral Ischemia ◽  
Cortical Cerebral Blood Flow ◽  
Doppler Flowmeter

Background & Aims: Remote ischemic conditioning (RIC) could induce brain protection in cerebral ischemia. The conditioning can be divided into pre-, per- and post-conditioning. The aim of this study is to clarify which RIC is the most effective in murine focal ischemia. Methods: Adult male C57BL/6 mice were used in this study. Transient focal cerebral ischemia was produced with nylon-suture model by occluding middle cerebral artery (MCAO) for 45 minutes. Cortical cerebral blood flow (rCBF) was continuously measured during ischemia with laser Doppler flowmeter. Twenty-four hours after MCAO, the animals were sacrificed and their brains were removed. After cutting coronal 1-mm brain sections, infarct volume was measured after TTC staining. Fifty mice were divided into five groups (each n=10); sham RIC group, delayed preRIC group (RIC 24 hours before MCAO), early preRIC group (RIC 5 minutes before MCAO), perRIC group (RIC during MCAO), and postRIC group (RIC 5 minutes after MCAO). Hind limb ischemia was induced by making the snare as tight as possible using a hemostatic forceps for 5 minutes followed by loosening it for 5 minutes. Four cycles were performed as RIC. Results: Infarct volume were 58.8±10.1 mm 3 in sham RIC, 54.8±19.4 mm 3 in delayed preRIC, 69.3±10.8 mm 3 in early preRIC, 38.0±22.1 mm 3 in perRIC, and 64.5±13.5 mm 3 in postRIC groups. Infarct volume in perRIC was significantly smaller than that in sham RIC and other groups (P<0.01). However, infarct volume of other RIC groups was not different with sham RIC group. After MCAO, rCBF reduced to 15.6% of baseline level in sham RIC, 11.2% in delayed preRIC, 11.9% in early preRIC, 13.4% in perRIC, and 10.8% in postRIC group. No difference was found in residual rCBF among all groups. At the end of MCAO, rCBF compared to rCBF immediate after occlusion was 102±21% in sham RIC, 112±25% in delayed preRIC, 98±22% in early preRIC, 131±33% in perRIC and 105±19% postRIC groups. Relative rCBF change at the end of MCAO in perRIC was significantly more than that in sham RIC group (P<0.05). Conclusions: Among four RIC procedures, only perRIC showed clear brain protection against transient MCAO. Change during rCBF may suggest that enhancement of collateral circulation play a role in part on brain protective effect of perRIC.

scholarly journals Remote Ischemic Conditioning Improves Post-Ischemic Cardiac Function: The Role of Neuregulin-1

2017 ◽  
Vol 65 (S 01) ◽  
pp. S1-S110
Author(s):  
A. Kiss ◽  
P. Pilz ◽  
I.F. Gonçalves ◽  
M. Inci ◽  
F. Nagel ◽  
...  
Keyword(s):  
Cardiac Function ◽  
Remote Ischemic Conditioning ◽  
Neuregulin 1 ◽  
Ischemic Conditioning

scholarly journals Immune Modulation as a Key Mechanism for the Protective Effects of Remote Ischemic Conditioning After Stroke

2021 ◽  
Vol 12 ◽  
Author(s):  
Sima Abbasi-Habashi ◽  
Glen C. Jickling ◽  
Ian R. Winship
Keyword(s):  
Immune Modulation ◽  
Ischemia Reperfusion ◽  
Treatment Strategies ◽  
Protective Effects ◽  
Humoral Factors ◽  
Remote Ischemic Conditioning ◽  
Ischemic Conditioning ◽  
Mediators Of Inflammation ◽  
The Brain

Remote ischemic conditioning (RIC), which involves a series of short cycles of ischemia in an organ remote to the brain (typically the limbs), has been shown to protect the ischemic penumbra after stroke and reduce ischemia/reperfusion (IR) injury. Although the exact mechanism by which this protective signal is transferred from the remote site to the brain remains unclear, preclinical studies suggest that the mechanisms of RIC involve a combination of circulating humoral factors and neuronal signals. An improved understanding of these mechanisms will facilitate translation to more effective treatment strategies in clinical settings. In this review, we will discuss potential protective mechanisms in the brain and cerebral vasculature associated with RIC. We will discuss a putative role of the immune system and circulating mediators of inflammation in these protective processes, including the expression of pro-and anti-inflammatory genes in peripheral immune cells that may influence the outcome. We will also review the potential role of extracellular vesicles (EVs), biological vectors capable of delivering cell-specific cargo such as proteins and miRNAs to cells, in modulating the protective effects of RIC in the brain and vasculature.

scholarly journals Neuroprotective therapy in acute ischemic stroke

2021 ◽  
Vol 13 (4) ◽  
pp. 94-102
Author(s):  
A. A. Kulesh
Keyword(s):  
Ischemic Stroke ◽  
Acute Ischemic Stroke ◽  
Ischemia Reperfusion ◽  
Interleukin 1 ◽  
Current Data ◽  
Remote Ischemic Conditioning ◽  
Ischemic Conditioning ◽  
Neuroprotective Therapy ◽  
Neuroprotective Strategies

The review discusses the role of neuroprotective therapy in the acute period of ischemic stroke in the era of active introduction of reperfusion treatment methods. The main mechanisms of brain damage during ischemia/reperfusion and the leading neuroprotective strategies studied in clinical trials are considered. Neuroprotective approaches aimed at suppressing excitotoxicity, oxidative stress, and neuroinflammation are presented. Current data on the safety and efficacy of uric acid, edaravone, fingolimod, natalizumab, interleukin 1 receptors antagonists, cerebrolysin, and other drugs have been analyzed. Non-drug methods of neuroprotection are characterized, including remote ischemic conditioning, therapeutic hypothermia, and neurostimulation. According to the author's position, the safest and most effective neuroprotective agent in acute ischemic stroke is cerebrolysin.

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