A Combination of Remote Ischemic Perconditioning and Cerebral Ischemic Postconditioning Inhibits Autophagy to Attenuate Plasma HMGB1 and Induce Neuroprotection Against Stroke in Rat

Wang, Jue; Han, Dong; Sun, Miao; Feng, Juan

doi:10.1007/s12031-016-0724-9

Cited by 32 publications

(37 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…IPOC was also demonstrated to reduce the translocation of HMGB1 from the nucleus to the cytoplasm, and that the autophagy inhibition effect of IPOC may be caused by reduced interaction between HMGB1 and Beclin1. These results are consistent with the findings of our previous study (35), which confirmed that IPOC decreased the translocation of HMGB1 from the nucleus to the cytoplasm to exert its autophagy inhibition effect in an in vivo model of focal cerebral ischemia and IPOC. The current study adds further evidence for the mechanism of HMGB1-induced autophagy in ischemic stroke and IPOC.…”

Section: Discussionsupporting

confidence: 93%

Cerebral ischemic post-conditioning induces autophagy inhibition and a HMGB1 secretion attenuation feedback loop to protect against ischemia reperfusion injury in an oxygen glucose deprivation cellular model

Wang

Han

Sun

et al. 2016

Molecular Medicine Reports

Self Cite

View full text Add to dashboard Cite

Cerebral ischemic postconditioning (IPOC) has been demonstrated to be neuroprotective against cerebral ischemia reperfusion injury. The present study aimed to determine whether IPOC could inhibit autophagy and high mobility group box 1 (HMGB1) release in a PC12 cell oxygen glucose deprivation/reperfusion (OGD/R) model. An 8 h OGD and 24 h reperfusion cellular model was developed to mimic cerebral ischemia reperfusion injury, with 3 cycles of 10 min OGD/5 min reperfusion treatment to imitate IPOC. Cell viability was determined to demonstrate the efficiency of OGD/R, IPOC and autophagy activator, rapamycin (RAP), treatment. Transmission electron microscopy was performed to observe the formation of autophagosomes, and immunofluorescence, western blot and co-immunoprecipitation were used to examine the expression of autophagy-associated proteins and HMGB1. Enzyme-linked immunosorbent assay analysis was conducted to examine the level of HMGB1 in cell supernatants. Additionally, PC12 cells were treated with RAP to examine the effect of autophagy on HMGB1 release, and the effect of recombinant human HMGB1 and Beclin1 small interfering RNA on autophagy was investigated. The present study confirmed that IPOC inhibited autophagy and HMGB1 secretion, autophagy inhibition induced a decrease in HMGB1 secretion, and HMGB1 secretion attenuation caused autophagy inhibition in return, as demonstrated by immunofluorescence and western blot analyses. Autophagy inhibition and HMGB1 secretion attenuation were, therefore, demonstrated to form a feedback loop under IPOC. These mechanisms illustrated the protective effects of IPOC and may accelerate the clinical use of IPOC.

show abstract

Section: Discussionsupporting

confidence: 93%

Cerebral ischemic post-conditioning induces autophagy inhibition and a HMGB1 secretion attenuation feedback loop to protect against ischemia reperfusion injury in an oxygen glucose deprivation cellular model

Wang

Han

Sun

et al. 2016

Molecular Medicine Reports

Self Cite

View full text Add to dashboard Cite

show abstract

“…They were able to ascertain that RIC was able to induce pro-autophagy signaling. Wang et al, in SD rat models, was able to show that RIC attenuated plasma HMGB1 levels and exerted a neuroprotective effect by inhibiting the autophagy process ( 51 ).…”

Section: Mechanisms Of Limb Remote Ischemic Pre- Per- and Postcondimentioning

confidence: 99%

Limb Remote Ischemic Conditioning: Mechanisms, Anesthetics, and the Potential for Expanding Therapeutic Options

et al. 2018

View full text Add to dashboard Cite

Novel and innovative approaches are essential in developing new treatments and improving clinical outcomes in patients with ischemic stroke. Remote ischemic conditioning (RIC) is a series of mechanical interruptions in blood flow of a distal organ, following end organ reperfusion, shown to significantly reduce infarct size through inhibition of oxidation and inflammation. Ischemia/reperfusion (I/R) is what ultimately leads to the irreversible brain damage and clinical picture seen in stroke patients. There have been several reports and reviews about the potential of RIC in acute ischemic stroke; however, the focus here is a comprehensive look at the differences in the three types of RIC (remote pre-, per-, and postconditioning). There are some limited uses of preconditioning in acute ischemic stroke due to the unpredictability of the ischemic event; however, it does provide the identification of biomarkers for clinical studies. Remote limb per- and postconditioning offer a more promising treatment during patient care as they can be harnessed during or after the initial ischemic insult. Though further research is needed, it is imperative to discuss the importance of preclinical data in understanding the methods and mechanisms involved in RIC. This understanding will facilitate translation to a clinically feasible paradigm for use in the hospital setting.

show abstract

“…These findings imply that autophagy exerts a pivotal function in RIC-induced neuroprotection with the possible involvement of AKT/GSK3β, AMPK, and mTOR/p70S6K signaling pathways, and AKT-dependent Bcl-2 phosphorylation. However, in contrast, studies also demonstrated that inhibition of the autophagy process contributed to the protection against cerebral ischemia injury in rats subjected with ischemic post-conditioning alone or combined with RIC [ 134 , 135 ]. The potential function of autophagy in RIC-induced protection needs to be further elucidated.…”

Section: Resultsmentioning

confidence: 99%

Remote ischemic conditioning: a promising therapeutic intervention for multi-organ protection

Zhou

Ding

et al. 2018

Aging

View full text Add to dashboard Cite

Despite decades of formidable exploration, multi-organ ischemia-reperfusion injury (IRI) encountered, particularly amongst elderly patients with clinical scenarios, such as age-related arteriosclerotic vascular disease, heart surgery and organ transplantation, is still an unsettled conundrum that besets clinicians. Remote ischemic conditioning (RIC), delivered via transient, repetitive noninvasive IR interventions to distant organs or tissues, is regarded as an innovative approach against IRI. Based on the available evidence, RIC holds the potential of affording protection to multiple organs or tissues, which include not only the heart and brain, but also others that are likely susceptible to IRI, such as the kidney, lung, liver and skin. Neuronal and humoral signaling pathways appear to play requisite roles in the mechanisms of RIC-related beneficial effects, and these pathways also display inseparable interactions with each other. So far, several hurdles lying ahead of clinical translation that remain to be settled, such as establishment of biomarkers, modification of RIC regimen, and deep understanding of underlying minutiae through which RIC exerts its powerful function. As this approach has garnered an increasing interest, herein, we aim to encapsulate an overview of the basic concept and postulated protective mechanisms of RIC, highlight the main findings from proof-of-concept clinical studies in various clinical scenarios, and also to discuss potential obstacles that remain to be conquered. More well designed and comprehensive experimental work or clinical trials are warranted in future research to confirm whether RIC could be utilized as a non-invasive, inexpensive and efficient adjunct therapeutic intervention method for multi-organ protection.

show abstract

A Combination of Remote Ischemic Perconditioning and Cerebral Ischemic Postconditioning Inhibits Autophagy to Attenuate Plasma HMGB1 and Induce Neuroprotection Against Stroke in Rat

Cited by 32 publications

References 28 publications

Cerebral ischemic post-conditioning induces autophagy inhibition and a HMGB1 secretion attenuation feedback loop to protect against ischemia reperfusion injury in an oxygen glucose deprivation cellular model

Cerebral ischemic post-conditioning induces autophagy inhibition and a HMGB1 secretion attenuation feedback loop to protect against ischemia reperfusion injury in an oxygen glucose deprivation cellular model

Limb Remote Ischemic Conditioning: Mechanisms, Anesthetics, and the Potential for Expanding Therapeutic Options

Remote ischemic conditioning: a promising therapeutic intervention for multi-organ protection

Contact Info

Product

Resources

About