Protective effects of remote ischemic conditioning against ischemia/reperfusion-induced retinal injury in rats

Zhang, Xuxiang; Jizhang, Yunneng; Xu, Xiaoying; Kwiecien, Timothy D.; Li, Ning; Zhang, Ying; Ji, Xunming; Ren, Chang­hong; Ding, Yuchuan

doi:10.1017/s0952523814000121

Cited by 29 publications

(25 citation statements)

References 36 publications

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“…Our evidence that RIP can induce the protection of photoreceptors complements recent reports of RIP-induced protection of the inner layers of retina from ischemiareperfusion injury and optic nerve transection. 21,25 It also complements our previous report that remote ischemia enhances the response of the retina to light, producing a supernormal ERG. 29 Remote ischemic preconditioning-induced enhancement of the function of an undamaged tissue had not been described previously; it was possible to detect in the retina because the ERG is a sensitive measure of retinal function, and remote ischemia can be delivered in a temporally precise way.…”

Section: Protecting Photoreceptors By Stress Conditioningsupporting

confidence: 87%

“…In humans, the conditioning ischemia is usually induced in one arm using a conventional tourniquet. Limb ischemia has been shown to reduce the cerebral lesion and functional loss caused by a stroke, 20 to reduce retinal damage caused by local ischemia, 21 to reduce acute renal injury in a range of clinical settings, and to reduce liver injury in ischemia (reviewed in Refs. [22][23][24].…”

mentioning

confidence: 99%

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Remote Ischemic Preconditioning Protects Retinal Photoreceptors: Evidence From a Rat Model of Light-Induced Photoreceptor Degeneration

Brandli

Johnstone

Stone

2016

Invest. Ophthalmol. Vis. Sci.

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Section: Protecting Photoreceptors By Stress Conditioningsupporting

confidence: 87%

mentioning

confidence: 99%

Remote Ischemic Preconditioning Protects Retinal Photoreceptors: Evidence From a Rat Model of Light-Induced Photoreceptor Degeneration

Brandli

Johnstone

Stone

2016

Invest. Ophthalmol. Vis. Sci.

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“…PerC was initiated immediately following the onset of focal ischemia by bilaterally occluding blood flow to the hind limbs ( Zhang, et al., 2014 ). Hind limb occlusion was accomplished by tightening a tourniquet (8 mm) around the upper thigh for 3 cycles, with each occlusion or release phase lasting 10 minutes.…”

Section: Methodsmentioning

confidence: 99%

Limb remote ischemic per-conditioning in combination with post-conditioning reduces brain damage and promotes neuroglobin expression in the rat brain after ischemic stroke

Ren

Wang

et al. 2015

RNN

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Purpose: Limb remote ischemic per-conditioning or post-conditioning has been shown to be neuroprotective after cerebral ischemic stroke. However, the effect of combining remote per-conditioning with post-conditioning on ischemic/reperfusion injury as well as the underlying mechanisms are largely unexplored. Methods: Here, adult male Sprague Dawley rats were subjected to middle cerebral artery occlusion (MCAO). The limb ischemic stimulus was immediately applied after onset of focal ischemia (per-conditioning), followed by repeated short episodes of remote ischemia 24 hr after reperfusion (post-conditioning). The infarct volume, motor function, and the expression of neuroglobin (Ngb) were measured at different durations after reperfusion. Results: We found that a single episode of limb remote per-conditioning afforded short-term protection, but combining repeated remote post-conditioning during the 14 days after reperfusion significantly ameliorated cerebral ischemia/reperfusion injury. Interestingly, we also found that ischemic per- and post-conditioning significantly increased expression of Ngb, an oxygen-binding globin protein that has been demonstrated to be neuroprotective against stroke, at peri-infarct regions from day 1 to day 14 following ischemia/reperfusion.Conclusion: Our results suggest that the conventional per-conditioning combined with post-conditioning may be used as a novel neuroprotective strategy against ischemia-reperfusion injury, and Ngb seems to be one of the important players in limb remote ischemia-mediated neuroprotection.

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“…PerC was initiated immediately after the onset of focal ischemia by occluding blood flow to the hind limbs bilaterally while under anesthesia [22]. Hind limb occlusion was accomplished by tightening a tourniquet (8 mm) around the upper thigh for 3 cycles, with each occlusion and release phase lasting 10 minutes.…”

Section: Remote Ischemic Perconditioningmentioning

confidence: 99%

Limb Ischemic Perconditioning Attenuates Blood-Brain Barrier Disruption by Inhibiting Activity of MMP-9 and Occludin Degradation after Focal Cerebral Ischemia

Ren¹,

Li²,

Wang³

et al. 2015

Aging and disease

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Remote ischemic perconditioning (PerC) has been proved to have neuroprotective effects on cerebral ischemia, however, the effect of PerC on the BBB disruption and underlying mechanisms remains largely unknown. To address these issues, total 90 adult male Sprague Dawley (SD) rats were used. The rats underwent 90-min middle cerebral artery occlusion (MCAO), and the limb remote ischemic PerC was immediately applied after the onset of MCAO. We found that limb remote PerC protected BBB breakdown and brain edema, in parallel with reduced infarct volume and improved neurological deficits, after MCAO. Immunofluorescence studies revealed that MCAO resulted in disrupted continuity of claudin-5 staining in the cerebral endothelial cells with significant gap formation, which was significantly improved after PerC. Western blot analysis demonstrated that expression of tight junction (TJ) protein occludin was significantly increased, but other elements of TJ proteins, claudin-5 and ZO-1, in the BBB endothelial cells were not altered at 48 h after PerC, compared to MCAO group. The expression of matrix metalloproteinase (MMP-9), which was involved in TJ protein degradation, was decreased after PerC. Interestingly, phosphorylated extracellular signal-regulated kinase 1/2 (pERK1/2), an upstream of MMP-9 signaling, was significantly reduced in the PerC group. Our data suggest that PerC inhibits MMP-9-mediated occludin degradation, which could lead to decreased BBB disruption and brain edema after ischemic stroke.Key words: ischemic stroke, remote ischemic perconditioning, blood-brain barrier, tight junction, matrix metalloproteinasesThe blood-brain barrier (BBB) is a physical and metabolic interface that segregates the central nervous system (CNS) from the peripheral circulation in addition to regulating the CNS microenvironment [1]. Under physiological conditions, BBB integrity is maintained by endothelial cell through tight junctions (TJs) and the basal lamina, limiting paracellular movement of ions, solutes, and water [2]. Yet, TJs are key components of the BBB structure that seal the gaps between adjacent endothelial cells and restrict paracellular permeability [3]. The TJ proteins, occludin and claudins, are important molecules in forming this seal [4]. In vivo, cerebral ischemia induces claudin-5

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Protective effects of remote ischemic conditioning against ischemia/reperfusion-induced retinal injury in rats

Cited by 29 publications

References 36 publications

Remote Ischemic Preconditioning Protects Retinal Photoreceptors: Evidence From a Rat Model of Light-Induced Photoreceptor Degeneration

Remote Ischemic Preconditioning Protects Retinal Photoreceptors: Evidence From a Rat Model of Light-Induced Photoreceptor Degeneration

Limb remote ischemic per-conditioning in combination with post-conditioning reduces brain damage and promotes neuroglobin expression in the rat brain after ischemic stroke

Limb Ischemic Perconditioning Attenuates Blood-Brain Barrier Disruption by Inhibiting Activity of MMP-9 and Occludin Degradation after Focal Cerebral Ischemia

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