Research Progress of the Application of Hypothermia in the Eye

There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

Abstract

Hypothermia is widely used in the medical field to protect organs or tissues from damage. Different research fields have different explanations of the protection mechanism of hypothermia. Hypothermia is also widely used in the field of ophthalmology, for example, in the eye bank, the preservation of corneal tissue and the preservation of the eyeball. Low temperature can also be applied to some ophthalmic diseases, such as allergic conjunctivitis, retinal ischemia, and retinal hypoxia. It is used to relieve eye symptoms or reduce tissue damage. Hypothermic techniques have important applications in ophthalmic surgery, such as corneal refractive surgery, vitrectomy surgery, and ciliary body cryotherapy for end-stage glaucoma. Hypothermia can reduce the inflammation of the cornea and protect the retinal tissue. The eyeball is a complex organ, including collagen tissue of the eyeball wall and retinal nerve tissue and retinal blood vessels. The mechanism of low temperature protecting eye tissue is complicated. It is important to understand the mechanism of hypothermia and its applications in ophthalmology. This review introduces the mechanism of hypothermia and its application in the eye banks, eye diseases (allergic conjunctivitis, retinal ischemia, and hypoxia), and eye surgeries (corneal transplant surgery, corneal refractive surgery, and vitrectomy).

Related collections

Most cited references 102

Record: found
Abstract: found
Article: not found

Retinal ischemia: mechanisms of damage and potential therapeutic strategies.

Neville N. Osborne, Robert J. Casson, John Wood … (2004)

Retinal ischemia is a common cause of visual impairment and blindness. At the cellular level, ischemic retinal injury consists of a self-reinforcing destructive cascade involving neuronal depolarisation, calcium influx and oxidative stress initiated by energy failure and increased glutamatergic stimulation. There is a cell-specific sensitivity to ischemic injury which may reflect variability in the balance of excitatory and inhibitory neurotransmitter receptors on a given cell. A number of animal models and analytical techniques have been used to study retinal ischemia, and an increasing number of treatments have been shown to interrupt the "ischemic cascade" and attenuate the detrimental effects of retinal ischemia. Thus far, however, success in the laboratory has not been translated to the clinic. Difficulties with the route of administration, dosage, and adverse effects may render certain experimental treatments clinically unusable. Furthermore, neuroprotection-based treatment strategies for stroke have so far been disappointing. However, compared to the brain, the retina exhibits a remarkable natural resistance to ischemic injury, which may reflect its peculiar metabolism and unique environment. Given the increasing understanding of the events involved in ischemic neuronal injury it is hoped that clinically effective treatments for retinal ischemia will soon be available.

0 comments Cited 291 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

Regulation of therapeutic hypothermia on inflammatory cytokines, microglia polarization, migration and functional recovery after ischemic stroke in mice.

Jin Lee, Zheng Wei, Wenyuan Cao … (2016)

Stroke is a leading threat to human life and health in the US and around the globe, while very few effective treatments are available for stroke patients. Preclinical and clinical studies have shown that therapeutic hypothermia (TH) is a potential treatment for stroke. Using novel neurotensin receptor 1 (NTR1) agonists, we have demonstrated pharmacologically induced hypothermia and protective effects against brain damages after ischemic stroke, hemorrhage stroke, and traumatic brain injury (TBI) in rodent models. To further characterize the mechanism of TH-induced brain protection, we examined the effect of TH (at ±33°C for 6h) induced by the NTR1 agonist HPI-201 or physical (ice/cold air) cooling on inflammatory responses after ischemic stroke in mice and oxygen glucose deprivation (OGD) in cortical neuronal cultures. Seven days after focal cortical ischemia, microglia activation in the penumbra reached a peak level, which was significantly attenuated by TH treatments commenced 30min after stroke. The TH treatment decreased the expression of M1 type reactive factors including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-12, IL-23, and inducible nitric oxide synthase (iNOS) measured by RT-PCR and Western blot analyses. Meanwhile, TH treatments increased the expression of M2 type reactive factors including IL-10, Fizz1, Ym1, and arginase-1. In the ischemic brain and in cortical neuronal/BV2 microglia cultures subjected to OGD, TH attenuated the expression of monocyte chemoattractant protein-1 (MCP-1) and macrophage inflammatory protein-1α (MIP-1α), two key chemokines in the regulation of microglia activation and infiltration. Consistently, physical cooling during OGD significantly decreased microglia migration 16h after OGD. Finally, TH improved functional recovery at 1, 3, and 7days after stroke. This study reveals the first evidence for hypothermia mediated regulation on inflammatory factor expression, microglia polarization, migration and indicates that the anti-inflammatory effect is an important mechanism underlying the brain protective effects of a TH therapy.

0 comments Cited 58 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

RBM3 mediates structural plasticity and protective effects of cooling in neurodegeneration

Diego Peretti, Amandine Bastide, Helois Radford … (2015)

In the healthy adult brain synapses are continuously remodelled through a process of elimination and formation known as structural plasticity 1 . Reduction in synapse number is a consistent early feature of neurodegenerative diseases 2, 3 , suggesting deficient compensatory mechanisms. While much is known about toxic processes leading to synaptic dysfunction and loss in these disorders 2,3 , how synaptic regeneration is affected is unknown. In hibernating mammals, cooling induces loss of synaptic contacts, which are reformed on rewarming, a form of structural plasticity 4, 5 . We have found that similar changes occur in artificially cooled laboratory rodents. Cooling and hibernation also induce a number cold-shock proteins in the brain, including the RNA binding protein, RBM3 6 . The relationship of such proteins to structural plasticity is unknown. Here we show that synapse regeneration is impaired in mouse models of neurodegenerative disease, in association with the failure to induce RBM3. In both prion-infected and 5×FAD (Alzheimer-type) mice 7 , the capacity to regenerate synapses after cooling declined in parallel with the loss of induction of RBM3. Enhanced expression of RBM3 in the hippocampus prevented this deficit and restored the capacity for synapse reassembly after cooling. Further, RBM3 over-expression, achieved either by boosting endogenous levels through hypothermia prior to the loss of the RBM3 response, or by lentiviral delivery, resulted in sustained synaptic protection in 5×FAD mice and throughout the course of prion disease, preventing behavioural deficits and neuronal loss and significantly prolonging survival. In contrast, knockdown of RBM3 exacerbated synapse loss in both models and accelerated disease and prevented the neuroprotective effects of cooling. Thus, deficient synapse regeneration, mediated at least in part by failure of the RBM3 stress response, contributes to synapse loss throughout the course of neurodegenerative disease. The data support enhancing cold shock pathways as potential protective therapies in neurodegenerative disorders.

0 comments Cited 49 times – based on 0 reviews      Review now

Bookmark

All references

Author and article information

Contributors

Lei Xi:

ORCID: https://orcid.org/0000-0003-3746-3132

Journal

Journal ID (nlm-ta): Oxid Med Cell Longev

Journal ID (iso-abbrev): Oxid Med Cell Longev

Journal ID (publisher-id): OMCL

Title: Oxidative Medicine and Cellular Longevity

Publisher: Hindawi

ISSN (Print): 1942-0900

ISSN (Electronic): 1942-0994

Publication date Collection: 2020

Publication date (Electronic): 15 December 2020

Volume: 2020

Electronic Location Identifier: 3897168

Affiliations

Division of Experimental Vitreoretinal Surgery, Centre for Ophthalmology, University of Tübingen, Schleichstrasse 12/1, 72076 Tübingen, Germany

Author notes

Academic Editor: Andrey V. Kozlov

Author information

Lei Xi https://orcid.org/0000-0003-3746-3132

Article

DOI: 10.1155/2020/3897168

PMC ID: 7758138

PubMed ID: 33381263

SO-VID: 003222a2-a891-491b-85f9-f905e884455e

License:

This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

History

Date received : 26 July 2020

Date revision received : 4 December 2020

Date accepted : 7 December 2020

Funding

Funded by: University of Tübingen, Germany

Comments

Comment on this article

scite_

Cited by 4

See all cited by

Most referenced authors 1,018

See all reference authors

- Version 1

Research Progress of the Application of Hypothermia in the Eye

Read this article at

Abstract

Related collections

Drug Repurposing Research Collection

Most cited references 102

Retinal ischemia: mechanisms of damage and potential therapeutic strategies.

Regulation of therapeutic hypothermia on inflammatory cytokines, microglia polarization, migration and functional recovery after ischemic stroke in mice.

RBM3 mediates structural plasticity and protective effects of cooling in neurodegeneration

Author and article information

Contributors

Journal

Affiliations

Author notes

Author information

Article

History

Funding

Categories

Comments

Comment on this article

Similar content 141

Cited by 4

Most referenced authors 1,018