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Molecular Research on Stress Response and Ocular Homeostasis

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (15 September 2020) | Viewed by 21324

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Dr. Toshihide Kurihara

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Laboratory of Photobiology, Department of Ophthalmology, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan
Interests: retina; hypoxia response; myopia; optogenetics
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Special Issue Information

Dear Colleagues,

Stress response is a fundamental cellular reaction contributing to developmental processes, tissue homeostasis, and organ pathogenesis. Physiologically, individual organs maintain their homeostasis, reacting to various stresses such as hypoxia, inflammation, and starvation. The eye is the organ which specifically exists in order to receive light and convert it to a signal. Thus, individual cells protect their functions from the distinctive microenvironment in respective ocular components including the cornea, the crystalline lens, the retina, and the uvea. Not only intraocular systems but also inter-organ systems such as the eye–gut axis utilize cellular stress response to maintain local and systemic homeostasis. Molecular components including, but not limited to, stress-responsive transcriptional factors such as hypoxia-inducible factors (HIFs), nuclear factor erythroid 2-related factor 2 (Nrf2), and nuclear factor-kappa B (NF-kB) have been revealed to play a critical role in cellular stress response. Dysfunction or rather ectopic activation of molecules in charge of cellular stress response can be observed in the pathophysiological process of multiple ocular components. This Special Issue will focus on ocular stress response in molecular, cellular, local, and systemic levels. The response and related molecules are conserved between species; therefore, the scope includes a large extent from the basic biological sciences to human diseases.

Assoc. Prof. Toshihide Kurihara
Guest Editor

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Keywords

Hypoxia response
Oxidative stress
Energy homeostasis
Light exposure

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Published Papers (5 papers)

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Research

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15 pages, 5161 KiB

Open AccessArticle

Autophagic Upregulation Is Cytoprotective in Ischemia/Reperfusion-Injured Retina and Retinal Progenitor Cells

by Larissa Ho Ching Tang, Frederic Khe Cheong Fung, Angela Ka Wai Lai, Ian Yat Hin Wong, Kendrick Co Shih and Amy Cheuk Yin Lo

Int. J. Mol. Sci. 2021, 22(16), 8446; https://doi.org/10.3390/ijms22168446 - 6 Aug 2021

Cited by 7 | Viewed by 3045

Abstract

The cytoprotective versus cytotoxic role of macroautophagy in ocular ischemia/reperfusion injuries remains controversial and its effects under hyperglycemia are unclear. We investigated the involvement of autophagy in in vitro and in vivo normoglycemic and hyperglycemic models of retinal ischemia/reperfusion injury. Retinal ischemia (2 h) and reperfusion (2 or 22 h) was induced in wild-type and type I diabetic Ins2^Akita/+ mice using a middle cerebral artery occlusion model. R28 retinal precursor cells were subjected to CoCl₂-induced hypoxia with or without autophagic inhibitor NH₄Cl. Autophagic regulation during ischemia/reperfusion was assessed through immunohistochemical detection and Western blotting of microtubule-associated protein 1A/1B-light chain 3 (LC3) and lysosomal associated membrane protein 1 (LAMP1). Effect of autophagic inhibition on cell viability and morphology under hypoxic conditions was also evaluated. Upregulation of autophagic markers in the inner retinae was seen after two hours reperfusion, with tapering of the response following 22 h of reperfusion in vivo. LC3-II turnover assays confirmed an increase in autophagic flux in our hypoxic in vitro model. Pharmacological autophagic inhibition under hypoxic conditions decreased cell survival and induced structural changes not demonstrated with autophagic inhibition alone. Yet no statistically significant different autophagic responses in ischemia/reperfusion injuries were seen between the two glycemic states. Full article

(This article belongs to the Special Issue Molecular Research on Stress Response and Ocular Homeostasis)

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22 pages, 7125 KiB

Open AccessArticle

Hypothermically Stored Adipose-Derived Mesenchymal Stromal Cell Alginate Bandages Facilitate Use of Paracrine Molecules for Corneal Wound Healing

by Olla Al-Jaibaji, Stephen Swioklo, Alex Shortt, Francisco C. Figueiredo and Che J. Connon

Int. J. Mol. Sci. 2020, 21(16), 5849; https://doi.org/10.3390/ijms21165849 - 14 Aug 2020

Cited by 6 | Viewed by 3829

Abstract

Adipose-derived mesenchymal stromal cells (Ad-MSCs) may alleviate corneal injury through the secretion of therapeutic factors delivered at the injury site. We aimed to investigate the therapeutic factors secreted from hypothermically stored, alginate-encapsulated Ad-MSCs’ bandages in in vitro and in vivo corneal wounds. Ad-MSCs were encapsulated in 1.2% w/v alginate gels to form bandages and stored at 15 °C for 72 h before assessing cell viability and co-culture with corneal scratch wounds. Genes of interest, including HGF, TSG-6, and IGF were identified by qPCR and a human cytokine array kit used to profile the therapeutic factors secreted. In vivo, bandages were applied to adult male mice corneas following epithelial debridement. Bandages were shown to maintain Ad-MSCs viability during storage and able to indirectly improve corneal wound healing in vivo. Soluble protein concentration and paracrine factors such as TSG-6, HGF, IL-8, and MCP-1 release were greatest following hypothermic storage. In vivo, Ad-MSCs bandages-treated groups reduced immune cell infiltration when compared to untreated groups. In conclusion, bandages were shown to maintain Ad-MSCs ability to produce a cocktail of key therapeutic factors following storage and that these soluble factors can improve in vitro and in vivo corneal wound healing. Full article

(This article belongs to the Special Issue Molecular Research on Stress Response and Ocular Homeostasis)

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13 pages, 1992 KiB

Open AccessArticle

Effects of Hyperoxia on the Refraction in Murine Neonatal and Adult Models

by Kiwako Mori, Toshihide Kurihara, Xiaoyan Jiang, Shin-ichi Ikeda, Ayako Ishida, Hidemasa Torii and Kazuo Tsubota

Int. J. Mol. Sci. 2019, 20(23), 6014; https://doi.org/10.3390/ijms20236014 - 29 Nov 2019

Cited by 2 | Viewed by 2435

Abstract

Whether hyperoxia affects the refraction in neonatal and adult mice is unknown. The mice exposed to 85% oxygen at postnatal 8 days (P8d) for 3 days and the mice exposed to normal air were assigned to the neonatal hyperoxia and normoxia groups, respectively. The refraction, the corneal curvature radius (CR) and the axial length (AL) were measured at P30d and P47d. Postnatal 6 weeks (P6w) adult mice were divided into the adult hyperoxia and normoxia groups. These parameters were measured before oxygen exposure, after 1 and 6 weeks, and every 7 weeks. The lens elasticity was measured at P7w and P26w by enucleation. The neonatal hyperoxia group showed a significantly larger myopic change than the neonatal normoxia group (P47d −6.56 ± 5.89 D, +4.11 ± 2.02 D, p < 0.001), whereas the changes in AL were not significantly different (P47d, 3.31 ± 0.04 mm, 3.31 ± 0.05 mm, p = 0.852). The adult hyperoxia group also showed a significantly larger myopic change (P12w, −7.20 ± 4.09 D, +7.52 ± 2.54 D, p < 0.001). The AL did not show significant difference (P12w, 3.44 ± 0.03 mm, 3.43 ± 0.01 mm, p = 0.545); however, the CR in the adult hyperoxia group was significantly smaller than the adult normoxia group (P12w, 1.44 ± 0.03 mm, 1.50 ± 0.03 mm, p = 0.003). In conclusion, hyperoxia was demonstrated to induce myopic shift both in neonatal and adult mice, which was attributed to the change in the CR rather than the AL. Elucidation of the mechanisms of hyperoxia and the application of this result to humans should be carried out in future studies. Full article

(This article belongs to the Special Issue Molecular Research on Stress Response and Ocular Homeostasis)

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Review

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18 pages, 1437 KiB

Open AccessReview

Novel Programmed Cell Death as Therapeutic Targets in Age-Related Macular Degeneration?

by Ming Yang, Kwok-Fai So, Wai Ching Lam and Amy Cheuk Yin Lo

Int. J. Mol. Sci. 2020, 21(19), 7279; https://doi.org/10.3390/ijms21197279 - 1 Oct 2020

Cited by 43 | Viewed by 6148

Abstract

Age-related macular degeneration (AMD) is a leading cause of severe visual loss among the elderly. AMD patients are tormented by progressive central blurring/loss of vision and have limited therapeutic options to date. Drusen accumulation causing retinal pigment epithelial (RPE) cell damage is the hallmark of AMD pathogenesis, in which oxidative stress and inflammation are the well-known molecular mechanisms. However, the underlying mechanisms of how RPE responds when exposed to drusen are still poorly understood. Programmed cell death (PCD) plays an important role in cellular responses to stress and the regulation of homeostasis and diseases. Apart from the classical apoptosis, recent studies also discovered novel PCD pathways such as pyroptosis, necroptosis, and ferroptosis, which may contribute to RPE cell death in AMD. This evidence may yield new treatment targets for AMD. In this review, we summarized and analyzed recent advances on the association between novel PCD and AMD, proposing PCD’s role as a therapeutic new target for future AMD treatment. Full article

(This article belongs to the Special Issue Molecular Research on Stress Response and Ocular Homeostasis)

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16 pages, 3201 KiB

Open AccessReview

Oxidative Stress and Microglial Response in Retinitis Pigmentosa

by Yusuke Murakami, Yusaku Nakabeppu and Koh-Hei Sonoda

Int. J. Mol. Sci. 2020, 21(19), 7170; https://doi.org/10.3390/ijms21197170 - 28 Sep 2020

Cited by 34 | Viewed by 5262

Abstract

An imbalance between the production of reactive oxygen species (ROS) and anti-oxidant capacity results in oxidative injury to cellular components and molecules, which in turn disturbs the homeostasis of cells and organs. Although retinitis pigmentosa (RP) is a hereditary disease, non-genetic biological factors including oxidative stress also modulate or contribute to the disease progression. In animal models of RP, the degenerating retina exhibits marked oxidative damage in the nucleic acids, proteins, and lipids, and anti-oxidant treatments substantially suppress photoreceptor cell death and microgliosis. Although the mechanisms by which oxidative stress mediates retinal degeneration have not been fully elucidated, our group has shown that oxidative DNA damage and its defense system are key regulators of microglial activation and photoreceptor degeneration in RP. In this review, we summarize the current evidence regarding oxidative stress in animal models and patients with RP. The clinical efficacy of anti-oxidant treatments for RP has not been fully established. Nevertheless, elucidating key biological processes that underlie oxidative damage in RP will be pivotal to understanding the pathology and developing a potent anti-oxidant strategy that targets specific cell types or molecules under oxidative stress. Full article

(This article belongs to the Special Issue Molecular Research on Stress Response and Ocular Homeostasis)

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