Upregulation of Homer1a Promoted Retinal Ganglion Cell Survival After Retinal Ischemia and Reperfusion via Interacting with Erk Pathway

Fei, Fei; Li, Juan; Rao, Wei; Liu, Wenbo; Chen, Xiaoyan; Su, Ning; Wang, Yusheng; Zhou, Fei

doi:10.1007/s10571-015-0198-2

Cited by 25 publications

(14 citation statements)

References 48 publications

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“…In general, Homer1a appears to be an important regulator of activity-induced remodeling at synaptic structures (Inoue et al, 2007 ). Previous studies have shown that activation of Homer1a improved neuronal survival after acute brain injury, such as traumatic neuronal injury, cerebral ischemia, and excitotoxic challenge (Luo et al, 2014 ; Fei et al, 2015 ; Wang et al, 2015 ). In line with these studies, our results indicated that the levels of Homer1a protein in HT-22 cells increased after H 2 O 2 treatment in a time-dependent manner.…”

Section: Discussionmentioning

confidence: 98%

Homer1a Attenuates Hydrogen Peroxide-Induced Oxidative Damage in HT-22 Cells through AMPK-Dependent Autophagy

Luo

Rao

et al. 2018

Front. Neurosci.

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Neuronal oxidative stress is involved in diverse neurological disorders. Homer1a, as an important member of the Homer family and localized at the postsynaptic density, is known to protect cells against oxidative injury. However, the exact neuroprotective mechanism of Homer1a has not been fully elucidated. Here, we found that Homer1a promoted cell viability and reduced H2O2-induced LDH release. The overexpression of Homer1a enhanced autophagy after H2O2 treatment, which was confirmed by increased expression of LC3II, Beclin-1, and greater autophagosome formation. In addition, we demonstrated that activating autophagy improved cell survival and reduced H2O2-induced oxidative stress and mitochondrial damage. Moreover, the autophagy inhibitor 3-MA partially prevented the protective effects of Homer1a against oxidative challenge. We also found that the upregulation of Homer1a after H2O2 treatment increased the phosphorylation of AMPK. Furthermore, the AMPK inhibitor compound C inhibited Homer1a-induced autophagy and abolished Homer1a-mediated neuroprotection. All the above data suggests that Homer1a confers protection against H2O2-induced oxidative damage via AMPK-dependent autophagy.

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Section: Discussionmentioning

confidence: 98%

Homer1a Attenuates Hydrogen Peroxide-Induced Oxidative Damage in HT-22 Cells through AMPK-Dependent Autophagy

Luo

Rao

et al. 2018

Front. Neurosci.

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“…It has been noted in this and other I/R injury models that increasing the pressure and duration of ischemia may increase injury severity 24 . For this reason, some practitioners have elected to use ischemic pressures and durations differing from those presented here 4,[6][7][8][9][10]12 . Therefore retinal I/R injury by elevated IOP offers an advantage over alternative retinal I/R techniques in that it allows one to adjust surgical parameters to accommodate one's particular experimental goals.…”

Section: Discussionmentioning

confidence: 99%

“…Using the drip of a saline reservoir to raise IOP above systolic blood pressure, these studies demonstrated that pressurized ocular cannulation was sufficient to suspend the retinal circulation and thereby initiate neuronal degeneration. More recent efforts using retinal I/R by elevated IOP have begun to elaborate the mechanisms underlying I/R-induced retinal neurodegeneration [5][6][7][8][9][10][11][12] . Multiple groups have reported additional pathologic changes including inflammation 13,14 , vascular permeability 15,16 , and capillary degeneration 14,17 .…”

Section: Introductionmentioning

confidence: 99%

A Mouse Model of Retinal Ischemia-Reperfusion Injury Through Elevation of Intraocular Pressure

Hartsock

Cho

et al. 2016

JoVE

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Retinal ischemia-reperfusion (I/R) is a pathophysiological process contributing to cellular damage in multiple ocular conditions, including glaucoma, diabetic retinopathy, and retinal vascular occlusions. Rodent models of I/R injury are providing significant insights into mechanisms and treatment strategies for human I/R injury, especially with regard to neurodegenerative damage in the retinal neurovascular unit. Presented here is a protocol for inducing retinal I/R injury in mice through elevation of intraocular pressure (IOP). In this protocol, the ocular anterior chamber is cannulated with a needle, through which flows the drip of an elevated saline reservoir. Using this drip to raise IOP above systolic arterial blood pressure, a practitioner temporarily halts inner retinal blood flow (ischemia). When circulation is reinstated (reperfusion) by removal of the cannula, severe cellular damage ensues, resulting ultimately in retinal neurodegeneration. Recent studies demonstrate inflammation, vascular permeability, and capillary degeneration as additional elements of this model. Compared to alternative retinal I/R methodologies, such as retinal arterial ligation, retinal I/R injury by elevated IOP offers advantages in its anatomical specificity, experimental tractability, and technical accessibility, presenting itself as a valuable tool for examining neuronal pathogenesis and therapy in the retinal neurovascular unit.

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“…Thus, the initial steps of corneal wound healing are cell migration with polarization and protrusion in the direction of migration [ 31 ], and the decrease in the wound area during the 12 h after corneal epithelial abrasion due to cell migration [ 32 ]. Moreover, the MAPK/ERK pathways participate in the regulation of the manifold pathological and physiological processes [ 33 , 34 , 35 , 36 ], and it is well known that MAPK family members, such as ERK1/2, are also important for cell migration [ 19 , 20 , 21 , 22 ]. In this study, sericin enhanced cell movement, since the corneal wound healing in rats instilled with sericin was greater 12 h after corneal epithelial abrasion than in saline instilled rats.…”

Section: Discussionmentioning

confidence: 99%

Instillation of Sericin Enhances Corneal Wound Healing through the ERK Pathway in Rat Debrided Corneal Epithelium

Nagai

Fukuoka

Ishii

et al. 2018

IJMS

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Sericin is a major constituent of silk produced by silkworms. We previously found that the instillation of sericin enhanced the proliferation of corneal epithelial cells, and acted to promote corneal wound healing in both normal and diabetic model rats. However, the mechanisms by which sericin promotes the proliferation of corneal cells have not been established. In this study, we investigated the effects of sericin on Akt and ERK activation in a human corneal epithelial cell line (HCE-T cells) and rat debrided corneal epithelium. Although Akt phosphorylation was not detected following the treatment of HCE-T cells with sericin, ERK1/2 phosphorylation was enhanced. The growth of HCE-T cells treated with sericin was significantly increased, with the cell growth of sericin-treated HCE-T cells being 1.7-fold higher in comparison with vehicle-treated HCE-T cells. On the other hand, both of an ERK inhibitor U0126 (non-specific specific inhibitor) and SCH772984 (specific inhibitor) attenuated the enhanced cell growth by sericin, and the growth level in the case of co-treatment with sericin and ERK1/2 inhibitor was similar to that of cells treated with ERK1/2 inhibitor alone. In an in vivo study using rat debrided corneal epithelium, the corneal wound healing rate was enhanced by the instillation of sericin, and this enhancement was also attenuated by the instillation of U0126. In addition, the corneal wound healing rate in rats co-instilled with sericin and U0126 was similar to that following the instillation of U0126 alone. In conclusion, we found that the instillation of sericin enhanced cell proliferation via the activation of the MAPK/ERK pathway, resulting in the promotion of corneal wound healing in rat eyes. These findings provide significant information for designing further studies to develop potent corneal wound-healing drugs.

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Upregulation of Homer1a Promoted Retinal Ganglion Cell Survival After Retinal Ischemia and Reperfusion via Interacting with Erk Pathway

Cited by 25 publications

References 48 publications

Homer1a Attenuates Hydrogen Peroxide-Induced Oxidative Damage in HT-22 Cells through AMPK-Dependent Autophagy

Homer1a Attenuates Hydrogen Peroxide-Induced Oxidative Damage in HT-22 Cells through AMPK-Dependent Autophagy

A Mouse Model of Retinal Ischemia-Reperfusion Injury Through Elevation of Intraocular Pressure

Instillation of Sericin Enhances Corneal Wound Healing through the ERK Pathway in Rat Debrided Corneal Epithelium

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