STAT3 activation protects retinal ganglion cell layer neurons in response to stress

Zhang, Chun; Li, Hong; Liu, Mu Gen; Kawasaki, Atsushi; Fu, Xin; Barnstable, Colin J.; Zhang, Samuel Shao-Min

doi:10.1016/j.exer.2008.03.020

Cited by 40 publications

(36 citation statements)

References 49 publications

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“…In the present study, it was shown that H 2 O 2 and oxLDL decreased SirT1 levels in RPEs. STAT3, which was activated at a basal level in the RPEs, was upregulated and activated following oxidative stress-induced RPE injury (36,37). The results of the present study were in accordance with those of previous studies (36,37).…”

Section: A B C Dsupporting

confidence: 82%

“…STAT3, which was activated at a basal level in the RPEs, was upregulated and activated following oxidative stress-induced RPE injury (36,37). The results of the present study were in accordance with those of previous studies (36,37). Dysregulation of SirT1 and STAT3 implied that the two molecules may have important roles in the modulation of oxidative stress in RPEs.…”

Section: A B C Dsupporting

confidence: 82%

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SirT1 and STAT3 protect retinal pigmented epithelium cells against oxidative stress

Wei

Zhang

et al. 2015

Molecular Medicine Reports

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Abstract.It has been previously demonstrated that there are interactions between sirtuin 1 (SirT1) and signal transducer and activator of transcription 3 (STAT3), which have versatile roles in various microenvironments. However, whether or not there is crosstalk between these two molecules during oxidative stress, and what mechanism of crosstalk occurs in retinal pigmented epithelium cells (RPEs), the protection of which may delay the process of age-related macular degeneration (AMD), has required further elucidation. The present study aimed to investigate the interactions between SirT1 and STAT3 in RPEs, following exposure to oxidative stress. The rates of proliferation and apoptosis, levels of intracellular reactive oxygen species and cell senescence of RPEs, induced by oxidants [H 2 O 2 and oxidized low density lipoprotein (oxLDL)], were evaluated. The results revealed a downregulation of SirT1 expression, and an upregulation of STAT3 expression during oxidative stress. Further investigation indicated that SirT1 protected RPEs from oxidative stress-induced damage. Furthermore, gain-and loss-of-function experiments indicated that SirT1 had negative effects on the regulation of STAT3 expression in RPEs during oxidative stress. Notably, STAT3 directly protected the cells from oxidative stress, rather than depending on SirT1. Additionally, the protective effects of STAT3 had no association with the modulation of cell senescence during oxidative stress. In conclusion, SirT1 had negative effects on the regulation of STAT3 expression during oxidative stress. However, SirT1 and STAT3 demonstrated protective roles against oxidative stress in RPEs. These results therefore suggested that there was an equilibrium mechanism between SirT1 and STAT3 against oxidative stress, meaning that an equilibrium mechanism is required to be considered when combined application of STAT3 and SirT1 were performed to treat AMD.

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Section: A B C Dsupporting

confidence: 82%

Section: A B C Dsupporting

confidence: 82%

SirT1 and STAT3 protect retinal pigmented epithelium cells against oxidative stress

Wei

Zhang

et al. 2015

Molecular Medicine Reports

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“…STAT3 but not MAPK (pp44/42) activation is responsible for the inhibitory role of CNTF on rod differentiation [31]. In additional studies, we and other groups have obtained results strongly suggesting that STAT3 signaling is an underlying component of neural responsiveness to stress stimuli, especially in retina ganglion cells [36,37].…”

Section: Discussionmentioning

confidence: 69%

MAPK signaling during Müller glial cell development in retina explant cultures

Zhang

Huang

et al. 2010

j ocul biol dis inform

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The Müller cell is the only glial cell type generated from the retinal neuroepithelium. This cell type controls normal retina homeostasis and has been suggested to play a neuroprotective role. Recent evidence suggests that mammalian Müller cells can de-differentiate and return to a progenitor or stem cell stage following injury or disease. In vivo exploration of the molecular mechanisms of Müller cell differentiation and proliferation will add essential information to manipulate Müller cell functions. Signal transduction pathways that regulate Müller cell responses and activity are a critical part of their cellular machinery. In this study, we focus on mitogen-activated protein kinase (MAPK) signaling pathway during Müller glial cell differentiation and proliferation. We found that both MAPK and STAT3 signaling pathways are present during Müller glial cell development. Ciliary neurotrophic factor (CNTF)-stimulated Müller glial cell proliferation is associated with early developmental stages. Specific inhibition of MAPK phosphorylation significantly reduced the number of Müller glial cells with or without CNTF stimulation. These results suggested that the MAPK signal transduction pathway is important in the formation of Müller glial cells during retina development.

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“…7D). Our data suggest that transient Stat3 signaling activation in RGCs may not be sufficient to protect these cells from cell death, 35 whereas P-Erk1 activation in Müller glial may regulate gliosis after I/R. 36 …”

Section: Intracellular Signaling Pathways Activated By I/r In Mouse Rmentioning

confidence: 90%

New Mouse Retinal Stroke Model Reveals Direction-Selective Circuit Damage Linked to Permanent Optokinetic Response Loss

Joly¹,

Guzik-Kornacka²,

Pernet³

2014

Invest. Ophthalmol. Vis. Sci.

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STAT3 activation protects retinal ganglion cell layer neurons in response to stress

Cited by 40 publications

References 49 publications

SirT1 and STAT3 protect retinal pigmented epithelium cells against oxidative stress

SirT1 and STAT3 protect retinal pigmented epithelium cells against oxidative stress

MAPK signaling during Müller glial cell development in retina explant cultures

New Mouse Retinal Stroke Model Reveals Direction-Selective Circuit Damage Linked to Permanent Optokinetic Response Loss

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