Pentose phosphate pathway activation via HSP27 phosphorylation by ATM kinase: A putative endogenous antioxidant defense mechanism during cerebral ischemia-reperfusion

Yamamoto, Yusuke; Hosoda, Kohkichi; Imahori, Taichiro; Tanaka, Jun; Matsuo, Kazuya; Nakai, Tomoaki; Irino, Yasuhiro; Shinohara, Masakazu; Sato, Naoko; Sasayama, Takashi; Tanaka, Kazuhiro; Nagashima, Hiroaki; Kohta, Masaaki; Kohmura, Eiji

doi:10.1016/j.brainres.2018.03.001

Cited by 19 publications

(22 citation statements)

References 52 publications

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“…Blocking the cathepsin-t Bid-mitochondrial apoptosis signaling pathway by inhibiting autophagy and stabilizing the lysosomal membrane is associated with up-regulation of lysosomal Hsp70.1B in astrocytes (Zhou et al, 2017). Further, other studies have found that HSP proteins are involved in the pathophysiology of cerebral ischemia (Qi et al, 2015; Shi et al, 2017; Choi et al, 2018; Yamamoto et al, 2018). This suggests that additional studies on heat shock proteins may provide new options for clinical treatment of stroke.…”

Section: Possible Molecular Mechanisms Of Autophagy Involved In Ischementioning

confidence: 95%

Crosstalk Between Autophagy and Cerebral Ischemia

Sun¹,

Zhu²,

Zhong³

et al. 2019

Front. Neurosci.

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With the use of advanced electron microscopy and molecular biology tools, several studies have shown that autophagy is involved in the development of ischemic stroke. A series of molecular mechanisms are involved in the regulation of autophagy. In this work, the possible molecular mechanisms involved in autophagy during ischemic stroke were reviewed and new potential targets for the study and treatment of ischemic stroke were provided.

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Section: Possible Molecular Mechanisms Of Autophagy Involved In Ischementioning

confidence: 95%

Crosstalk Between Autophagy and Cerebral Ischemia

Sun¹,

Zhu²,

Zhong³

et al. 2019

Front. Neurosci.

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“…C57BL/6 mice of the sham group were injected with normal saline for 8 h under 50 mg/kg pentobarbital sodium pentobarbital sodium. C57BL/6 mice with IP were injected with 2 mg/kg of LPS (Sigma-Aldrich Merck KGaA) under 50 mg/kg pentobarbital sodium (intraperitoneal) (17,18). A total of 8 h later, peripheral blood (100 μ l) was collected from a leg vein under 50 mg/kg pentobarbital sodium and serum was centrifuged at 1,000 × g for 10 min at 4°C.…”

Section: Methodsmentioning

confidence: 99%

“…no. sc-29410; Santa Cruz Biotechnology, Inc.), 100 ng of miRNA-302e, 100 ng of anti-miRNA-302e and 100 ng of negative mimics were transfected into cells (1×10 5 cell/ml) using Lipofectamine 2000 (Thermo Fisher Scientific, Inc.) for 48 h. Following 48 h, cells were treated with 100 ng/ml of LPS for 6 h (3,6,17) and used for western blotting or RT-qPCR.…”

Section: Methodsmentioning

confidence: 99%

miRNA-302e attenuates inflammation in infantile pneumonia though the RelA/BRD4/NF-κB signaling pathway

Cui

et al. 2019

Int J Mol Med

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In the present study, the main focus was investigating the role of microRNA (miRNA)-302e in infantile pneumonia (IP) and exploring the potential protective mechanisms. Briefly, the expression of miRNA-302e was reduced in a mouse model of IP. In addition, the administration of anti-miRNA-302e increased inflammation and induced the protein expression of RelA, bromodomain-containing protein 4 (BRD4) and nuclear factor (NF)-κB in the in vitro model of IP. In contrast, over-expression of miRNA-302e reduced inflammation and suppressed the protein expression of RelA, BRD4 and NF-κB in an in vitro model of IP. Small interfering (si)-RelA attenuated the effects of miRNA-302e on inflammation in an in vitro model of IP. Consistently, si-BRD4 or si-NF-κB attenuated the effects of miRNA-302e on inflammation in an in vitro model of IP. Taken together, the results of the present study demonstrated that miRNA-302e attenuated inflammation in IP through the RelA/ BRD4/ NF-κB signaling pathway.

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“…Studies have shown that the expression of HspB1 can significantly decrease cellular the ROS level and upregulate the total glutathione level [82,83]. HspB1 may act in different ways to modulate cell intracellular redox status: (a) decreasing free radical production by reducing the activities of enzymes, including superoxide dismutase (SOD) [84,85] and catalase [85,86], or decreasing of intracellular iron to prevent its participation in free radical formation [87]; (b) scavenging free radicals by modulating the activity of antioxidant enzymes such as glucose 6-phosphate dehydrogenase (G6PDH) [88,89], glutathione reductase (GR) [90], and glutathione peroxidase (GPx) [85,90] to increase reduced glutathione (GSH) levels and downregulate ROS; (c) activating transcription factors, such as nuclear factor erythroid 2-related factor 2 (NRF2), thereby activating their target antioxidative enzymes [91]. Consistent with the abovementioned mechanisms, increased levels of sHSPs, together with multiple antioxidant molecules, including superoxide dismutase (MnSOD), thioredoxin reductase 2 (TXNRD2), glutathione (GSH), glutathione peroxidase (Gpx), were identified in thyroid tumors [92].…”

Section: Tumorigenesismentioning

confidence: 99%

Small Heat Shock Proteins in Cancers: Functions and Therapeutic Potential for Cancer Therapy

Xiong

Tan

et al. 2020

IJMS

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Small heat shock proteins (sHSPs) are ubiquitous ATP-independent chaperones that play essential roles in response to cellular stresses and protein homeostasis. Investigations of sHSPs reveal that sHSPs are ubiquitously expressed in numerous types of tumors, and their expression is closely associated with cancer progression. sHSPs have been suggested to control a diverse range of cancer functions, including tumorigenesis, cell growth, apoptosis, metastasis, and chemoresistance, as well as regulation of cancer stem cell properties. Recent advances in the field indicate that some sHSPs have been validated as a powerful target in cancer therapy. In this review, we present and highlight current understanding, recent progress, and future challenges of sHSPs in cancer development and therapy.

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Pentose phosphate pathway activation via HSP27 phosphorylation by ATM kinase: A putative endogenous antioxidant defense mechanism during cerebral ischemia-reperfusion

Cited by 19 publications

References 52 publications

Crosstalk Between Autophagy and Cerebral Ischemia

Crosstalk Between Autophagy and Cerebral Ischemia

miRNA-302e attenuates inflammation in infantile pneumonia though the RelA/BRD4/NF-κB signaling pathway

Small Heat Shock Proteins in Cancers: Functions and Therapeutic Potential for Cancer Therapy

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