Zinc induces reactive astrogliosis through ERK dependent activation of Stat3 and promotes synaptic degeneration

2021 ◽  
Author(s):  
Huiliang Zhang ◽  
Mengzhe Yang ◽  
Xiaochuan Wang ◽  
Hui Wei ◽  
Min Du ◽  
...  
Keyword(s):  
Reactive Astrogliosis ◽  
Synaptic Degeneration

scholarly journals P3-209: CIP2A INDUCES ALZHEIMER-LIKE SYNAPTIC DEGENERATION AND COGNITIVE DEFICITS THROUGH PROMOTING REACTIVE ASTROGLIOSIS

2019 ◽  
Vol 15 ◽  
pp. P1010-P1010
Author(s):  
Yangping Shentu ◽  
Wenting Hu ◽  
Xiaochuan Wang ◽  
Jianzhi Wang ◽  
Rong Liu
Keyword(s):  
Cognitive Deficits ◽  
Reactive Astrogliosis ◽  
Synaptic Degeneration

scholarly journals CDDO-Me Distinctly Regulates Regional Specific Astroglial Responses to Status Epilepticus via ERK1/2-Nrf2, PTEN-PI3K-AKT and NFκB Signaling Pathways

Antioxidants ◽  
2020 ◽  
Vol 9 (10) ◽  
pp. 1026
Author(s):  
Ji-Eun Kim ◽  
Hana Park ◽  
Tae-Cheon Kang
Keyword(s):  
Status Epilepticus ◽  
Signaling Pathways ◽  
Seizure Activity ◽  
Molecular Layer ◽  
Antioxidant Properties ◽  
Acid Methyl Ester ◽  
Related Factor ◽  
Nuclear Factor ◽  
Reactive Astrogliosis ◽  
Nrf2 Expression

2-Cyano-3,12-dioxo-oleana-1,9(11)-dien-28-oic acid methyl ester (CDDO-Me) is a triterpenoid analogue of oleanolic acid. CDDO-Me shows anti-inflammatory and neuroprotective effects. Furthermore, CDDO-Me has antioxidant properties, since it activates nuclear factor-erythroid 2-related factor 2 (Nrf2), which is a key player of redox homeostasis. In the present study, we evaluated whether CDDO-Me affects astroglial responses to status epilepticus (SE, a prolonged seizure activity) in the rat hippocampus in order to understand the underlying mechanisms of reactive astrogliosis and astroglial apoptosis. Under physiological conditions, CDDO-Me increased Nrf2 expression in the hippocampus without altering activities (phosphorylations) of phosphatase and tensin homolog deleted on chromosome 10 (PTEN), phosphatidylinositol-3-kinase (PI3K), and AKT. CDDO-Me did not affect seizure activity in response to pilocarpine. However, CDDO-Me ameliorated reduced astroglial Nrf2 expression in the CA1 region and the molecular layer of the dentate gyrus (ML), and attenuated reactive astrogliosis and ML astroglial apoptosis following SE. In CA1 astrocytes, CDDO-Me inhibited the PI3K/AKT pathway by activating PTEN. In contrast, CDDO-ME resulted in extracellular signal-related kinases 1/2 (ERK1/2)-mediated Nrf2 upregulation in ML astrocytes. Furthermore, CDDO-Me decreased nuclear factor-κB (NFκB) phosphorylation in both CA1 and ML astrocytes. Therefore, our findings suggest that CDDO-Me may attenuate SE-induced reactive astrogliosis and astroglial apoptosis via regulation of ERK1/2-Nrf2, PTEN-PI3K-AKT, and NFκB signaling pathways.

Melatonin attenuates reactive astrogliosis and glial scar formation following cerebral ischemia and reperfusion injury mediated by GSK‐3β and RIP1K

2021 ◽  
Author(s):  
Nuttapong Yawoot ◽  
Jirakhamon Sengking ◽  
Piyawadee Wicha ◽  
Piyarat Govitrapong ◽  
Chainarong Tocharus ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Reperfusion Injury ◽  
Glial Scar ◽  
Scar Formation ◽  
Ischemia And Reperfusion ◽  
Ischemia And Reperfusion Injury ◽  
Reactive Astrogliosis ◽  
Cerebral Ischemia And Reperfusion ◽  
Gsk 3Β

NEK6 is an injury‐responsive kinase cooperating with STAT3 in regulation of reactive astrogliosis

Glia ◽  
2021 ◽  
Author(s):  
Ying Yu ◽  
Tianjin Shen ◽  
Xiaoling Zhong ◽  
Lei‐Lei Wang ◽  
Wenjiao Tai ◽  
...  
Keyword(s):  
Reactive Astrogliosis
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