Neuronic autophagy contributes to p-connexin 43 degradation in hippocampal astrocytes following traumatic brain injury in rats

Sun, Li Qian; Gao, Jun; Cui, Ying; Zhao, Man; Jing, Xiao; Li, Ran; Tian, Yan; Cui, Jian; Wu, Zhongxue

doi:10.3892/mmr.2015.3264

Cited by 16 publications

(7 citation statements)

References 19 publications

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“…Next, the GFP-LC3 transfected N2a cells were incubated with M 3 -Cy5&Aβ 42 (20 μg·mL −1 /20 μM) for 4 h, followed by CLSM observation. Generally, LC3-II was recruited to the autophagosome membrane and thereby formed a green dot of GFP-LC3 when autophagy was activated 36 , 37 . As expected, the CLSM images revealed that most of the M 3 -Cy5 (red signal) colocalized with autophagosomes (GFP-LC3, green signal) (Fig.…”

Section: Resultsmentioning

confidence: 99%

A self-destructive nanosweeper that captures and clears amyloid β-peptides

et al. 2018

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Cerebral amyloid β-peptide (Aβ) accumulation resulting from an imbalance between Aβ production and clearance is one of the most important causes in the formation of Alzheimer’s disease (AD). In order to preserve the maintenance of Aβ homeostasis and have a notable AD therapy, achieving a method to clear up Aβ plaques becomes an emerging task. Herein, we describe a self-destructive nanosweeper based on multifunctional peptide-polymers that is capable of capturing and clearing Aβ for the effective treatment of AD. The nanosweeper recognize and bind Aβ via co-assembly through hydrogen bonding interactions. The Aβ-loaded nanosweeper enters cells and upregulates autophagy thus promoting the degradation of Aβ. As a result, the nanosweeper decreases the cytotoxicity of Aβ and rescues memory deficits of AD transgenic mice. We believe that this resourceful and synergistic approach has valuable potential as an AD treatment strategy.

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Section: Resultsmentioning

confidence: 99%

A self-destructive nanosweeper that captures and clears amyloid β-peptides

et al. 2018

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“…57 Following traumatic brain injury (TBI), autophagy inhibition caused increased levels of phosphorylated connexin 43 (pCx43) in hippocampal astrocytes, indicating autophagy based degradation of GJs. 58 A single or several AGJs can be engulfed simultaneously within an individual autophagosome. 54 Furthermore, plasma-membrane bound connexin proteins have been shown to be involved in early biogenesis of autophagosome.…”

Section: Autophagy Regulation Of Gap Junctionmentioning

confidence: 99%

Role of autophagy in the regulation of epithelial cell junctions

Nighot

2016

Tissue Barriers

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“…Autophagy is involved in the pathological and physiological process of numerous diseases. However, no consensus has been reached on the effect of autophagy on organ function (16). A previous study has indicated that autophagy may lead to autophagic cell death or apoptosis, thus aggravating organ dysfunction (17).…”

Section: Discussionmentioning

confidence: 99%

Effect of poly‑arginine R18 on neurocyte cell growth via autophagy in traumatic brain injury

Batulu

et al. 2019

Exp Ther Med

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The present study assessed the effects of poly-arginine R18 and its promotion of neurocyte cell growth via autophagy in traumatic brain injury (TBI), and aimed to determine the possible mechanism by which this occurs. Brain water content was measured to analyze the effects of poly-arginine R18 in TBI. MTT and lactate dehydrogenase activity assays were performed to measure N2A cell growth. Western blotting and immunofluorescence staining were also performed to determine the protein expression of Bcl-2 associated X, LC3, Beclin-1 and p62. The results demonstrated that poly-arginine R18 treatment reduced neurocyte apoptosis and promoted neurocyte cell growth via the activation of autophagy in a rat model of TBI. Furthermore, poly-arginine R18 treatment promoted neurocyte cell growth, reduced apoptosis, induced the protein expression of LC3 and Beclin-1, and suppressed p62 expression by promoting autophagy in vitro . In addition, the inhibition of autophagy attenuated the effects of poly-arginine R18 on cell growth in vitro . Collectively, the results demonstrate the effects of poly-arginine R18 on neurocyte cell growth via autophagy activation in a model of TBI, and poly-arginine R18 is therefore a potential therapeutic target in TBI.

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Neuronic autophagy contributes to p-connexin 43 degradation in hippocampal astrocytes following traumatic brain injury in rats

Cited by 16 publications

References 19 publications

A self-destructive nanosweeper that captures and clears amyloid β-peptides

A self-destructive nanosweeper that captures and clears amyloid β-peptides

Role of autophagy in the regulation of epithelial cell junctions

Effect of poly‑arginine R18 on neurocyte cell growth via autophagy in traumatic brain injury

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