Autophagy ameliorates cognitive impairment through activation of PVT1 and apoptosis in diabetes mice

Li, Zhigui; Hao, Shuang; Yin, Hongqiang; Gao, Jing; Yang, Zhuo

doi:10.1016/j.bbr.2016.03.023

Cited by 64 publications

(43 citation statements)

References 65 publications

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“…Additionally, another group studied PVT1-mediated autophagy in cognitive impairment of diabetes mellitus. They found that autophagy inhibitor 3-methyladenine (3-MA) could significantly induce apoptotic cell death by decreasing hippocampal PVT1 expression, which subsequently heightened cognitive impairment (52). This was the first time that lncRNA homeostasis was shown to be controlled by cell autophagy, but the specific mechanisms need to be further elucidated.…”

Section: Other Lncrnas On Autophagy Regulationmentioning

confidence: 99%

Long non-coding RNAs act as regulators of cell autophagy in diseases

Xu¹,

Yan²,

Qian³

et al. 2017

Oncology Reports

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Identification of long non-coding RNAs (lncRNAs) has provided a substantial increase in our understanding of the non-coding transcriptome. Studies have revealed a crucial function of lncRNAs in the modulation of cell autophagy in vitro and in vivo, further contributing to the hallmarks of disease phenotypes. These findings have profoundly altered our understanding of disease pathobiology, and may lead to the emergence of new biological concepts underlying autophagy-associated diseases, such as the carcinomas. Studies on the molecular mechanism of the lncRNA-autophagy axis may offer additional avenues for therapeutic intervention and biomarker assessment. In this review, we discuss recent findings on the multiple molecular roles of regulatory lncRNAs in the signaling pathways of cell autophagy. The emerging knowledge in this rapidly advancing field will offer novel insights into human diseases, especially cancers.

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Section: Other Lncrnas On Autophagy Regulationmentioning

confidence: 99%

Long non-coding RNAs act as regulators of cell autophagy in diseases

Xu¹,

Yan²,

Qian³

et al. 2017

Oncology Reports

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show abstract

“…Investigations on streptozotocin-induced diabetes in mice showed that LTP impairment in diabetic mice was exacerbated in the presence of an inhibitor of autophagy called 3-methyl adenine (Li et al, 2016). In the context of chemically induced LTD, it has been shown that neuronal stimulation induces autophagy (Shehata et al, 2012).…”

Section: Other Proteolytic Pathways That Play a Role In Synaptic Pmentioning

confidence: 99%

“…Therefore, it is likely that autophagy has a role in memory formation in humans as well. In the study on diabetic mice, it was found that spatial memory was not impaired but spatial reversal memory was and the memory impairment was exacerbated by inhibition of autophagy (Li et al, 2016). Even though these results are suggestive of the link between autophagy and memory, the caveat is that the studies were conducted in the context of diabetes.…”

Section: Other Proteolytic Pathways That Play a Role In Synaptic Pmentioning

confidence: 99%

Proteolysis, synaptic plasticity and memory

Hegde

2017

Neurobiology of Learning and Memory

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Protein degradation has many critical functions in the nervous system such as refinement of synaptic connections during development and synaptic plasticity and memory in the adult organisms. A major cellular machinery of proteolysis is the ubiquitin-proteasome pathway (UPP). The UPP precisely regulates proteolysis by covalently attaching ubiquitin, a small protein, to substrates through sequential enzymatic reactions and the proteins marked with the ubiquitin tag are degraded by complex containing many subunits called the proteasome. Research over the years has shown a role for the UPP in regulating presynaptic and postsynaptic proteins critical for neurotransmission and synaptic plasticity. Studies have also revealed a role for the UPP in various forms of memory. Mechanistic investigations suggest that the function of the UPP in neurons is not homogenous and is subject to local regulation in different neuronal sub-compartments. In both invertebrate and vertebrate model systems, local roles have been found for enzymes that attach ubiquitin to substrate proteins as well as for enzymes that remove ubiquitin from substrates. The proteasome also has disparate functions in different parts of the neuron. In addition to the UPP, proteolysis by the lysosome and autophagy play a role in synaptic plasticity and memory. This review details the functions of proteolysis in synaptic plasticity and summarizes the findings on the connection between proteolysis and memory mainly focusing on the UPP including its local roles.

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“…It has been recognized that autophagy exhibits a dual function in neurodegenerative diseases. Recently, several studies have implied that autophagy impairment may contribute to diabetic encephalopathy, and targeting the autophagic signaling to restore autophagic flux may be neuroprotective in this setting …”

Section: Introductionmentioning

confidence: 99%

“…Recently, several studies have implied that autophagy impairment may contribute to diabetic encephalopathy, and targeting the autophagic signaling to restore autophagic flux may be neuroprotective in this setting. [13][14][15] Curcumin, a major bioactive component of turmeric, can prevent cognitive impairment via its various pharmacological activities including regulation of autophagy, anti-oxidative stress, and anti-inflammation. [16][17][18] However, the poor aqueous solubility and relatively low bioavailability of curcumin limits its utilization.…”

mentioning

confidence: 99%