Role of microglia-neuron interactions in diabetic encephalopathy

2018 ◽  
Vol 42 ◽  
pp. 28-39 ◽  
Author(s):  
Yuan Liu ◽  
Mingchao Li ◽  
Zuo Zhang ◽  
Yun Ye ◽  
Jiyin Zhou
2003 ◽  
Vol 16 (67) ◽  
pp. 440-449 ◽  
Author(s):  
María A. García-Espinosa ◽  
María L. García-Martín ◽  
Sebastián Cerdán

2021 ◽  
Author(s):  
Olli Pietilainen ◽  
Ralda Nehme ◽  
Aditi Trehan ◽  
Kevin Eggan

Recent genetic discoveries in schizophrenia have highlighted neuronal genes with functions in the synapse. Although emblematic of neurons, the development of synapses and neuronal maturation relies on interactions with glial cells including astrocytes. To study the role of glia-neuron interactions in schizophrenia, we generated RNA sequence data from human pluripotent stem cell (hPSC) derived neurons that were cocultured with glial cells. We found that expression of genes characteristic of astrocytes induced the expression of post-synaptic genetic programs in neurons, consistent with advanced neuronal maturation. We further found that the astrocyte-induced genes in neurons were associated with risk for schizophrenia. To understand how glial cells promoted neuronal maturation, we studied the association of transcript abundances in glial cells to gene expression in neurons. We found that expression of synaptic cell adhesion molecules in glial cells corresponded to induced synaptic transcripts in neurons and were associated with genetic risk for schizophrenia. These included 11 genes in significant GWAS loci and three with direct genetic evidence for the disorder (MAGI2, NRXN1, LRRC4B, and MSI2). Our results suggest that astrocyte-expressed genes with functions in the synapse are associated with schizophrenia and promote synaptic genetic programs in neurons, and further highlight the potential role for astrocyte-neuron interactions in schizophrenia.


2005 ◽  
Vol 1037 (1-2) ◽  
pp. 12-24 ◽  
Author(s):  
Zhen-guo Li ◽  
Weixian Zhang ◽  
Anders A.F. Sima

2019 ◽  
Vol 10 ◽  
Author(s):  
Anup Bhusal ◽  
Md Habibur Rahman ◽  
In-Kyu Lee ◽  
Kyoungho Suk

Molecules ◽  
2018 ◽  
Vol 23 (3) ◽  
pp. 522 ◽  
Author(s):  
Yadong Zhai ◽  
Xiangbao Meng ◽  
Tianyuan Ye ◽  
Weijie Xie ◽  
Guibo Sun ◽  
...  

Diabetes is associated with a high risk of developing cognitive dysfunction and neuropsychiatric disabilities, and these disease symptomsare termed diabetic encephalopathy (DEP). Inflammation is involved in the development of DEP. The cleavage and maturation of the proinflammatory cytokine interleukin (IL)-1β is regulated by the NLRP3 inflammasome. Obese and type 2 diabetic db/db mice show anxiety- and depression-like behaviors and cognitive disorders associated with hippocampal inflammation. The purpose of this study was to explore the role of NLRP3 inflammasome in DEP. Results showed that expression levels of inflammasome components including NLRP3, apoptosis-associated speck-like protein (ASC), and caspase-1, as well as IL-1β in the hippocampus of diabetic db/db mice were higher than those of non-diabetic db/m mice. Treatment of db/db mice with NLRP3 inflammasome inhibitor MCC950 ameliorated anxiety- and depression-like behaviors as well as cognitive dysfunction, and reversed increased NLRP3, ASC, and IL-1βexpression levels and caspase-1 activity in hippocampus. Moreover, MCC950 treatment significantly improved insulin sensitivity in db/db mice. These results demonstrate that inhibition of NLRP3 inflammasome activation may prove to be a potential therapeutic approach for DEP treatment.


2019 ◽  
Vol 10 ◽  
Author(s):  
Anup Bhusal ◽  
Md Habibur Rahman ◽  
In-Kyu Lee ◽  
Kyoungho Suk

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