Analysis of genes associated with Alzheimer's disease and endoplasmic reticulum stress DOI Creative Commons
Ziyu Liu, Fei Li

Research Square (Research Square), Journal Year: 2024, Volume and Issue: unknown

Published: June 11, 2024

Abstract Objecitve Endoplasmic reticulum (ER) stress can activate the unfolded protein response (UPR), and sustained activation of UPR is closely associated with inflammation neuronal dysfunction, ultimately leading to neurodegeneration. This study aims identify potential targets related ER stress, aiming provide new insights into treatment Alzheimer's disease (AD). Methods We conducted differential expression analysis GSE4757 dataset in Gene Expression Omnibus (GEO) database using GEO2R tool performed Venn differentially expressed genes (DEGs) stress. Subsequently, we annotated functions DEGs genes, constructed a protein-protein interaction network Cytoscape, identified hub genes. Results The contained total 407 DEGs, 33 overlapping those The biological processes involved these mainly include mesenchymal morphogenesis, muscle growth, ossification regulation. KEGG revealed that participate cellular pathways such as basal cell carcinoma signaling pathway, breast cancer, pertussis pathway. We also four AD by Cytoscape. Conclusion used bioinformatics role AD, analyzed their involvement processes, for intervening thereby providing direction treating AD.

Language: Английский

Microglia aggravate white matter injury via C3/C3aR pathway after experimental subarachnoid hemorrhage DOI

Lei Yang,

Jinpeng Wu, Fan Zhang

et al.

Experimental Neurology, Journal Year: 2024, Volume and Issue: 379, P. 114853 - 114853

Published: June 10, 2024

Language: Английский

Citations

2
The mechanisms, hallmarks, and therapies for brain aging and age-related dementia DOI Creative Commons
Shiyun Jin, Wenping Lü,

Juan Zhang

et al.

Science Bulletin, Journal Year: 2024, Volume and Issue: unknown

Published: Sept. 1, 2024

Language: Английский

Citations

2
AIBP controls TLR4 inflammarafts and mitochondrial dysfunction in a mouse model of Alzheimer’s disease DOI Creative Commons
Yi Sak Kim, Soo‐Ho Choi, Keunyoung Kim

et al.

bioRxiv (Cold Spring Harbor Laboratory), Journal Year: 2024, Volume and Issue: unknown

Published: Feb. 21, 2024

ABSTRACT Microglia-driven neuroinflammation plays an important role in the development of Alzheimer’s disease (AD). Microglia activation is accompanied by formation and chronic maintenance TLR4 inflammarafts, defined as enlarged cholesterol-rich lipid rafts serving assembly platform for dimers complexes other inflammatory receptors. The secreted apoA-I binding protein (APOA1BP or AIBP) binds selectively targets cholesterol depletion machinery to inflammaraft expressing inflammatory, but not homeostatic microglia. Here we demonstrated that amyloid-beta (Aβ) induced inflammarafts microglia vitro brain APP/PS1 mice. Mitochondria Apoa1bp -/- were hyperbranched cupped, which was increased ROS dilated ER. size number Aβ plaques neuronal cell death significantly increased, animal survival decreased compared female These results suggest AIBP exerts control mitochondrial dynamics a protective AD associated oxidative stress neurodegeneration.

Language: Английский

Citations

1
Geniposide alleviates cholesterol-induced endoplasmic reticulum stress and apoptosis in osteoblasts by mediating the GLP-1R/ABCA1 pathway DOI Creative Commons

Mingliang Zhong,

Zhenyu Wu, Zhixi Chen

et al.

Journal of Orthopaedic Surgery and Research, Journal Year: 2024, Volume and Issue: 19(1)

Published: March 11, 2024

Abstract Background Cholesterol (CHO) is an essential component of the body. However, high CHO levels in body can damage bone mass and promote osteoporosis. accumulation cause osteoblast apoptosis, which has a negative effect on formation. The pathogenesis osteoporosis complicate process that includes oxidative stress, endoplasmic reticulum (ER) inflammation. Geniposide (GEN) natural compound with anti-osteoporotic effect. roles GEN osteopathogenesis are still unclear. Our previous studies demonstrated could reduce osteoblasts activation ER stress osteoblasts. molecular mechanism inhibiting CHO-induced apoptosis needs to be further investigated. Methods MC3T3-E1 cells were treated osteogenic induction medium (OIM). Ethanol-solubilized cholesterol (100 µM) was used as stimulator, 10 µM 25 geniposide added for treatment. alterations protein expression detected by western blot, cell analyzed flow cytometer. Results promoted activating osteoblasts, while alleviated reduced GLP-1R/ABCA1 pathway. Inhibition ABCA1 or GLP-1R eliminate protective activity against apoptosis. Conclusion mediating

Language: Английский

Citations

0
Analysis of genes associated with Alzheimer's disease and endoplasmic reticulum stress DOI Creative Commons
Ziyu Liu, Fei Li

Research Square (Research Square), Journal Year: 2024, Volume and Issue: unknown

Published: June 11, 2024

Abstract Objecitve Endoplasmic reticulum (ER) stress can activate the unfolded protein response (UPR), and sustained activation of UPR is closely associated with inflammation neuronal dysfunction, ultimately leading to neurodegeneration. This study aims identify potential targets related ER stress, aiming provide new insights into treatment Alzheimer's disease (AD). Methods We conducted differential expression analysis GSE4757 dataset in Gene Expression Omnibus (GEO) database using GEO2R tool performed Venn differentially expressed genes (DEGs) stress. Subsequently, we annotated functions DEGs genes, constructed a protein-protein interaction network Cytoscape, identified hub genes. Results The contained total 407 DEGs, 33 overlapping those The biological processes involved these mainly include mesenchymal morphogenesis, muscle growth, ossification regulation. KEGG revealed that participate cellular pathways such as basal cell carcinoma signaling pathway, breast cancer, pertussis pathway. We also four AD by Cytoscape. Conclusion used bioinformatics role AD, analyzed their involvement processes, for intervening thereby providing direction treating AD.

Language: Английский

Citations

0