HSP22 and its Role in Human Neurological Disease

Guan, Xiaomei; Tu, Chao; Li, Mengjun; Hu, Zhiping

doi:10.2174/156720211798121034

Cited by 4 publications

(2 citation statements)

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“…Apoptosis is a form of the process of inducing programmed cell death that is induced by gene expression to maintain homeostasis under certain physiological and pathological conditions [ 44 ]. Previous studies have shown that LPS-induced cognitive impairment is related to apoptosis [ 17 ].…”

Section: Resultsmentioning

confidence: 99%

Hsp22 pretreatment protects against LPS-induced hippocampal injury by alleviating neuroinflammation and apoptosis by regulating the NLRP3/Caspase1/IL-1β signaling pathway in mice

Peng

et al. 2023

Aging

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Neuroinflammation is an important reason for the occurrence and development of cognitive impairment. The Lentiviral vector Hsp22 was constructed for intracerebroventricular injection pretreatment, LPS was used to induce the cognitive impairment model in mice, and the Morris water maze was used to examine the changes in cognitive behavior in mice. LPS was used to induce BV-2 microglial cells, and plasmid pretreatment was used to overexpress Hsp22. HE staining, Nissl staining, immunohistochemistry, immunofluorescence, ELISA and protein blotting were used to examine microglial activation, changes in inflammatory factors, changes in pathway proteins and apoptosis. The results showed that LPS induced microglial expression of NLRP3/Caspase-1/IL-1β signaling pathway protein Iba1, and the inflammatory protein and inflammatory factors IL-1β, IL-6 and TNF-α, the expression of Bax increased significantly, Bcl2 expression decreased, and the learning and memory abilities of mice decreased significantly. Preconditioning with the Hsp22-overexpressing lentivirus attenuated LPS-induced activation of hippocampal microglia, the expression of inflammatory factors and pathway proteins, and apoptosis, and improved cognitive impairment in mice. In addition, plasmid-mediated Hsp22 overexpression reversed LPS-induced inflammation. These findings suggest that Hsp22 overexpression is a promising method for the treatment of cognitive impairment.

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Section: Resultsmentioning

confidence: 99%

Hsp22 pretreatment protects against LPS-induced hippocampal injury by alleviating neuroinflammation and apoptosis by regulating the NLRP3/Caspase1/IL-1β signaling pathway in mice

Peng

et al. 2023

Aging

View full text Add to dashboard Cite

show abstract

“…14,15 Phosphorylation or mutation in definite sites of HspB8 leads to the development of clinical diseases, such as hereditary nerve ending disease, Charcot-MarieTooth, desmin-related cardiomyopathy, and breast cancer. [16][17][18][19][20] Failure to regulate the amyloid-beta peptide aggregation of HspB8 could cause the development of classic senile plaques in Alzheimer's disease. 21 HspB8 also has an important function in the stress reaction due to cerebral ischemia.…”

Section: Introductionmentioning

confidence: 99%