HSP90 Inhibition Attenuated Isoflurane-Induced Neurotoxicity in Mice and Human Neuroglioma Cells

Zhang, Chunlu; Chen, Xi; Liu, Ruizhu; Zhao, Guoqing

doi:10.1007/s11064-023-04060-1

Cited by 1 publication

(1 citation statement)

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“…4B, C). HSP90 could contribute to enhancing hippocampal neuroplasticity [52,53]. Patients with Alzheimer’s disease (AD) exhibit lower levels of HSP90 in their hippocampus compared to subjects without AD [54], and HSP90 may be related to the association between T2DM and AD [55].…”

Section: Discussionmentioning

confidence: 99%

Muscle-derived miR-200a-3p through light-intensity exercise may contribute to improve memory dysfunction in type 2 diabetic mice

Shima,

Onishi,

Terashima

2024

Preprint

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Background: Memory dysfunction associated with type 2 diabetes mellitus (T2DM) poses a considerable threat to overall well-being. Engaging in light-intensity exercise has been shown to exert favorable effects on hippocampal function and molecular profiles, including Mct2 mRNA and miR-200a-3p. Nonetheless, a comprehensive understanding of the mechanisms underlying the positive impact of light-intensity exercise remains elusive. Here, we assessed the influence of exosomal miR-200a-3p secretion from gastrocnemius muscles in T2DM mice undergoing light-intensity exercise intervention, focusing on its potential to ameliorate memory dysfunction. Basic procedures: We initially assessed the effects of light-intensity exercise (7.0 m/min for healthy mice, 5.0 m/min for ob/ob mice, 30 min/day, five days/week, over a four-week period) on memory function, hippocampal mRNA associated with memory function, and the secretion of exosomal miR-200a-3p from their gastrocnemius muscle. Subsequently, the impact of a daily intraperitoneal injection of the miR-200a-3p mimic over a four-week duration was investigated, focusing on its influence on hippocampal dysregulation in ob/ob mice. Main findings: The light-intensity exercise intervention increased gastrocnemius muscle-derived and plasma exosomal miR-200a-3p levels in ob/ob mice, concomitant with improved memory dysfunction. Intriguingly, the daily intraperitoneal injection of mmu-miR-200a-3p mimic also demonstrated an ameliorative effect on memory function in ob/ob mice. Notably, both the exercise intervention and miR-200a-3p mimic treatment induced downregulation in hippocampal Keap1 mRNA and upregulation in mRNA of Hsp90aa1 and Mct2 in ob/ob mice. Principal conclusions: The current results imply that the augmentation of exosomal miR-200a-3p derived from the gastrocnemius muscle contributes to the amelioration of memory dysfunction in T2DM undergoing light-intensity exercise. Additionally, it is proposed that miR-200a-3p emulates the effects of light-intensity exercise, suggesting a potential therapeutic pathway for addressing hippocampal complications in the context of T2DM.

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