Department of Pathology, Beijing Hospital; National Center of Gerontology; Institute of Geriatric Medicine; Chinese Academy of Medical Sciences, Beijing, China.
National Center for Clinical Laboratories, Beijing Hospital, National Center of Gerontology; Institute of Geriatric Medicine, Chinese Academy of Medical Sciences, P.R. China; Graduate School of Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, China.
Front Endocrinol (Lausanne). 2022 Oct 3;13:892897. doi: 10.3389/fendo.2022.892897. eCollection 2022.
Girdin, as an actin-binding protein, plays a major role in maintaining the stability of the actin skeleton structure and affects the growth, development, and migration of neurons. This study discusses the mechanism of Girdin in brain degeneration caused by high glucose stimulation. We examined the expression of Girdin in diabetic patients. The positive expression rate of Girdin in the diabetic group was 17.2% (5/29), which was obviously lower than the positive expression rate of 83.3% (20/24) in the non-diabetic group. We examined the expression of Girdin and its signaling pathway-related proteins Akt and STAT3 in hippocampal neurons induced by high glucose. The results showed that, in contrast to the control group (glucose concentration = 25 mmol/L), the expression of Girdin in the high-glucose group (glucose concentration = 225 mmol/L) was reduced ( < 0.05); the phosphorylation levels of Akt and STAT3 related to Girdin signaling pathway were also reduced ( < 0.05). Under high-glucose stimulation, the structure of neurons is abnormal, such as the reduction or disappearance of dendritic spines, and the number of neurons is reduced. In addition, Girdin and Akt were less expressed in neurons and synapses, especially the most obvious reduction in synaptic terminals. The activity of Girdin and its signaling pathway-related proteins Akt and STAT3 decreased in neurons under high glucose stimulation, indicating that the mechanism of Girdin in brain degeneration caused by high glucose stimulation was closely related to the Akt and STAT3 pathways.
The mechanism of Girdin in degenerative brain disease caused by high glucose stimulation. This article discusses the mechanism of Girdin in brain degeneration induced by high glucose stimulation. The expression of Girdin in the diabetic group was significantly lower than that in the non-diabetic group. The expression of Girdin and its signaling pathway-related proteins Akt and STAT3 in hippocampal neurons was significantly reduced under high glucose stimulation. Under high glucose stimulation, the structure of neurons is abnormal and the number decreases; synapses become shorter. It indicates that the mechanism of brain degeneration caused by high glucose stimulation by Girdin is closely related to the Akt and STAT3 pathways.
Girdin 作为一种肌动蛋白结合蛋白，在维持肌动蛋白骨架结构的稳定性方面发挥着重要作用，并影响神经元的生长、发育和迁移。本研究探讨了 Girdin 在高糖刺激引起的脑退行性变中的作用机制。我们检测了糖尿病患者中 Girdin 的表达。糖尿病组 Girdin 的阳性表达率为 17.2%（5/29），明显低于非糖尿病组 83.3%（20/24）的阳性表达率。我们检测了高糖诱导的海马神经元中 Girdin 及其信号通路相关蛋白 Akt 和 STAT3 的表达。结果表明，与对照组（葡萄糖浓度=25mmol/L）相比，高糖组（葡萄糖浓度=225mmol/L）Girdin 的表达减少（<0.05）；Girdin 信号通路相关的 Akt 和 STAT3 的磷酸化水平也降低（<0.05）。在高糖刺激下，神经元的结构异常，如树突棘减少或消失，神经元数量减少。此外，Girdin 和 Akt 在神经元和突触中的表达减少，尤其是突触末梢减少最为明显。高糖刺激下神经元中 Girdin 及其信号通路相关蛋白 Akt 和 STAT3 的活性降低，提示 Girdin 在高糖刺激引起的脑退行性变中的作用机制与 Akt 和 STAT3 通路密切相关。
高糖刺激引起的退行性脑疾病中 Girdin 的作用机制。本文探讨了高糖刺激引起的脑退行性变中 Girdin 的作用机制。糖尿病组 Girdin 的表达明显低于非糖尿病组。高糖刺激下，海马神经元中 Girdin 及其信号通路相关蛋白 Akt 和 STAT3 的表达明显减少。高糖刺激下，神经元结构异常，数量减少；突触变短。表明 Girdin 引起的高糖刺激脑退行性变的机制与 Akt 和 STAT3 通路密切相关。
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