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层粘连蛋白经基质金属蛋白酶 9 降解可促进早期发育大鼠视网膜内氯胺酮诱导的神经元凋亡。

Laminin degradation by matrix metalloproteinase 9 promotes ketamine-induced neuronal apoptosis in the early developing rat retina.

机构信息

Department of Anesthesiology, Shanghai Children's Medical Center Affiliated to School of Medicine, Shanghai Jiao Tong University, Shanghai, China.

出版信息

CNS Neurosci Ther. 2020 Oct;26(10):1058-1068. doi: 10.1111/cns.13428. Epub 2020 Jun 20.

DOI:10.1111/cns.13428
PMID:32562453
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7539835/
Abstract

AIMS

During early development, laminin degradation contributes to the death of neurons. This study aims to investigate the role and regulation of laminin in ketamine-induced apoptosis.

METHODS

We performed terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling (TUNEL) and immunohistochemical assays to investigate the roles of the non-integrin laminin receptor, matrix metalloproteinase 9 (MMP9) in ketamine-induced neuronal apoptosis. In situ zymography, Western blot, and immunofluorescence were used to explore the relationships between laminin, MMP9 activity, and Zn . Experiments were performed using whole-mount retinas dissected from Sprague Dawley rats.

RESULTS

The TUNEL and immunohistochemical assays indicated that ketamine-induced neuronal apoptosis in early developing rat retina. Blockade of non-integrin laminin receptor promoted ketamine-induced apoptosis, while non-integrin laminin receptor activation attenuated ketamine-induced apoptosis. Ketamine-induced laminin degradation, possibly by enhancing the activity of MMP9. MMP9 inhibition reduced ketamine-induced apoptosis by reducing laminin degradation. Downregulation of Zn attenuated the increased MMP9 activity, laminin degradation caused by ketamine and significantly reduced ketamine-induced neuronal apoptosis.

CONCLUSION

Laminin degradation by MMP9 promoted ketamine-induced neuronal apoptosis in early developing rat retina. The non-integrin laminin receptor may be a pathway involved in ketamine-induced apoptosis. Zn downregulation may play a protective role against ketamine-induced neuronal apoptosis through inhibiting MMP9 activity.

摘要

目的

在早期发育过程中，层粘连蛋白的降解有助于神经元的死亡。本研究旨在探讨层粘连蛋白在氯胺酮诱导的细胞凋亡中的作用和调节机制。

方法

我们通过末端脱氧核苷酸转移酶生物素-dUTP 缺口末端标记（TUNEL）和免疫组织化学检测，研究了非整联层粘连蛋白受体、基质金属蛋白酶 9（MMP9）在氯胺酮诱导的神经元凋亡中的作用。原位酶谱法、Western blot 和免疫荧光法用于探讨层粘连蛋白、MMP9 活性与 Zn之间的关系。实验采用 Sprague Dawley 大鼠全视网膜铺片进行。

结果

TUNEL 和免疫组织化学检测表明，氯胺酮诱导早期发育大鼠视网膜神经元凋亡。非整联层粘连蛋白受体阻断促进氯胺酮诱导的凋亡，而非整联层粘连蛋白受体激活则减弱氯胺酮诱导的凋亡。氯胺酮诱导的层粘连蛋白降解可能通过增强 MMP9 活性来实现。MMP9 抑制通过减少层粘连蛋白降解，减轻氯胺酮诱导的凋亡。Zn 的下调通过抑制 MMP9 活性、层粘连蛋白降解，显著减轻氯胺酮诱导的神经元凋亡。

结论

MMP9 介导的层粘连蛋白降解促进了早期发育大鼠视网膜中氯胺酮诱导的神经元凋亡。非整联层粘连蛋白受体可能是氯胺酮诱导凋亡的途径之一。Zn 的下调可能通过抑制 MMP9 活性发挥对氯胺酮诱导的神经元凋亡的保护作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f66/7539835/3aac980bd574/CNS-26-1058-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f66/7539835/6c1004d98020/CNS-26-1058-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f66/7539835/c88902c6997a/CNS-26-1058-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f66/7539835/dedb8743182a/CNS-26-1058-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f66/7539835/f391861c49a4/CNS-26-1058-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f66/7539835/ad68f17f1bf5/CNS-26-1058-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f66/7539835/3aac980bd574/CNS-26-1058-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f66/7539835/6c1004d98020/CNS-26-1058-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f66/7539835/c88902c6997a/CNS-26-1058-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f66/7539835/dedb8743182a/CNS-26-1058-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f66/7539835/f391861c49a4/CNS-26-1058-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f66/7539835/ad68f17f1bf5/CNS-26-1058-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f66/7539835/3aac980bd574/CNS-26-1058-g006.jpg

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