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半乳糖凝集素3和激活转录因子3在6-羟基多巴胺诱导的帕金森病大鼠模型黑质多巴胺能神经元中的表达

Expression of Galectin 3 and Activating Transcription Factor 3 in Nigral Dopaminergic Neurons of 6-Hydroxydopamine Induced Parkinsonian Rat Model.

作者信息

Lee Eun-Jin, Choy Yoon-Jung, Woo Ran-Sook, Baik Tai-Kyoung, Yoo Hong-Il, Song Dae-Yong

机构信息

Department of Anatomy and Neurosciences, Eulji University School of Medicine, Daejeon, Republic of Korea.

Department of Optometry, Eulji University, Seongnam, Republic of Korea.

出版信息

In Vivo. 2025 May-Jun;39(3):1341-1354. doi: 10.21873/invivo.13938.

DOI:10.21873/invivo.13938
PMID:40295017
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12041963/
Abstract

BACKGROUND/AIM: Parkinson's disease (PD) is an age-related neurodegenerative disease marked by the relatively progressive dopaminergic neuronal loss in the substantia nigra (SN). Retrograde degeneration of the nigrostriatal dopaminergic neurons by 6-hydroxydopamine (6-OHDA) has been widely used as a PD animal model, while endogenous 6-OHDA promotes the progression of PD pathology. Galectin 3 (Gal3) and activating transcription factor 3 (ATF3) have been implicated in neurodegenerative processes. The aim of this study was to investigate the expression pattern and roles of Gal3 and ATF3 in a Parkinson's disease animal model induced by 6-OHDA.

MATERIALS AND METHODS

We investigated temporal and spatial profiles of Gal3 expression in 6-OHDA rat model of PD. Lesions were induced by unilateral stereotactic injections of 6-OHDA into the striatum. Three days prior to 6-OHDA lesion, Fluorogold (FG) was injected at the same coordinates as the subsequent 6-OHDA injection. 6-OHDA induced retrograde degeneration of tyrosine hydroxylase immunopositive and FG immunopositive neurons within SN in a time-dependent manner.

RESULTS

Activating transcription factor 3 (ATF3) expression was also upregulated in the SN, in a pattern similar to that of Gal3 immunoreactivity. Finally, we confirmed through triple immunofluorescence staining that ATF3 and Gal3 were colocalized in the dopaminergic neurons labeled with FG. These neurons were damaged by 6-OHDA.

CONCLUSION

Gal3 may play a key role in the signaling pathway of dopaminergic neuronal cell death induced by 6-OHDA. This is the first demonstration that Gal3 is expressed in dopaminergic neurons injured by 6-OHDA.

摘要

背景/目的：帕金森病（PD）是一种与年龄相关的神经退行性疾病，其特征是黑质（SN）中多巴胺能神经元相对进行性丧失。6-羟基多巴胺（6-OHDA）诱导的黑质纹状体多巴胺能神经元逆行变性已被广泛用作帕金森病动物模型，而内源性6-OHDA会促进帕金森病病理进展。半乳糖凝集素3（Gal3）和激活转录因子3（ATF3）与神经退行性过程有关。本研究旨在探讨Gal3和ATF3在6-OHDA诱导的帕金森病动物模型中的表达模式及作用。

材料与方法

我们研究了帕金森病6-OHDA大鼠模型中Gal3表达的时空分布。通过向纹状体单侧立体定向注射6-OHDA诱导损伤。在6-OHDA损伤前3天，在与随后6-OHDA注射相同的坐标处注射荧光金（FG）。6-OHDA以时间依赖性方式诱导黑质中酪氨酸羟化酶免疫阳性和FG免疫阳性神经元的逆行变性。

结果

激活转录因子3（ATF3）在黑质中的表达也上调，其模式与Gal3免疫反应性相似。最后，我们通过三重免疫荧光染色证实，ATF3和Gal3共定位于用FG标记的多巴胺能神经元中。这些神经元被6-OHDA损伤。

结论

Gal3可能在6-OHDA诱导的多巴胺能神经元细胞死亡信号通路中起关键作用。这是首次证明Gal3在6-OHDA损伤的多巴胺能神经元中表达。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c676/12041963/74a5a601b808/in_vivo-39-1349-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c676/12041963/884475f51654/in_vivo-39-1346-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c676/12041963/884475f51654/in_vivo-39-1346-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c676/12041963/a43acc0cd2d9/in_vivo-39-1348-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c676/12041963/74a5a601b808/in_vivo-39-1349-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c676/12041963/884475f51654/in_vivo-39-1346-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c676/12041963/884475f51654/in_vivo-39-1346-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c676/12041963/a43acc0cd2d9/in_vivo-39-1348-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c676/12041963/74a5a601b808/in_vivo-39-1349-g0001.jpg

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