{"title":"Expression of Galectin 3 and Activating Transcription Factor 3 in Nigral Dopaminergic Neurons of 6-Hydroxydopamine Induced Parkinsonian Rat Model.","authors":"Eun-Jin Lee, Yoon-Jung Choy, Ran-Sook Woo, Tai-Kyoung Baik, Hong-Il Yoo, Dae-Yong Song","doi":"10.21873/invivo.13938","DOIUrl":null,"url":null,"abstract":"<p><strong>Background/aim: </strong>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.</p><p><strong>Materials and methods: </strong>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.</p><p><strong>Results: </strong>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.</p><p><strong>Conclusion: </strong>Gal3 may play a key role in the signaling pathway of dopaminergic neuronal cell death induced by 6-OHDA. This is the first <i>in vivo</i> demonstration that Gal3 is expressed in dopaminergic neurons injured by 6-OHDA.</p>","PeriodicalId":13364,"journal":{"name":"In vivo","volume":"39 3","pages":"1341-1354"},"PeriodicalIF":1.8000,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12041963/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"In vivo","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.21873/invivo.13938","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"MEDICINE, RESEARCH & EXPERIMENTAL","Score":null,"Total":0}
引用次数: 0
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 in vivo demonstration that Gal3 is expressed in dopaminergic neurons injured by 6-OHDA.
期刊介绍：
IN VIVO is an international peer-reviewed journal designed to bring together original high quality works and reviews on experimental and clinical biomedical research within the frames of physiology, pathology and disease management.
The topics of IN VIVO include: 1. Experimental development and application of new diagnostic and therapeutic procedures; 2. Pharmacological and toxicological evaluation of new drugs, drug combinations and drug delivery systems; 3. Clinical trials; 4. Development and characterization of models of biomedical research; 5. Cancer diagnosis and treatment; 6. Immunotherapy and vaccines; 7. Radiotherapy, Imaging; 8. Tissue engineering, Regenerative medicine; 9. Carcinogenesis.
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