ArticleCellular and molecular neurobiology2013
Dynamic expressions of Beclin 1 and tyrosine hydroxylase in different areas of 6-hydroxydopamine-induced Parkinsonian rats.
Article in Cellular and molecular neurobiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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6 citing papers in PubMed, 20 citations in OpenAlex.
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- Triggering of inflammasome by impaired autophagy in response to acute experimental Parkinson's disease: involvement of the PI3K/Akt/mTOR pathway.Neuroreport · 2017Article
- Neurotoxin mechanisms and processes relevant to Parkinson's disease: an update.Neurotoxicity research · 2015Article
- Impairment of autophagy in the central nervous system during lipopolysaccharide-induced inflammatory stress in mice.Molecular brain · 2014Article
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7 authors at 1 institution in 1 country.
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Abstract
Beclin 1, a regulator of the autophagy pathway, plays an important role in Parkinson's disease (PD). However, the crucial mechanism of Beclin 1 in PD remains unclear. Therefore, we investigated dynamic expressions of Beclin 1 and tyrosine hydroxylase (TH) in different brain areas of 6-OHDA-induced rats. Beclin 1 and TH expressions were analyzed by flow cytometry and immunohistochemistry, respectively. The results showed that Beclin 1 expressions were low in the sham group, but rose significantly after 6-OHDA injection. In the striatum and cortex, Beclin 1 increased at 3 h, peaking at 12 h, while in the hippocampus, it increased at 3 h and peaked at 24 h, then it declined slowly and remained steady at 72 h. Beclin 1 expression in the striatum and cortex areas was higher than that of the hippocampus area at 12 h. In addition, the time-course of TH expression in the striatum was similar to that in the mesencephalon. TH expression declined dramatically between 0 and 12 h. Pearson analysis showed significant negative correlations between TH and Beclin 1 expression in the areas we analyzed. While TH expression declined gradually between 12 and 72 h, significant positive correlations between TH and Beclin 1 were detected during that interval. This indicated that activation of Beclin 1-dependent autophagy may inhibit the loss of TH-positive neurons.
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