| Title |
Regulation and the Mechanism of Estrogen on Cav1.2 Gene in Rat-Cultured Cortical Astrocytes
|
|---|---|
| Published in |
Journal of Molecular Neuroscience, August 2016
|
| DOI | 10.1007/s12031-016-0803-y |
| Pubmed ID | |
| Authors |
Ling He, Xiao-Tong Hu, Yu-Jie Lai, Yan Long, Lu Liu, Bing-lin Zhu, Guo-Jun Chen |
| Abstract |
L-type calcium channel (LTCC) gene Cav1.2 is believed to play an important role in the alteration of Ca(2+) homeostasis in brain astrocytes. Increasing evidence shows that alteration of intracellular Ca(2+) concentration is related to the effect of 17β-estradiol (E2) in a variety of neurophysiological and neuropathological conditions. In this study, we measured immunoreactivity of Cav1.2 protein expression in rat primary cortical astrocytes by using Western blots. We demonstrated that E2 upregulated Cav1.2 expression in a dose- and time-dependent manner and the effect of E2 on Cav1.2 expression were blocked by an estrogen receptor (ER) antagonist, ICI-182,780. The ER subtype-selective ERα agonists propylpyrazole triole (PPT) and ERβ agonist diarylpropionitrile (DPN) both increase the expression of Cav1.2 in a dose-dependent manner. Also, the PPT most closely mimicked the upregulation of Cav1.2 protein expression by E2. Similar experiments of 10 nM E2-treated ERα- or ERβ-knockdown astrocytes have also shown that the E2 regulation of Cav1.2 protein expression is mediated through an ERα-dependent pathway. Furthermore, we established that E2 did not change the level of Cav1.2 mRNA. The induction of E2-mediated Cav1.2 expression was inhibited by cycloheximide (CHX) but not by actinomycin D (Act-D), suggesting that E2 regulation of Cav1.2 expression occurred at a posttranscriptional level. We also found that E2 may increase Cav1.2 levels by decreasing its ubiquitination and degradation rate. These findings provide new information about the effect of E2 on Cav1.2 in astrocytes, particularly necessary for the treatment of neurological disease. |
X Demographics
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Geographical breakdown
| Country | Count | As % |
|---|---|---|
| United States | 1 | 50% |
| Unknown | 1 | 50% |
Demographic breakdown
| Type | Count | As % |
|---|---|---|
| Members of the public | 2 | 100% |
Mendeley readers
The data shown below were compiled from readership statistics for 15 Mendeley readers of this research output. Click here to see the associated Mendeley record.
Geographical breakdown
| Country | Count | As % |
|---|---|---|
| Unknown | 15 | 100% |
Demographic breakdown
| Readers by professional status | Count | As % |
|---|---|---|
| Researcher | 3 | 20% |
| Other | 2 | 13% |
| Professor > Associate Professor | 2 | 13% |
| Student > Ph. D. Student | 2 | 13% |
| Student > Doctoral Student | 1 | 7% |
| Other | 3 | 20% |
| Unknown | 2 | 13% |
| Readers by discipline | Count | As % |
|---|---|---|
| Agricultural and Biological Sciences | 4 | 27% |
| Neuroscience | 3 | 20% |
| Biochemistry, Genetics and Molecular Biology | 1 | 7% |
| Nursing and Health Professions | 1 | 7% |
| Pharmacology, Toxicology and Pharmaceutical Science | 1 | 7% |
| Other | 0 | 0% |
| Unknown | 5 | 33% |
Attention Score in Context
This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 25 March 2017.
All research outputs
#19,945,185
of 25,374,917 outputs
Outputs from Journal of Molecular Neuroscience
#1,094
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#285,271
of 381,520 outputs
Outputs of similar age from Journal of Molecular Neuroscience
#36
of 48 outputs
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