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本文引用的文献

1
Expression of connexin 30 and connexin 32 in hippocampus of rat during epileptogenesis in a kindling model of epilepsy.在癫痫点燃模型中，癫痫发生过程中海马中连接蛋白 30 和连接蛋白 32 的表达。
Neurosci Bull. 2012 Dec;28(6):729-36. doi: 10.1007/s12264-012-1279-6. Epub 2012 Nov 12.
2
Effect of chronic intracerebroventricluar administration of lipopolysaccharide on connexin43 protein expression in rat hippocampus.慢性脑室内注射脂多糖对大鼠海马中连接蛋白43蛋白表达的影响。
Iran Biomed J. 2012;16(1):25-32. doi: 10.6091/ibj.1030.2012.
3
Astroglial networks scale synaptic activity and plasticity.星形胶质细胞网络调节突触活动和可塑性。
Proc Natl Acad Sci U S A. 2011 May 17;108(20):8467-72. doi: 10.1073/pnas.1016650108. Epub 2011 May 2.
4
Role of astroglial connexin30 in hippocampal gap junction coupling.星形胶质细胞缝隙连接蛋白 30 在海马缝隙连接偶联中的作用。
Glia. 2011 Mar;59(3):511-9. doi: 10.1002/glia.21120. Epub 2010 Dec 29.
5
Neuroinflammation leads to region-dependent alterations in astrocyte gap junction communication and hemichannel activity.神经炎症导致星形胶质细胞缝隙连接通讯和半通道活性的区域依赖性改变。
J Neurosci. 2011 Jan 12;31(2):414-25. doi: 10.1523/JNEUROSCI.5247-10.2011.
6
Inhibition of cytokine-induced connexin43 hemichannel activity in astrocytes is neuroprotective.细胞因子诱导的星形胶质细胞缝隙连接蛋白 43 半通道活性抑制具有神经保护作用。
Mol Cell Neurosci. 2010 Sep;45(1):37-46. doi: 10.1016/j.mcn.2010.05.007.
7
Temporal and spatial profile of phosphorylated connexin43 after traumatic brain injury in rats.大鼠创伤性脑损伤后磷酸化连接蛋白 43 的时空特征。
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Dexamethasone prevents LPS-induced microglial activation and astroglial impairment in an experimental bacterial meningitis co-culture model.地塞米松可预防实验性细菌性脑膜炎共培养模型中 LPS 诱导的小胶质细胞激活和星形胶质细胞损伤。
Brain Res. 2010 May 6;1329:45-54. doi: 10.1016/j.brainres.2010.03.012. Epub 2010 Mar 15.
9
Lipopolysaccharide-induced inhibition of connexin43 gap junction communication in astrocytes is mediated by downregulation of caveolin-3.脂多糖诱导的星形胶质细胞缝隙连接通讯抑制是通过下调窖蛋白-3实现的。
Int J Biochem Cell Biol. 2010 May;42(5):762-70. doi: 10.1016/j.biocel.2010.01.016. Epub 2010 Jan 20.
10
Cannabinoids prevent the opposite regulation of astroglial connexin43 hemichannels and gap junction channels induced by pro-inflammatory treatments.大麻素可预防促炎处理诱导的星形胶质细胞缝隙连接蛋白 43 半通道和缝隙连接通道的相反调节。
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慢性中枢注射脂多糖在转录水平上上调大鼠海马中连接蛋白30和32间隙连接。

Upregulation of connexins 30 and 32 gap junctions in rat hippocampus at transcription level by chronic central injection of lipopolysaccharide.

作者信息

Abbasian Mohammad, Sayyah Mohammad, Babapour Vahab, Mahdian Reza, Choopani Samira, Kaviani Bahar

机构信息

Dept. of Physiology and Pharmacology, Pasteur Institute of Iran, Tehran, Iran.

Dept. of Physiology and Pharmacology, Pasteur Institute of Iran, Tehran; 3Dept. of Physiology, Faculty of Veterinary Medicine, Tehran University, Tehran, Iran.

出版信息

Iran Biomed J. 2012;16(3):127-32. doi: 10.6091/ibj.1099.2012.

DOI:10.6091/ibj.1099.2012
PMID:23023213
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3629930/
Abstract

BACKGROUND

Gap junctions composed of connexins (Cx) are functional in cell defense by propagation of toxic/death molecules to neighboring cells. Hippocampus, one of the brain regions with particular vulnerability to damage, has a wide network of gap junctions. Functional response of astrocytic Cx30 and neuronal Cx32 to hippocampal damage is unknown.

METHODS

We infused lipopolysaccharide (LPS) intracerebroventricularly (2.5 mug/rat) once daily for two weeks to create neuroinflammation. The mRNA and protein levels of the Cx were measured in the hippocampus after 1st, 7th and 14th injection by real-time PCR and Western-blot techniques.

RESULTS

A significant increase in Cx32 and Cx30 gene expression was observed after 7th and 14th injection of LPS with no significant change in their protein abundance.

CONCLUSION

Transcriptional overexpression of hippocampal Cx30 and Cx32 could be an adaptive response to production of intracellular toxic molecules but it is not accompanied with post- transcriptional overexpression and might have no functional impact.

摘要

背景

由连接蛋白（Cx）组成的间隙连接通过将毒性/死亡分子传播到邻近细胞在细胞防御中发挥作用。海马体是特别易受损伤的脑区之一，具有广泛的间隙连接网络。星形胶质细胞Cx30和神经元Cx32对海马体损伤的功能反应尚不清楚。

方法

我们每天一次脑室内注射脂多糖（LPS，2.5微克/只大鼠），持续两周以引发神经炎症。在第1次、第7次和第14次注射后，通过实时PCR和蛋白质印迹技术测量海马体中Cx的mRNA和蛋白质水平。

结果

在第7次和第14次注射LPS后，观察到Cx32和Cx30基因表达显著增加，但其蛋白质丰度无显著变化。

结论

海马体Cx30和Cx32的转录过表达可能是对细胞内毒性分子产生的一种适应性反应，但不伴有转录后过表达，可能没有功能影响。