Regulation of T‐type Ca 2+ channel expression by interleukin‐6 in sensory‐like ND7/23 cells post‐herpes simplex virus (HSV‐1) infection
Autor: | Shao-Chung Hsia, Qiaojuan Zhang, Miguel Martin-Caraballo |
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Rok vydání: | 2019 |
Předmět: |
0301 basic medicine
Protein subunit Gene Expression Sensory system Herpesvirus 1 Human Biochemistry Article Calcium Channels T-Type Mice 03 medical and health sciences Cellular and Molecular Neuroscience 0302 clinical medicine Cell Line Tumor medicine Animals Humans Secretion Interleukin 6 Messenger RNA biology Interleukin-6 Chemistry Calcium channel Interleukin Herpes Simplex Molecular biology Sensory neuron Rats 030104 developmental biology medicine.anatomical_structure biology.protein 030217 neurology & neurosurgery |
Zdroj: | J Neurochem |
ISSN: | 1471-4159 0022-3042 |
Popis: | Herpes simplex virus-type 1 (HSV-1) infection of sensory neurons may lead to a significant reduction in the expression of voltage-activated Na(+) and Ca(2+) channels, which can disrupt the transmission of pain information. Viral infection also results in the secretion of various pro-inflammatory cytokines, including interleukin (IL)-6. In this work, we tested whether IL-6 regulates the expression of Na(+) and Ca(2+) channels post HSV-1 infection in ND7/23 sensory-like neurons. Our results demonstrate that HSV-1 infection causes a significant decrease in the protein expression of the Cav3.2 T-type Ca(2+) channel subunit, despite increasing Cav3.2 mRNA synthesis. Neither Cav3.2 mRNA nor total protein content was affected by IL-6 treatment post HSV-1 infection. In ND7/23 cells, HSV-1 infection caused a significant reduction in the expression of Na(+) and T-type Ca(2+) channels within 48 h. Exposure of ND7/23 cells to IL-6 for 24 h post infection reverses the effect of HSV-1, resulting in a significant increase in T-type Ca(2+) current density. However, Na(+) currents were not restored by 24 h-treatment with IL-6 post HSV-1 infection of ND7/23 cells. The ability of IL-6 to increase the functional expression of T-type Ca(2+) channels on the membrane was blocked by inhibition of protein trafficking with brefeldin-A and ERK1/2 activation. These results indicate that IL-6 release following HSV-1 infection regulates the expression of T-type Ca(2+) channels, which may alter the transmission of pain information. |
Databáze: | OpenAIRE |
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