A potential role for T-type calcium channels in homocysteinemia-induced peripheral neuropathy
Homocysteinemia is a metabolic condition characterized by abnormally high level of homocysteine in the blood and is considered to be a risk factor for peripheral neuropathy. However, the cellular mechanisms underlying toxic effects of homocysteine on the processing of peripheral nociception have not...
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| Published in: | Pain (Amsterdam) Vol. 160; no. 12; pp. 2798 - 2810 |
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| Main Authors: | , , , , , , , , , , , |
| Format: | Journal Article |
| Language: | English |
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Wolters Kluwer
01-12-2019
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| Abstract | Homocysteinemia is a metabolic condition characterized by abnormally high level of homocysteine in the blood and is considered to be a risk factor for peripheral neuropathy. However, the cellular mechanisms underlying toxic effects of homocysteine on the processing of peripheral nociception have not yet been investigated comprehensively. Here, using a rodent model of experimental homocysteinemia, we report the causal association between homocysteine and the development of mechanical allodynia. Homocysteinemia-induced mechanical allodynia was reversed on pharmacological inhibition of T-type calcium channels. In addition, our in vitro studies indicate that homocysteine enhances recombinant T-type calcium currents by promoting the recycling of Cav3.2 channels back to the plasma membrane through a protein kinase C-dependent signaling pathway that requires the direct phosphorylation of Cav3.2 at specific loci. Altogether, these results reveal an unrecognized signaling pathway that modulates the expression of T-type calcium channels, and may potentially contribute to the development of peripheral neuropathy associated with homocysteinemia. |
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| AbstractList | Homocysteinemia is a metabolic condition characterized by abnormally high level of homocysteine in the blood and is considered to be a risk factor for peripheral neuropathy. However, the cellular mechanisms underlying toxic effects of homocysteine on the processing of peripheral nociception have not yet been investigated comprehensively. Here, using a rodent model of experimental homocysteinemia, we report the causal association between homocysteine and the development of mechanical allodynia. Homocysteinemia-induced mechanical allodynia was reversed on pharmacological inhibition of T-type calcium channels. In addition, our in vitro studies indicate that homocysteine enhances recombinant T-type calcium currents by promoting the recycling of Cav3.2 channels back to the plasma membrane through a protein kinase C-dependent signaling pathway that requires the direct phosphorylation of Cav3.2 at specific loci. Altogether, these results reveal an unrecognized signaling pathway that modulates the expression of T-type calcium channels, and may potentially contribute to the development of peripheral neuropathy associated with homocysteinemia. Homocysteinemia is a metabolic condition characterized by abnormally high level of homocysteine in the blood and is considered to be a risk factor for peripheral neuropathy. However, the cellular mechanisms underlying toxic effects of homocysteine on the processing of peripheral nociception have not yet been investigated comprehensively. Here, using a rodent model of experimental homocysteinemia, we report the causal association between homocysteine and the development of mechanical allodynia. Homocysteinemia-induced mechanical allodynia was reversed on pharmacological inhibition of T-type calcium channels. In addition, our in vitro studies indicate that homocysteine enhances recombinant T-type calcium currents by promoting the recycling of Ca v 3.2 channels back to the plasma membrane through a protein kinase C–dependent signaling pathway that requires the direct phosphorylation of Ca v 3.2 at specific loci. Altogether, these results reveal an unrecognized signaling pathway that modulates the expression of T-type calcium channels, and may potentially contribute to the development of peripheral neuropathy associated with homocysteinemia. |
| Author | Zamponi, Gerald W. Weiss, Norbert Huang, Junting Rivas-Ramirez, Paula Sitdikova, Guzel F. Burkhanova, Gulshat F. Rzhepetskyy, Yuriy Tomin, Andriy Cmarko, Leos Gaifullina, Aisylu S. Gerasimova, Elena V. Lazniewska, Joanna |
| AuthorAffiliation | Institute of Organic Chemistry and Biochemistry, Czech Academy of Sciences, Prague, Czech Republic Department of Physiology and Pharmacology, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada Department of Human and Animal Physiology, Institute of Fundamental Medicine and Biology, Kazan Federal University, Kazan, Russia |
| AuthorAffiliation_xml | – name: Department of Physiology and Pharmacology, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada – name: Department of Human and Animal Physiology, Institute of Fundamental Medicine and Biology, Kazan Federal University, Kazan, Russia – name: Institute of Organic Chemistry and Biochemistry, Czech Academy of Sciences, Prague, Czech Republic |
| Author_xml | – sequence: 1 givenname: Aisylu S. surname: Gaifullina fullname: Gaifullina, Aisylu S. organization: Institute of Organic Chemistry and Biochemistry, Czech Academy of Sciences, Prague, Czech Republic – sequence: 2 givenname: Joanna surname: Lazniewska fullname: Lazniewska, Joanna organization: Institute of Organic Chemistry and Biochemistry, Czech Academy of Sciences, Prague, Czech Republic – sequence: 3 givenname: Elena V. surname: Gerasimova fullname: Gerasimova, Elena V. organization: Department of Human and Animal Physiology, Institute of Fundamental Medicine and Biology, Kazan Federal University, Kazan, Russia – sequence: 4 givenname: Gulshat F. surname: Burkhanova fullname: Burkhanova, Gulshat F. organization: Department of Human and Animal Physiology, Institute of Fundamental Medicine and Biology, Kazan Federal University, Kazan, Russia – sequence: 5 givenname: Yuriy surname: Rzhepetskyy fullname: Rzhepetskyy, Yuriy organization: Institute of Organic Chemistry and Biochemistry, Czech Academy of Sciences, Prague, Czech Republic – sequence: 6 givenname: Andriy surname: Tomin fullname: Tomin, Andriy organization: Institute of Organic Chemistry and Biochemistry, Czech Academy of Sciences, Prague, Czech Republic – sequence: 7 givenname: Paula surname: Rivas-Ramirez fullname: Rivas-Ramirez, Paula organization: Institute of Organic Chemistry and Biochemistry, Czech Academy of Sciences, Prague, Czech Republic – sequence: 8 givenname: Junting surname: Huang fullname: Huang, Junting organization: Department of Physiology and Pharmacology, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada – sequence: 9 givenname: Leos surname: Cmarko fullname: Cmarko, Leos organization: Institute of Organic Chemistry and Biochemistry, Czech Academy of Sciences, Prague, Czech Republic – sequence: 10 givenname: Gerald W. surname: Zamponi fullname: Zamponi, Gerald W. organization: Department of Physiology and Pharmacology, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada – sequence: 11 givenname: Guzel F. surname: Sitdikova fullname: Sitdikova, Guzel F. organization: Department of Human and Animal Physiology, Institute of Fundamental Medicine and Biology, Kazan Federal University, Kazan, Russia – sequence: 12 givenname: Norbert surname: Weiss fullname: Weiss, Norbert organization: Institute of Organic Chemistry and Biochemistry, Czech Academy of Sciences, Prague, Czech Republic |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/31365467$$D View this record in MEDLINE/PubMed |
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| Snippet | Homocysteinemia is a metabolic condition characterized by abnormally high level of homocysteine in the blood and is considered to be a risk factor for... |
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| SubjectTerms | Animals Calcium - metabolism Calcium Channels, T-Type - metabolism Cell Membrane - metabolism Disease Models, Animal Ganglia, Spinal - metabolism Homocysteine - blood Hyperalgesia - etiology Hyperalgesia - metabolism Hyperhomocysteinemia - complications Nociception - physiology Peripheral Nervous System Diseases - etiology Peripheral Nervous System Diseases - metabolism Rats Rats, Wistar |
| Title | A potential role for T-type calcium channels in homocysteinemia-induced peripheral neuropathy |
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