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Transcriptomic analysis of glycan-processing genes in the dorsal root ganglia of diabetic mice and functional characterization on Cav3.2 channels

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    0523563 - ÚOCHB 2021 RIV US eng J - Journal Article
    Stringer, Robin Nicholas - Lazniewska, Joanna - Weiss, Norbert
    Transcriptomic analysis of glycan-processing genes in the dorsal root ganglia of diabetic mice and functional characterization on Cav3.2 channels.
    Channels. Roč. 14, č. 1 (2020), s. 132-140. ISSN 1933-6950. E-ISSN 1933-6969
    Institutional support: RVO:61388963
    Keywords : glycosylation * transcriptome * DRG neurons * diabetes * calcium channel * Cav3.2 channel * T-type channel
    OECD category: Biochemistry and molecular biology
    Impact factor: 2.581, year: 2020
    Method of publishing: Open access
    https://www.tandfonline.com/doi/full/10.1080/19336950.2020.1745406

    Cav3.2 T-type calcium channels play an essential role in the transmission of peripheral nociception in the dorsal root ganglia (DRG) and alteration of Cav3.2 expression is associated with the development of peripheral painful diabetic neuropathy (PDN). Several studies have previously documented the role of glycosylation in the expression and functioning of Cav3.2 and suggested that altered glycosylation of the channel may contribute to the aberrant expression of the channel in diabetic conditions. In this study, we aimed to analyze the expression of glycan-processing genes in DRG neurons from a leptin-deficient genetic mouse model of diabetes (db/db). Transcriptomic analysis revealed that several glycan-processing genes encoding for glycosyltransferases and sialic acid-modifying enzymes were upregulated in diabetic conditions. Functional analysis of these enzymes on recombinant Cav3.2 revealed an unexpected loss-of-function of the channel. Collectively, our data indicate that diabetes is associated with an alteration of the glycosylation machinery in DRG neurons. However, individual action of these enzymes when tested on recombinant Cav3.2 cannot explain the observed upregulation of T-type channels under diabetic conditions.
    Permanent Link: http://hdl.handle.net/11104/0307903

     
     
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