Počet záznamů: 1
Transcriptomic analysis of glycan-processing genes in the dorsal root ganglia of diabetic mice and functional characterization on Cav3.2 channels
- 1.0523563 - ÚOCHB 2021 RIV US eng J - Článek v odborném periodiku
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
Institucionální podpora: RVO:61388963
Klíčová slova: glycosylation * transcriptome * DRG neurons * diabetes * calcium channel * Cav3.2 channel * T-type channel
Obor OECD: Biochemistry and molecular biology
Impakt faktor: 2.581, rok: 2020
Způsob publikování: 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.
Trvalý link: http://hdl.handle.net/11104/0307903
Počet záznamů: 1