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.Abbreviations: Galnt16: Polypeptide N-acetylgalactosaminyltransferase 16; B3gnt8: UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 8; B4galt1: Beta-1,4-galactosyltransferase 1; St6gal1: Beta-galactoside alpha-2,6-sialyltransferase 1; Neu3: Sialidase-3.

中文翻译：

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糖尿病小鼠背根神经节中聚糖加工基因的转录组分析和Cav3.2通道的功能表征。

Cav3.2 T型钙通道在背根神经节（DRG）的外周伤害感受传递中起着至关重要的作用，Cav3.2表达的改变与周围疼痛性糖尿病性神经病（PDN）的发展有关。先前有数项研究记录了糖基化在Cav3.2的表达和功能中的作用，并建议在糖尿病条件下，通道糖基化的改变可能会导致通道异常表达。在这项研究中，我们旨在分析糖尿病的瘦素缺陷型遗传小鼠模型（db / db）中DRG神经元中聚糖加工基因的表达。转录组分析显示，在糖尿病条件下，编码糖基转移酶和唾液酸修饰酶的几种聚糖加工基因被上调。这些酶在重组Cav3.2上的功能分析显示，通道功能意外丧失。总体而言，我们的数据表明糖尿病与DRG神经元中糖基化机制的改变有关。但是，在重组Cav3.2上测试这些酶的个别作用不能解释在糖尿病条件下观察到的T型通道上调。缩写：Galnt16：多肽N-乙酰半乳糖胺基转移酶16；B3gnt8：UDP-GlcNAc：betaGal beta-1，3-N-乙酰氨基葡糖基转移酶8；B4galt1：β-1,4-半乳糖基转移酶1；St6gal1：β​​-半乳糖苷α-2,6-唾液酸转移酶1；Neu3：唾液酸酶-3。我们的数据表明糖尿病与DRG神经元糖基化机制的改变有关。但是，在重组Cav3.2上测试这些酶的个别作用不能解释在糖尿病条件下观察到的T型通道上调。缩写：Galnt16：多肽N-乙酰半乳糖胺基转移酶16；B3gnt8：UDP-GlcNAc：betaGal beta-1，3-N-乙酰氨基葡糖基转移酶8；B4galt1：β-1,4-半乳糖基转移酶1；St6gal1：β​​-半乳糖苷α-2,6-唾液酸转移酶1；Neu3：唾液酸酶-3。我们的数据表明，糖尿病与DRG神经元糖基化机制的改变有关。但是，在重组Cav3.2上测试这些酶的个别作用不能解释在糖尿病条件下观察到的T型通道上调。缩写：Galnt16：多肽N-乙酰半乳糖胺基转移酶16；B3gnt8：UDP-GlcNAc：betaGal beta-1，3-N-乙酰氨基葡糖基转移酶8；B4galt1：β-1,4-半乳糖基转移酶1；St6gal1：β​​-半乳糖苷α-2,6-唾液酸转移酶1；Neu3：唾液酸酶-3。3-N-乙酰基氨基葡萄糖氨基转移酶8; B4galt1：β-1,4-半乳糖基转移酶1；St6gal1：β​​-半乳糖苷α-2,6-唾液酸转移酶1；Neu3：唾液酸酶-3。3-N-乙酰基氨基葡萄糖氨基转移酶8; B4galt1：β-1,4-半乳糖基转移酶1；St6gal1：β​​-半乳糖苷α-2,6-唾液酸转移酶1；Neu3：唾液酸酶-3。