TY - JOUR
T1 - Analysis of O-glycoforms of the IgA1 hinge region by sequential deglycosylation
AU - Ohyama, Yukako
AU - Yamaguchi, Hisateru
AU - Nakajima, Kazuki
AU - Mizuno, Tomohiro
AU - Fukamachi, Yukihiro
AU - Yokoi, Yasuto
AU - Tsuboi, Naotake
AU - Inaguma, Daijo
AU - Hasegawa, Midori
AU - Renfrow, Matthew B.
AU - Novak, Jan
AU - Yuzawa, Yukio
AU - Takahashi, Kazuo
N1 - Funding Information:
The work was funded by the JSPS KAKENHI (grant numbers 24890268, 26860652, 15H05292, 16K09632, 19K08715, and 19K08691); by a Grant-in-Aid for Practical Research Project for Renal Diseases, from the Japan Agency for Medical Research and Development; by Takeda Science Foundation; and by Aichi Jinzou Foundation. JN and MBR were supported in part by NIH grants DK078244, GM098539, and DK082753. The authors appreciate assistance of Ms. Yuri Yoshida, Ms. Maki Okada, and Ms. Ikumi Matsui in the purification of serum IgA1 and Ms. Stacy Hall for preparation of IgA-specific protease-digested and neuraminidase-treated samples. Plasmid for expression of IgA-specific protease from Clostridium ramosum AK183 was kindly provided by Dr. Mogens Kilian.
Publisher Copyright:
© 2020, The Author(s).
PY - 2020/12/1
Y1 - 2020/12/1
N2 - A common renal disease, immunoglobulin A (IgA) nephropathy (IgAN), is associated with glomerular deposition of IgA1-containing immune complexes. IgA1 hinge region (HR) has up to six clustered O-glycans consisting of Ser/Thr-linked N-acetylgalactosamine with β1,3-linked galactose and variable sialylation. IgA1 glycoforms with some galactose-deficient (Gd) HR O-glycans play a key role in IgAN pathogenesis. The clustered and variable O-glycans make the IgA1 glycomic analysis challenging and better approaches are needed. Here, we report a comprehensive analytical workflow for IgA1 HR O-glycoform analysis. We combined an automated quantitative analysis of the HR O-glycopeptide profiles with sequential deglycosylation to remove all but Gd O-glycans from the HR. The workflow was tested using serum IgA1 from healthy subjects. Twelve variants of glycopeptides corresponding to the HR with three to six O-glycans were detected; nine glycopeptides carried up to three Gd O-glycans. Sites with Gd O-glycans were unambiguously identified by electron-transfer/higher-energy collision dissociation tandem mass spectrometry. Extracted ion chromatograms of isomeric glycoforms enabled quantitative assignment of Gd sites. The most frequent Gd site was T236, followed by S230, T233, T228, and S232. The new workflow for quantitative profiling of IgA1 HR O-glycoforms with site-specific resolution will enable identification of pathogenic IgA1 HR O-glycoforms in IgAN.
AB - A common renal disease, immunoglobulin A (IgA) nephropathy (IgAN), is associated with glomerular deposition of IgA1-containing immune complexes. IgA1 hinge region (HR) has up to six clustered O-glycans consisting of Ser/Thr-linked N-acetylgalactosamine with β1,3-linked galactose and variable sialylation. IgA1 glycoforms with some galactose-deficient (Gd) HR O-glycans play a key role in IgAN pathogenesis. The clustered and variable O-glycans make the IgA1 glycomic analysis challenging and better approaches are needed. Here, we report a comprehensive analytical workflow for IgA1 HR O-glycoform analysis. We combined an automated quantitative analysis of the HR O-glycopeptide profiles with sequential deglycosylation to remove all but Gd O-glycans from the HR. The workflow was tested using serum IgA1 from healthy subjects. Twelve variants of glycopeptides corresponding to the HR with three to six O-glycans were detected; nine glycopeptides carried up to three Gd O-glycans. Sites with Gd O-glycans were unambiguously identified by electron-transfer/higher-energy collision dissociation tandem mass spectrometry. Extracted ion chromatograms of isomeric glycoforms enabled quantitative assignment of Gd sites. The most frequent Gd site was T236, followed by S230, T233, T228, and S232. The new workflow for quantitative profiling of IgA1 HR O-glycoforms with site-specific resolution will enable identification of pathogenic IgA1 HR O-glycoforms in IgAN.
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U2 - 10.1038/s41598-020-57510-z
DO - 10.1038/s41598-020-57510-z
M3 - Article
C2 - 31959827
AN - SCOPUS:85078287733
SN - 2045-2322
VL - 10
JO - Scientific Reports
JF - Scientific Reports
IS - 1
M1 - 671
ER -