Open AccessDistinct Glycosylation Responses to Spinal Cord Injury in Regenerative and Nonregenerative Models
Author(s) -
Rachel Ronan,
Aniket Kshirsagar,
Ana Lúcia Rebelo,
Abbah Sunny,
Michelle Kilcoyne,
Roisin O’ Flaherty,
Pauline M. Rudd,
Gerhard Schlosser,
Radka Saldova,
Abhay Pandit,
Siobhán S. McMahon
Publication year - 2022
Publication title -
journal of proteome research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.644
H-Index - 161
eISSN - 1535-3907
pISSN - 1535-3893
DOI - 10.1021/acs.jproteome.2c00043
Subject(s) - xenopus , glycosylation , spinal cord , glycan , regeneration (biology) , spinal cord injury , microbiology and biotechnology , sialic acid , microglia , chemistry , glycoprotein , biochemistry , biology , inflammation , immunology , neuroscience , gene
Traumatic spinal cord injury (SCI) results in disruption of tissue integrity and loss of function. We hypothesize that glycosylation has a role in determining the occurrence of regeneration and that biomaterial treatment can influence this glycosylation response. We investigated the glycosylation response to spinal cord transection in Xenopus laevis and rat. Transected rats received an aligned collagen hydrogel. The response compared regenerative success, regenerative failure, and treatment in an established nonregenerative mammalian system. In a healthy rat spinal cord, ultraperformance liquid chromatography (UPLC) N-glycoprofiling identified complex, hybrid, and oligomannose N-glycans. Following rat SCI, complex and outer-arm fucosylated glycans decreased while oligomannose and hybrid structures increased. Sialic acid was associated with microglia/macrophages following SCI. Treatment with aligned collagen hydrogel had a minimal effect on the glycosylation response. In Xenopus , lectin histochemistry revealed increased levels of N -acetyl-glucosamine (GlcNAc) in premetamorphic animals. The addition of GlcNAc is required for processing complex-type glycans and is a necessary foundation for additional branching. A large increase in sialic acid was observed in nonregenerative animals. This work suggests that glycosylation may influence regenerative success. In particular, loss of complex glycans in rat spinal cord may contribute to regeneration failure. Targeting the glycosylation response may be a promising strategy for future therapies.