Abstract
β-1,4 Galactosyltransferase V (β-1,4-GalT V) belongs to the β-1,4 galactosyltransferase family, which modifies proteins and plays a vital role in biological function. Our previous study revealed that β-1,4-GalT V was expressed in the cortex and hippocampus and participated in the recovery of spatial learning and memory in rats with traumatic brain injury. However, the expression of β-1,4-GalT V in microglia, resident immune cells in the central nervous system, and its impact on microglia in resting and lipopolysaccharide-triggered activated stages are elusive. In this study, we clarified that β-1,4-GalT V expresses in microglia, and it regulates microglial migration, proliferation, and release of the inflammatory factors. We also observed that β-1,4-GalT V affects the expression level of tumor necrosis factor receptor (TNFR)2 instead of TNFR1. These results strongly support the fact that β-1,4-GalT V is involved in microglial function.
Highlights
Microglial cells, the resident and primary immune cells of the central nervous system (CNS), are derived from the erythro-myeloid precursor cell that originates in the yolk sac during the early stages of development (Ginhoux et al, 2010; Casali and Reed-Geaghan, 2021)
Β-1,4-galactosyltransferase V was observed in Highly aggressive proliferating immortalized (HAPI) microglial cell (Figure 1A), which is a novel brain-derived microglial cell line (Cheepsunthorn et al, 2001), and expression of β1,4-GalT V was confirmed by immunofluorescence staining in primary cultured microglia cells, which were verified by location of ionized calcium-binding adaptor molecule 1 (Iba1) (Supplementary Figure 1)
The results showed that LPS-induced secretion levels of IL-1β from HAPI microglia cells were significantly increased compared with that in the nontreated sham group (Figure 1B). β-1,4-GalT V RNAi blocked the effect of LPS on the expression level of IL-1β, but the scrambled sequence could not (Figure 1B)
Summary
Microglial cells, the resident and primary immune cells of the central nervous system (CNS), are derived from the erythro-myeloid precursor cell that originates in the yolk sac during the early stages of development (Ginhoux et al, 2010; Casali and Reed-Geaghan, 2021). Microglial cells reside in a resting state which has the characteristic feature of a ramified morphology, and they play the role of immunological surveillance of the CNS. With diverse brain insults and a variety of neuroinflammatory stimuli, microglial cells are activated into a phagocytic state characterized by a motile ameboid form (Fan et al, 2018), and they perform the neuroinflammatory responses (Streit, 2002). Proliferation is a common accompaniment to hyperactivation (Gehrmann et al, 1995) and chronic activation of microglia (Nowacki et al, 2019), and it makes the neuroinflammatory process develop into neurotoxicity and pathogenic role for the above-mentioned neurological diseases (Kreutzberg, 1996; Nelson et al, 2002; Streit, 2004; Feng et al, 2019). Therapeutic targeting of neuroinflammation, that is microglial activation underlying neurological injury and disease pathogenesis, represents an exciting approach for novel neuroprotective strategies
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