Selenoprotein K Is Essential for the Migration and Phagocytosis of Immature Dendritic Cells.

Antioxidants (Basel)

Key Laboratory of Infectious Immune and Antibody Engineering of Guizhou Province, Cellular Immunotherapy Engineering Research Center of Guizhou Province, School of Biology and Engineering/School of Basic Medical Sciences, Guizhou Medical University, Guiyang 550025, China.

Published: June 2022

AI Article Synopsis

Article Abstract

Selenoprotein K (SELENOK) is an endoplasmic reticulum stress (ERS)-regulated protein required for the calcium (Ca) flux-mediated migration of T cells and neutrophils, and the migration and phagocytosis of macrophages and microglia. However, the effect of SELENOK on the regulation of the immune function of dendritic cells (DCs), including immature DCs (imDCs) and mature DCs (mDCs), is still unclear. In this study, imDCs prepared from SELENOK knockout mice were used to evaluate the effect of SELENOK on the migration and phagocytosis of imDCs. The results showed that ERS-induced downregulation of imDCs phenotypic markers led to a reduction in Ras homolog gene family member A (RhoA)-dependent migration and enhanced Ca/CD205-mediated phagocytosis. SELENOK deficiency-induced upregulation of selenoprotein S (SELENOS) attenuated ERS levels in imDCs. An increase in Ca levels resulted in increased migration and decreased phagocytosis with or without ERS conditions. The migration was RhoA-dependent, and Ca or CD205 was associated with regulating phagocytosis in imDCs. Our study found that SELENOK is required for imDC migration and phagocytosis.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9311522PMC
http://dx.doi.org/10.3390/antiox11071264DOI Listing

Publication Analysis

Top Keywords

migration phagocytosis
16
migration
8
dendritic cells
8
phagocytosis imdcs
8
phagocytosis
7
selenok
6
imdcs
6
selenoprotein essential
4
essential migration
4
phagocytosis immature
4

Similar Publications

Recombinant Abelson Tyrosine Protein Kinase (rAbl) Regulates Various Functions of Buffalo Peripheral Blood Mononuclear Cells.

Animals (Basel)

January 2025

Guangxi Colleges and Universities Key Laboratory of Prevention and Control for Animal Disease, College of Animal Science and Technology, Guangxi University, Nanning 530005, China.

can modulate host immune mechanisms through excretory-secretory products (ESP). As one of the components of ESP, it is unknown whether Abelson tyrosine protein kinase (Abl) is involved in parasite-host immune interaction. To investigate the immunoregulatory function of Abl in , we cloned and expressed the gigantica Abl protein and assessed its effect on specific immune functions of buffalo peripheral blood mononuclear cells (PBMCs).

View Article and Find Full Text PDF

Amyloid-β peptide (Aβ) is a critical cause of Alzheimer's disease (AD). It is generated from amyloid precursor protein (APP) through cleavages by β-secretase and γ-secretase. γ-Secretase, which includes presenilin, is regulated by several stimuli.

View Article and Find Full Text PDF

Cell adhesion molecule protocadherin-γC5 ameliorates Aβ plaque pathogenesis by modulating astrocyte function in Alzheimer's disease.

J Neurosci

January 2025

Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, School of Medicine, Xiamen University, Xiamen, Fujian 361102, China

Accumulation of astrocytes around β-amyloid (Aβ) plaques is one of the earliest neuropathological changes in Alzheimer's disease (AD), but the underlying mechanisms and significance remain unclear. Cell adhesion molecule protocadherin-γC5 (Pcdh-γC5) has been reported to implicate in AD. Here we find elevated expression level of Pcdh-γC5 in the brain of 5×FAD mice and Aβ-treated astrocytes, and further reveal that Pcdh-γC5 deficiency leads to exacerbated Aβ deposition in 5×FAD mice.

View Article and Find Full Text PDF

Introduction: Endoplasmic reticulum aminopeptidases 1 (ERAP1) and 2 (ERAP2) modulate a plethora of physiological processes for the maintenance of homeostasis in different cellular subsets at both intra and extracellular level.

Materials And Methods: In this frame, the extracellular supplementation of recombinant human (rh) ERAP1 and ERAP2 (300 ng/ml) was used to mimic the effect of stressor-induced secretion of ERAPs on neutrophils isolated from 5 healthy subjects. In these cells following 3 h or 24 h rhERAP stimulation by Western Blot, RT-qPCR, Elisa, Confocal microscopy, transwell migration assay, Oxygraphy and Flow Cytometry we assessed: i) rhERAP internalization; ii) activation; iii) migration; iv) oxygen consumption rate; v) reactive oxygen species (ROS) accumulation; granule release; vi) phagocytosis; and vii) autophagy.

View Article and Find Full Text PDF

Chitinase 1 (CHIT1), as a chitin-specific hydrolase, significantly influences the progression of Alzheimer's disease (AD) through microglia-associated inflammation and amyloid beta (Aβ) plaque accumulation. However, the precise mechanism of CHIT1 action in AD remains uncertain. The effects of CHIT1 on cerebral blood flow (CBF), hippocampal volume, and cognitive function were investigated in APP/PS1 mice.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!