The developmental expression of C3 receptor, an important surface marker of murine epidermal Langerhans cells (LCs), was quantitatively studied using an immunohistochemical technique on epidermal sheets and then compared with developmental expression of Ia antigen and membrane ATPase. Anti-Mac-1 monoclonal antibody associated with CR3 was used for detecting C3 receptor and proved positive for LCs by immunoelectron microscopy. Mac-1 positive (Mac-1+) cells showed quite a different distribution from those of ATPase+ and Ia+ cells. Almost the same number of Mac-1+ and ATPase+ cells were present during the embryonic period. The number of Mac-1+ cells gradually decreased from day 1 to day 5 of postnatal life, after which they increased again. Using the double-labeling technique on epidermal sheets at day 1 of postnatal life, it was shown that Ia+ cells possessed membrane ATPase activity and some Mac-1+ cells expressed Ia antigen. On days 4 and 7 of postnatal life all Mac-1+ cells expressed Ia antigen. These findings suggest that Mac-1 antigen observed during the embryonic period gradually fades after birth and is re-expressed after day 5 of postnatal life.
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Front Cell Dev Biol
January 2025
Dipartimento di Scienze Biomediche e Cliniche, Università degli Studi di Milano, Milano, Italy.
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.
Brain Commun
December 2024
San Diego Biomedical Research Institute, San Diego, CA 92121, USA.
Hypoxia triggers blood-brain barrier disruption and a strong microglial activation response around leaky cerebral blood vessels. These events are greatly amplified in aged mice which is translationally relevant because aged patients are far more likely to suffer hypoxic events from heart or lung disease, and because of the pathogenic role of blood-brain barrier breakdown in vascular dementia. Importantly, it is currently unclear if disrupted cerebral blood vessels spontaneously repair and if they do, whether surrounding microglia deactivates.
View Article and Find Full Text PDFJ Med Case Rep
October 2024
Department of Diagnostic Pathology, Tokyo Women's Medical University Adachi Medical Center, 4-33-1, Kohoku, Adachi-ku, 123-8558, Tokyo, Japan.
Adv Sci (Weinh)
December 2024
Institute of Lung Health and Immunity (LHI), Comprehensive Pneumology Center (CPC), Helmholtz Center Munich, Member of the German Center for Lung Research (DZL), 85764, Munich, Germany.
Exposure to nanoparticles (NPs) is frequently associated with adverse cardiovascular effects. In contrast, NPs in nanomedicine hold great promise for precise lung-specific drug delivery, especially considering the extensive pulmonary capillary network that facilitates interactions with bloodstream-suspended particles. Therefore, exact knowledge about effects of engineered NPs within the pulmonary microcirculation are instrumental for future application of this technology in patients.
View Article and Find Full Text PDFRedox Biol
November 2024
School of Public Health, Dalian Medical University, No. 9 W. Lvshun South Road, Dalian, 116044, China; National-Local Joint Engineering Research Center for Drug-Research and Development (R & D) of Neurodegenerative Diseases, Dalian Medical University, No. 9 W. Lvshun South Road, Dalian, 116044, China. Electronic address:
The activation of complement receptor 3 (CR3) in microglia contributes to neurodegeneration in neurological disorders, including Parkinson's disease (PD). However, it remains unclear for mechanistic knowledge on how CR3 mediates neuronal damage. In this study, the expression of CR3 and its ligands iC3b and ICAM-1 was found to be up-regulated in the midbrain of rotenone PD mice, which was associated with elevation of iron content and disruption of balance of iron metabolism proteins.
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