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Takei, F.

Publications and source records attributed to Takei, F..

2 recordsLinked to original sources

High +Gz Exposure Alters Urinary Extracellular Vesicle miRNAs in Humans

High +Gz exposure elicits complex cardiovascular, autonomic, and endocrine responses, but the associated molecular responses in humans remain poorly understood. We investigated whether microRNAs (miRNAs) encapsulated in urinary extracellular vesicles (uEVs) are altered following acute high +Gz exposure. Twenty-one healthy young men undergoing human centrifuge training provided urine samples before, immediately after, and on the morning after exposure. Candidate uEV-encapsulated miRNAs were identified by RNA sequencing and Gene Ontology analysis, and 16 miRNAs related to ischemia, hypoxia, blood pressure regulation, and mechanical stress were quantified by quantitative PCR. Salivary cortisol, urinary catecholamines, and heart rate were also assessed. Six uEV-encapsulated miRNAs increased significantly after high +Gz exposure. miR-20b-5p, miR-125b-5p, and miR-130a-3p increased immediately after exposure and returned to baseline by the following morning, whereas miR-335-5p, miR-17-5p, and miR-92a-3p remained elevated. Urinary adrenaline, noradrenaline, and dopamine increased immediately after exposure; adrenaline returned to baseline by the following morning, whereas noradrenaline and dopamine remained elevated. Salivary cortisol and heart rate also increased. These findings demonstrate distinct transient and sustained temporal responses of uEV-encapsulated miRNAs to high +Gz in humans, paralleling different catecholamine response patterns. Although their tissue origins and functional roles remain unresolved, these findings provide new molecular-level insights into the human physiological response to high +Gz.

physiology↗

Human CD127 negative ILC2s show immunological memory

Group 2 Innate Lymphoid Cells (ILC2s) serve as key players in type 2 immunity and contribute significantly to maintaining homeostasis and responding to inflammation. Notably, ILC2s are closely implicated in the development of allergic disorders like asthma. While previous research has demonstrated immunological memory in mouse ILC2s, it has remained unclear whether human ILC2s can acquire this form of memory. In this study, we demonstrate the persistence of CD45RO, a marker previously linked to inflammatory ILC2s, in resting ILC2s that have undergone prior activation. These cells concurrently reduce the expression of the canonical ILC marker CD127. Through in vitro experiments involving the isolation and stimulation of CD127-CD45RO+ ILC2s, we observed an augmented ability to produce cytokines and undergo proliferation. CD127-CD45RO+ ILC2s are found in both healthy and inflamed tissues and display a gene signature of cell activation. Memory ILC2s may play a significant role in chronic type 2 diseases, such as allergic asthma and atopic dermatitis. HIGHLIGHTS- Inflamed and healthy tissues contain CD127-ILC2s with a gene signature of cell activation - CD127-CD45RO+ ILC2s from healthy tissues show immunological memory features - Mouse memory ILC2s downregulate CD127 - In vitro stimulation of naive ILC2s generates memory CD127-CD45RO+ ILC2s

immunology↗