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Kanninen, K.

Publications and source records attributed to Kanninen, K..

2 recordsLinked to original sources

Plasma untargeted metabolomics reveals distinct metabolic disturbances between sexes following inhalation of ultrafine particles and exposure to aircraft noise in mice

Traffic noise and air pollution, particularly ultrafine particles (UFP), are significantly associated with health risks. However, the systemic metabolic consequences of the combined effects of UFP and aircraft noise (AN) exposure on health remain poorly understood. We aimed to investigate changes in plasma metabolites in healthy wildtype C57BL/6J mice following whole-body inhalation exposure to UFP (average diameter <40 nm), AN and their combination (UFP+AN). Liquid chromatography-mass spectrometry (LC-MS)-based untargeted plasma metabolomics analysis was undertaken for UFP, AN, and combined UFP+AN-exposed mice of both sexes. This study identified a total of 1146 plasma metabolites. Across exposure groups, AN induced the greatest plasma metabolomic changes in both sexes, while UFP significantly altered metabolites only in females, indicating a sex-specific response. The combined UFP+AN exposure produced a modestly enhanced effect in males compared with either single exposure but showed an attenuated effect in females. Pathway analyses revealed that lipid and amino acid metabolism were the most affected, followed by xenobiotics, and cofactors and vitamins, after exposure in both female and male mice. Additionally, in the clean air control group, we identified sex differences in 49 plasma metabolites, which mostly included lipids and amino acids. Following exposure, however, sex-dependent metabolic differences became more pronounced and exposure-specific, suggesting that UFP and AN have distinct effects on plasma metabolome of male and female mice that extend beyond baseline sexual dimorphism observed in unexposed animals. To our knowledge, this study is the first comprehensive characterization of systemic metabolic changes in mice after combination of UFP and AN exposure, providing new insight into the interplay between traffic noise and air pollution health risks.

pharmacology and toxicology↗

Microglial amyloid beta clearance is driven by PIEZO1 channels

BackgroundMicroglia are the endogenous immune cells of the brain and act as sensors of pathology to maintain brain homeostasis and eliminate potential threats. In Alzheimers disease (AD), toxic amyloid beta (A{beta}) accumulates in the brain and forms stiff plaques. In late-onset AD accounting for 95% of all cases, this is thought to be due to reduced clearance of A{beta}. Human genome-wide association studies and animal models suggest that reduced clearance results from aberrant function of microglia. While the impact of neurochemical pathways on microglia have been broadly studied, mechanical receptors regulating microglial functions remain largely unexplored. MethodsHere we showed that a mechanotransduction ion channel, PIEZO1, is expressed and functional in human and mouse microglia. We used a small molecule agonist, Yoda1, to study how activation of PIEZO1 affects AD-related functions in human induced pluripotent stem cell (iPSC) -derived microglia-like cells (iMGL) under controlled laboratory experiments. Cell survival, metabolism, phagocytosis and lysosomal activity were assessed using real-time functional assays. To evaluate the effect of activation of PIEZO1 in vivo, 5-month-old 5xFAD male mice were infused daily with Yoda1 for two weeks through intracranial cannulas. Microglial Iba1 expression and A{beta} pathology were quantified with immunohistochemistry and confocal microscopy. Published human and mouse AD datasets were used for in-depth analysis of PIEZO1 gene expression and related pathways in microglial subpopulations. ResultsWe show that PIEZO1 orchestrates A{beta} clearance by enhancing microglial survival, phagocytosis, and lysosomal activity. A{beta} inhibited PIEZO1-mediated calcium transients, whereas activation of PIEZO1 with a selective agonist, Yoda1, improved microglial phagocytosis resulting in A{beta} clearance both in human and mouse models of AD. Moreover, PIEZO1 expression was associated with a unique microglial transcriptional phenotype in AD as indicated by assessment of cellular metabolism, and human and mouse single cell datasets. ConclusionThese results indicate that the compromised function of microglia in AD could be improved by controlled activation of PIEZO1 channels resulting in alleviated A{beta} burden. Pharmacological regulation of these mechanoreceptors in microglia could represent a novel therapeutic paradigm for AD. GRAPHICAL ABSTRACT O_FIG O_LINKSMALLFIG WIDTH=176 HEIGHT=200 SRC="FIGDIR/small/484831v1_ufig1.gif" ALT="Figure 1"> View larger version (43K): org.highwire.dtl.DTLVardef@832eadorg.highwire.dtl.DTLVardef@6d8719org.highwire.dtl.DTLVardef@c09740org.highwire.dtl.DTLVardef@9fa85_HPS_FORMAT_FIGEXP M_FIG C_FIG

neuroscience↗