ArticleMolecular medicine (Cambridge, Mass.)2026
LPS-induced inflammation differentially affects endogenous Ca
Article in Molecular medicine (Cambridge, Mass.), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Written in the Stars: Astrocyte Biology From Evolution to Disease.Acta physiologica (Oxford, England) · 2026Review
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11 authors.
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Abstract
backgroundMouse and human astrocytes exhibit substantial species-specific differences in both morphology and function. Their response to inflammatory stimuli, however, remains underexplored despite being crucial for understanding bidirectional astrocyte-neuron signaling dynamics and for translating preclinical findings to human-relevant applications. Induced pluripotent stem cell-based models thus offer a powerful platform to investigate these mechanisms in the context of the human neural connectome.
methodsWe apply two well-established in vitro protocols by exposing cultured astrocytes to lipopolysaccharide (LPS) for either 3 or 24 h to trigger an inflammatory response. We investigated how LPS-induced inflammation affects the endogenous Ca2+ activity in astrocytes derived from the mouse hippocampus (HC) and prefrontal cortex (PFC), as well as human induced pluripotent stem cell (hiPSC)-derived astrocytes. Both, morphological changes and Ca2+ activity were analyzed using the volume fraction (VF) approach and our previously developed multi-threshold event detection (MTED) combined with machine learning-driven non-negative matrix factorization (NMF).
resultsThe comprehensive assessment of Ca2+ activity patterns and their relation to cell morphology revealed significant alterations in response to LPS treatment, and further between mouse and human hiPSC-derived astrocytes. While both mouse and human astrocytes show increased Ca2+ event frequency after short-term LPS exposure, after 24 h of LPS treatment Ca2+ activity is severely restricted in PFC astrocytes but substantially increased in human astrocytes.
conclusionsOur findings highlight the unique properties of human iPSC-derived astrocytes and provide detailed insights into how Ca2+ signaling becomes dysregulated under neuroinflammatory conditions. Understanding the species-specific responses is essential for advancing stem cell-based models of human astrocyte-neuron signaling circuits and for developing targeted therapeutic strategies to alleviate neuroinflammation and Ca2+-related dysregulation in neurological diseases.
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