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Di Valentin, E.

Publications and source records attributed to Di Valentin, E..

2 recordsLinked to original sources

Tanycytic annexinA1-containing extracellular vesicles control thermogenesis by orchestrating microglial and neuronal functions.

Obesity, a major global health issue, results from disrupted energy balance driven by chronic hypothalamic inflammation and altered intercellular communication. Among the diverse cells orchestrating this regulation, tanycytes--specialized ependymal cells at the brain-blood interface--have emerged as key modulators, yet the molecular mechanisms by which they influence surrounding cells remain poorly understood. Here, we identify Annexin A1 (ANXA1) as a tanycyte-derived anti-inflammatory signal whose expression, localization, and secretion are dynamically regulated by nutritional state and altered under high-fat diet. During positive energy balance, ANXA1 is secreted in CD9 extracellular vesicles (EV), remodeling hypothalamic networks by altering microglial morphology, synaptic density, and neuronal activation. These EV-mediated effects extend systemically to regulate brown adipose tissue thermogenesis, glucose homeostasis, and overall energy balance. Our findings reveal a previously unrecognized tanycyte-microglia-neuron signaling axis and highlight EV-mediated glial communication as a potential therapeutic target in obesity-associated neuroinflammation.

neuroscience↗

SARS-CoV2 infection triggers reactive astrocyte states and inflammatory conditions in long-term Human Cortical Organoids

SARS-CoV2, severe acute respiratory syndrome coronavirus 2, is frequently associated with neurological manifestations. Despite the presence of mild to severe CNS-related symptoms in a cohort of patients, there is no consensus whether the virus can infect directly brain tissue or if the symptoms in patients are a consequence of peripheral infectivity of the virus. Here, we use long-term human stem cell-derived cortical organoids to assess SARS-CoV2 infectivity of brain cells and unravel the cell-type tropism and its downstream pathological effects. Our results show consistent and reproducible low levels of SARS-CoV2 infection of astrocytes, deep projection neurons, upper callosal neurons and inhibitory neurons in 6 months human cortical organoids. Interestingly, astrocytes showed the highest infection rate among all infected cell populations that led to increased presence of reactive states. Further, transcriptomic analysis revealed overall changes in expression of genes related to cell metabolism, astrocyte activation and, inflammation and further, upregulation of cell survival pathways. Thus, local and minor infectivity of SARS-CoV2 in the brain may induce widespread adverse effects and may lead to resilience of dysregulated neurons and astrocytes within an inflammatory environment.

neuroscience↗