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Fidalgo, M.

Publications and source records attributed to Fidalgo, M..

2 recordsLinked to original sources

An astrocytic AMPK clock drives circadian behaviour

Circadian clocks coordinate behaviour and physiology with daily cycles of light and nutrient availability, but how metabolic signals influence brain timing remains incompletely understood. Astrocytes integrate metabolic and hormonal cues and exhibit time-of-day-dependent responses, suggesting that they may convey temporal information to hypothalamic circuits. Here, we show that hypothalamic AMP-activated protein kinase (AMPK) exhibits circadian regulation independently of light and feeding cues, is modulated by nutrient availability and astrocytic Ca{superscript 2} signalling, and regulates the temporal organisation of the hypothalamic phosphoproteome. Genetic manipulation of astrocytic AMPK signalling alters PER2 abundance and phosphorylation, including at a conserved residue implicated in circadian period regulation. At the behavioural level, AMPK and PER2 in ventromedial hypothalamic astrocytes contribute to food-anticipatory activity, whereas disruption of astrocytic AMPK signalling alters SCN-dependent circadian locomotor rhythms and energy homeostasis in a sex-dependent manner. Together, these findings identify astrocytic AMPK signalling as a temporally regulated pathway that couples metabolic signals to hypothalamic circadian timing and systemic homeostasis.

neuroscience↗

Transcription factor 19 is an androgen responsive gene that modulates vessel homeostasis and sustains metastatic prostate cancer

Prostate cancer is a prevalent tumor type that, despite being highly curable, progresses to metastatic disease in a fraction of patients, thus accounting for more than 350.000 annual deaths worldwide. In turn, uncovering the molecular insights of metastatic disease is instrumental to improve the survival rate of prostate cancer patients. By means of gene expression metanalysis in multiple prostate cancer patient cohorts, we identified a set of genes that are differentially expressed in aggressive prostate cancer. Transcription factor 19 (TCF19) stood out as an unprecedented epithelial gene upregulated in metastatic disease, with prognostic potential and associated with the activity of androgen receptor. By combining computational and empiric approaches, our data revealed that TCF19 is required for full metastatic capacity and its depletion influences core cancer-related processes, such as vascular permeability, supporting the role of this gene in the dissemination of prostate tumor cells.

cancer biology↗