Project Title
Mesenchymal stem cell-derived secretome: A multitarget intervention to reduce long-term disabilities induced by in utero opioid exposure
Partner Organisations
Internal ID
1240162
Principal Investigator
Type
applied research
Status
VIGENTE
Start Date
April 1, 2024
End Date
March 31, 2027
Organisations
University of Chile
Fields of Science and Technology (OECD)
Medical and Health sciences
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Item type:Publication, Gut Microbiota‐Derived Extracellular Vesicles Influence Alcohol Intake Preferences in Rats(Wiley, 2025-03)7 - Some of the metrics are blocked by yourconsent settings
Item type:Publication, Morphine self-administration is inhibited by the antioxidant N‐acetylcysteine and the anti-inflammatory ibudilast; an effect enhanced by their co-administration(2024)1Scopus© Citations 3 - Some of the metrics are blocked by yourconsent settings
Item type:Publication, Two-Month Voluntary Ethanol Consumption Promotes Mild Neuroinflammation in the Cerebellum but Not in the Prefrontal Cortex, Hippocampus, or Striatum of Mice(2024); ; María Rosa Bono<jats:p>Chronic ethanol exposure often triggers neuroinflammation in the brain’s reward system, potentially promoting the drive for ethanol consumption. A main marker of neuroinflammation is the microglia-derived monocyte chemoattractant protein 1 (MCP1) in animal models of alcohol use disorder in which ethanol is forcefully given. However, there are conflicting findings on whether MCP1 is elevated when ethanol is taken voluntarily, which challenges its key role in promoting motivation for ethanol consumption. Here, we studied MCP1 mRNA levels in areas implicated in consumption motivation—specifically, the prefrontal cortex, hippocampus, and striatum—as well as in the cerebellum, a brain area highly sensitive to ethanol, of C57BL/6 mice subjected to intermittent and voluntary ethanol consumption for two months. We found a significant increase in MCP1 mRNA levels in the cerebellum of mice that consumed ethanol compared to controls, whereas no significant changes were observed in the prefrontal cortex, hippocampus, or striatum or in microglia isolated from the hippocampus and striatum. To further characterize cerebellar neuroinflammation, we measured the expression changes in other proinflammatory markers and chemokines, revealing a significant increase in the proinflammatory microRNA miR-155. Notably, other classical proinflammatory markers, such as TNFα, IL6, and IL-1β, remained unaltered, suggesting mild neuroinflammation. These results suggest that the onset of neuroinflammation in motivation-related areas is not required for high voluntary consumption in C57BL/6 mice. In addition, cerebellar susceptibility to neuroinflammation may be a trigger to the cerebellar degeneration that occurs after chronic ethanol consumption in humans.</jats:p>Scopus© Citations 2 6 - Some of the metrics are blocked by yourconsent settings
Item type:Publication, Mitochondrial dynamics and sex-specific responses in the developing rat hippocampus: Effect of perinatal asphyxia and mesenchymal stem cell Secretome treatment(2024)2 - Some of the metrics are blocked by yourconsent settings
Item type:Publication, Mesenchymal stem cells as a promising therapy for alcohol use disorder(2024)Scopus© Citations 1 12 - Some of the metrics are blocked by yourconsent settings
Item type:Publication, Paw Skin as a Translational Model for Investigating Fibrotic and Inflammatory Wound Healing Defects in Recessive Dystrophic Epidermolysis Bullosa(MDPI AG, 2025-04-30); ; Recessive dystrophic epidermolysis bullosa (RDEB) is a severe genetic disease caused by COL7A1 mutations. It leads to skin fragility, chronic inflammation, and impaired wound healing. The condition often results in fibrotic scarring, pseudosyndactyly, and cutaneous squamous cell carcinoma (SCC). However, current animal models fail to fully replicate chronic RDEB wounds. In this study, we used Collagen VII-hypomorphic mice (Col7a1flNeo/flNeo) and created full-thickness wounds on their paw skin, an area prone to fibrosis due to mechanical stress. We analyzed the healing process using histology, immunofluorescence, and electron microscopy. The RDEB mice showed delayed wound closure, increased inflammation, and poor granulation tissue formation. At 30 days post-injury, we observed persistent fibrosis, with elevated levels of Collagen I, α-SMA+ myofibroblasts, and tenascin-C. These mice also had fewer intraepidermal nerve fibers, which may help explain the neuropathic pain associated with RDEB. Our model reproduces the main features of chronic RDEB wounds. It offers a useful tool for evaluating therapies aimed at reducing inflammation, fibrosis, and tumor risk in these patients.Scopus© Citations 3 4 - Some of the metrics are blocked by yourconsent settings
Item type:Publication, Intragastric administration of short chain fatty acids greatly reduces voluntary ethanol intake in rats(2024)Scopus© Citations 6 3