Publications by authors named "F Merigo"

SARS-CoV-2 infection has been recently shown to induce cellular senescence in vivo. A senescence-like phenotype has been reported in cystic fibrosis (CF) cellular models. Since the previously published data highlighted a low impact of SARS-CoV-2 on CFTR-defective cells, here we aimed to investigate the senescence hallmarks in SARS-CoV-2 infection in the context of a loss of CFTR expression/function.

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Article Synopsis
  • Richter's syndrome (RS) is a severe form of cancer resulting from the evolution of chronic lymphocytic leukemia (CLL) into a high-grade B-cell malignancy, characterized by decreased reliance on BCL-2, a key protein that prevents apoptosis (cell death).
  • Studies comparing CLL and RS revealed that RS cells display lower apoptotic priming and may depend on different anti-apoptotic proteins, complicating treatment strategies like using BH3 mimetics that target cell death pathways.
  • Transcriptomic analyses showed that as CLL transforms into RS, there is a downregulation of pro-apoptotic factors and changes in mitochondrial structure that contribute to enhanced resistance to apoptosis, making it harder to target RS directly.
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SARS-CoV-2 replicates in host cell cytoplasm. People with cystic fibrosis, considered at risk of developing severe symptoms of COVID-19, instead, tend to show mild symptoms. We, thus, analyzed at the ultrastructural level the morphological effects of SARS-CoV-2 infection on wild-type (WT) and F508del (ΔF) CFTR-expressing CFBE41o- cells at early and late time points post infection.

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People with cystic fibrosis should be considered at increased risk of developing severe symptoms of COVID-19. Strikingly, a broad array of evidence shows reduced spread of SARS-CoV-2 in these subjects, suggesting a potential role for CFTR in the regulation of SARS-CoV-2 infection/replication. Here, we analyzed SARS-CoV-2 replication in wild-type and CFTR-modified human bronchial epithelial cell lines and primary cells to investigate SARS-CoV-2 infection in people with cystic fibrosis.

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Multipotent stem cells persist within the stromal vascular fraction (SVF) of adipose tissue during adulthood. These cells, commonly referred to as adipose-derived stromal cells (ASC), have been extensively investigated over the past years as a promising therapeutic tool based on their regenerative and immunomodulatory properties. However, how ASC might mirror the age-related alteration of the fat they reside in remains unclear.

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