Publications by authors named "P Braghetta"
The core component of the class III phosphatidylinositol 3-kinase complex, Beclin 1, takes part in different protein networks, thus switching its role from inducing autophagy to regulating autophagosomal maturation and endosomal trafficking. While assessed in neurons, astrocytes, and microglia, its role is far less investigated in myelinating glia, including Schwann cells (SCs), responsible for peripheral nerve myelination. Remarkably, the dysregulation in endosomal trafficking is emerging as a pathophysiological mechanism underlying peripheral neuropathies, such as demyelinating Charcot-Marie-Tooth (CMT) diseases.
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- * This study examined how pericytes function in elderly individuals and those with muscular dystrophies linked to collagen VI mutations, highlighting the challenges of aging and muscle degeneration.
- * The research demonstrated that aging affects pericytes negatively, impairing their ability to help form blood vessels, while young patients with collagen VI issues showed some similar traits but retained a stronger ability to cope with oxidative stress and support blood vessel formation.
Article Synopsis
- Mutations in the GBA1 gene, linked to Gaucher disease, are common genetic risk factors for Parkinson's disease, but the role of oligodendrocytes in this relationship has not been well studied.
- A new in vitro system was used to investigate how β-glucocerebrosidase affects oligodendrocyte differentiation and myelination, employing an inhibitor and a transgenic mouse model to analyze the impacts of gene inactivation.
- Results indicate that loss of β-glucocerebrosidase function in oligodendrocytes leads to lysosomal dysfunction and decreased myelination, highlighting its potential role in neurodegenerative processes associated with Parkinson's disease.
Microenvironmental factors are known fundamental regulators of the phenotype and aggressiveness of glioblastoma (GBM), the most lethal brain tumor, characterized by fast progression and marked resistance to treatments. In this context, the extracellular matrix (ECM) is known to heavily influence the behavior of cancer cells from several origins, contributing to stem cell niches, influencing tumor invasiveness and response to chemotherapy, mediating survival signaling cascades, and modulating inflammatory cell recruitment. Here, we show that collagen VI (COL6), an ECM protein widely expressed in both normal and pathological tissues, has a distinctive distribution within the GBM mass, strongly correlated with the most aggressive and phenotypically immature cells.
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