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Aiello, V.

Publications and source records attributed to Aiello, V..

2 recordsLinked to original sources
bioRxiv2024

Apelin-13 alleviate inflammatory reaction of ischemia reperfusion in rat kidney transplantation via NF-kappa B signaling pathway

Withdrawal statementThis manuscript has been withdrawn after a request from the Dean of the Department of Medical and Surgical Sciences (DIMEC) at the University of Bologna. This manuscript constitutes a fraudulent submission by a third party impersonating Prof. Gaetano La Manna of said university. The email address listed for the corresponding author is invalid and not the institutional email address of Prof. La Manna, a member of DIMEC. Additionally, there are no other faculty members or researchers named Gaetano La Manna employed at the University of Bologna (UNIBO). Furthermore, the department (DIMES) associated with the publication in question was dissolved on December 31, 2022, and no longer exists. The individuals falsely listed as authors were not responsible for its submission and have no knowledge of or involvement in the work presented. Therefore, this article should not be cited as reference for this project.

cell biology↗
bioRxiv2024

YY1 mutations disrupt corticogenesis and cytoarchitecture through a cell-type specific rewiring of cell-autonomous and non-cell-autonomous transcriptional programs

Germline mutations of YY1 cause Gabriele-de Vries syndrome (GADEVS), a neurodevelopmental disorder featuring intellectual disability and a wide range of systemic manifestations. To dissect the cellular and molecular mechanisms underlying GADEVS, we combined large-scale imaging, single-cell multiomics and gene regulatory network reconstruction in 2D and 3D patient-derived physiopathologically relevant cell lineages. YY1 haploinsufficiency causes a pervasive alteration of cell type specific transcriptional networks, disrupting corticogenesis at the level of neural progenitors and terminally differentiated neurons, including cytoarchitectural defects reminiscent of GADEVS clinical features. Transcriptional alterations in neurons propagated to neighboring astrocytes through a major non-cell autonomous pro-inflammatory effect that grounds the rationale for modulatory interventions. Together, neurodevelopmental trajectories, synaptic formation and neuronal-astrocyte cross talk emerged as salient domains of YY1 dosage-dependent vulnerability. Mechanistically, cell-type resolved reconstruction of gene regulatory networks uncovered the regulatory interplay between YY1, NEUROG2 and ETV5 and its aberrant rewiring in GADEVS. Our findings underscore the reach of advanced in vitro models in capturing developmental antecedents of clinical features and exposing their underlying mechanisms to guide the search for targeted interventions.

neuroscience↗