In JoVE (1)
Other Publications (1)
Articles by Jacopo Morini in JoVE
A Co-culture Method to Investigate the Crosstalk Between X-ray Irradiated Caco-2 Cells and PBMC Gabriele Babini*1, Jacopo Morini*1, Sofia Barbieri1, Giorgio Baiocco1, Giovanni Battista Ivaldi2, Marco Liotta2, Paola Tabarelli de Fatis2, Andrea Ottolenghi1 1Dipartimento di Fisica, Università degli Studi di Pavia, 2IRCCS Istituti Clinici Scientifici Maugeri We present a protocol to investigate the crosstalk between X-ray-irradiated Caco-2 and peripheral blood mononuclear cells (PBMC). The protocol starts with Caco-2 irradiation and set-up of the co-culture with PBMC; subsequently, trans-epithelial electrical resistance is measured regularly over 48 h and western blot performed in both Caco-2 and PBMC.
Other articles by Jacopo Morini on PubMed
Functional Analysis of a Novel ENG Variant in a Patient with Hereditary Hemorrhagic Telangiectasia (HHT) Identifies a New Sp1 Binding-site Gene. Jan, 2018 | Pubmed ID: 29305977 Hereditary Hemorrhagic Telangiectasia (HHT) is a rare disease, with an autosomal dominant inheritance and a worldwide incidence of about 1: 5000 individuals. In >80% of patients, HHT is caused by mutations in either ENG or ACVRL1, which code for ENDOGLIN and Activin A Receptor Type II-Like Kinase 1 (ALK1), belonging to the TGF-β/BMP signalling pathway. Typical HHT clinical features are mucocutaneous telangiectases, arteriovenous malformations, spontaneous and recurrent epistaxis, as well as gastrointestinal bleedings. An additional, but less frequent, clinical manifestation in some HHT patients is the presence of Pulmonary Arterial Hypertension (PAH). The aim of this work is to describe the functional role of a novel ENG intronic variant found in a patient affected by both HHT and PAH, in order to assess whether it has a pathogenic role. We proved that the variant lies in a novel binding-site for the transcription factor Sp1, known to be involved in the regulation of ENG and ACVRL1 transcription. We confirmed a pathogenic role for this intronic variant, as it significantly reduces ENG transcription by affecting this novel Sp1 binding-site.