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Biology subjects

Follenzi, A.

Publications and source records attributed to Follenzi, A..

2 recordsLinked to original sources

Bioengineering of the implantable vascularized endocrine constructs for insulin delivery suitable for clinical upscaling

Beta cell replacement therapy for type 1 diabetes is hindered by poor graft survival and suboptimal function, largely due to inadequate vascularization and lack of supportive microenvironment. To address these challenges, we developed a clinically scalable, extracellular matrix (ECM)-mimetic hydrogel, termed Amniogel, derived from human amniotic membrane via streamlined, clinically compliant process. Co-encapsulation of pancreatic islets with blood outgrowth endothelial cells (BOECs) within Amniogel facilitated the formation of prevascularized endocrine constructs (VECs). These constructs demonstrated enhanced {beta}-cell viability and function through ECM-bound pro-survival signals, rapid self-assembly of perfusable endothelial networks enabling efficient glucose sensing, and deposition of laminin-rich basement membranes enhancing {beta}-cell coupling and insulin secretion kinetics. In preclinical diabetic mouse models, VECs rapidly integrated with the host vasculature and provided sustained glycemic control when implanted subcutaneously. This integrative approach, combining a scalable, cost-effective biological scaffold with autologous vascularization potential, represents a significant advancement toward durable and clinically translatable {beta}-cell replacement therapies for T1DM. One Sentence SummaryA clinically scalable, biological hydrogel based vascularized endocrine constructs show sustained diabetes reversal.

bioengineering↗

FVIII interacts with cell surface to regulate endothelial cell functionality

Haemophilia A (HA) is a rare bleeding disorder caused by factor 8 (F8) mutations. Clinical manifestations are spontaneous bleedings that primarily consist of hemarthrosis and intracranial haemorrhages. To date, the impairment of vessel stability in HA patients and the correlation between FVIII and endothelial functionality is poorly understood. Here we show that FVIII plays a role in endothelial cell functionality. Blood Outgrowth endothelial cells (BOECs) knockout generated by CRISPR/Cas9, HA BOECs and HA iPSCs-derived ECs showed alteration of vessel-formation, endothelial cell migration, and vessel permeability. Importantly, the impaired EC phenotype was rescued by treatment with recombinant human FVIII or by lentiviral vector (LV) expressing FVIII. The FVIII function on endothelium was confirmed in vivo in a mouse model of severe HA which showed that an altered angiogenesis and vesselpermeability could be treated by exogenous FVIII. BOECstranscriptomic profiles revealed that FVIIIregulates the expression of endothelial basement membrane and extracellular matrix genes. Furthermore, exogenous expression of Nidogen2, identified as a FVIII regulated gene, restored the extracellular matrix integrity and EC functionality of HA ECs. In conclusion, FVIII is not only a coagulation factor but also an endothelial cell autocrine factor which promotes vessel stability.

molecular biology↗