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Seamless integration of bioelectronic interface in an animal model via in vivo polymerization of conjugated oligomers

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Bioactive Materials 2022年第4期7卷 107-116页

作者： Giuseppina Tommasini Gwennael Dufil Federica Fardella Xenofon Strakosas Eugenio Fergola Tobias Abrahamsson David Bliman Roger Olsson Magnus Berggren Angela Tino Eleni Stavrinidou Claudia tortiglione Istituto di Scienze Applicate e Sistemi Intelligenti“E.Caianiello” Consiglio Nazionale delle RicercheVia Campi Flegrei 3480078PozzuoliItaly Laboratory of Organic Electronics Department of Science and TechnologyLinkoping UniversitySE-60174NorrkopingSweden Department of Chemistry and Molecular Biology University of GothenburgSE-40530GothenburgSweden Chemical Biology&Therapeutics Department of Experimental Medical ScienceLund UniversitySE-22184LundSweden

Leveraging the biocatalytic machinery of living organisms for fabricating functional bioelectronic interfaces,in vivo,defines a new class of micro-biohybrids enabling the seamless integration of technology with living biological ***,we have demonstrated the in vivo polymerization of conjugated oligomers forming conductors within the structures of ***,we expand this concept by reporting that Hydra,an invertebrate animal,polymerizes the conjugated oligomer ETE-S both within cells that expresses peroxidase activity and within the adhesive material that is secreted to promote underwater surface *** resulting conjugated polymer forms electronically conducting and electrochemically activeμm-sized domains,which are inter-connected resulting in percolative conduction pathways extending beyond 100μm,that are fully integrated within the Hydra tissue and the secreted ***,the introduction and in vivo polymerization of ETE-S can be used as a biochemical marker to follow the dynamics of Hydra budding(reproduction)and *** work paves the way for well-defined self-organized electronics in animal tissue to modulate biological functions and in vivo biofabrication of hybrid functional materials and devices.

关键词： In vivo polymerization Bioelectronics interfaces Conjugated oligomers Model organism

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Na+ - Ca2+ Exchanger Gene Products. NCX1, NCX2 and NCX3, as Putative Targets for Neuroprotection in Brain Ischemia

Na+ - Ca2+ Exchanger Gene Products. NCX1, NCX2 and NCX3, as ...

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第十五届国际药理学大会

作者： Annunziato L Pignataro G Sirabella R Saggese M Cuomo O Gala R Sec-ondo A Viggiano D Boscia F Molinaro P Valsecchi V tortiglione a Di Renzo GF Division of Pharmacology Depof NeuroscienceSchool of MedicineUniv.of Naples Federico IIItaly Division of Pharmacology Depof NeuroscienceSchool of MedicineUniv.of Naples Federico IIItaly Division of Pharmacology Depof NeuroscienceSchool of MedicineUniv.of Naples Federico IIItaly Division of Pharmacology Depof NeuroscienceSchool of MedicineUniv.of Naples Federico IIItaly Division of Pharmacology Depof NeuroscienceSchool of MedicineUniv.of Naples Federico IIItaly Division of Pharmacology Depof NeuroscienceSchool of MedicineUniv.of Naples Federico IIItaly Division of Pharmacology Depof NeuroscienceSchool of MedicineUniv.of Naples Federico IIItaly Division of Pharmacology Depof NeuroscienceSchool of MedicineUniv.of Naples Federico IIItaly Division of Pharmacology Depof NeuroscienceSchool of MedicineUniv.of Naples Federico IIItaly Division of Pharmacology Depof NeuroscienceSchool of MedicineUniv.of Naples Federico IIItaly Division of Pharmacology Depof NeuroscienceSchool of MedicineUniv.of Naples Federico IIItaly Division of Pharmacology Depof NeuroscienceSchool of MedicineUniv.of Naples Federico IIItaly Division of Pharmacology Depof NeuroscienceSchool of MedicineUniv.of Naples Federico IIItaly

＜正＞ NCX is a neuronal plasmamembrane antiporter, which, by coupling Ca2 + and Na+ fluxes, plays a relevant role in brain ischemia. In the CNS there are 3 different NCX gene products NCX1, NCX2, and NCX3. NCX transcript and protein expression is differently regulated after ischemia in the focal region and in the peri-infarct area. The pharmacological inhibition of NCX activity is detrimental in the development of ischemic damage. NCX knocking out through antisense strategy showed that NCX1 and NCX3 play a major role in NCX neuroprotective action. Accordingly. NCX3 transfected BHK cells are less vulnerable to chemical hypoxia. Interestingly, the expression of NCX1 and NCX3 is up-regulated by NGF in PC12 cells. This modulation occurs via two pathways activated by tyro-sine kinase receptors. Ras-Raf-Mek-MAPK pathway and PI-3K/AKT pathway. In fact, the Mek inhibitor PD 98059 or the PI-3K inhibitor LY 294002 prevented this up-regulation. whereas AKT-1 PC12 cell positive mutants showed an increase in NCX1 and NCX3 expression. These data demonstrate that NCX products display a differential expression in the development of ischemic damage and can be selectively upregulated through NGF-mediated trasductional pathways

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