Relevant bibliographies by topics / Cellule neuronali

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Academic literature on the topic 'Cellule neuronali'

Author: Grafiati
Published: 9 March 2023
Last updated: 10 March 2023

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Journal articles on the topic "Cellule neuronali"

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Lledo, Pierre-Marie. "Cellules souches neuronales." Morphologie 99, no. 327 (December 2015): 154. http://dx.doi.org/10.1016/j.morpho.2015.09.012.

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Corner, M. A. "Neuronal and cellular oscillators." Journal of the Neurological Sciences 92, no. 2-3 (September 1989): 349. http://dx.doi.org/10.1016/0022-510x(89)90150-0.

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Korn, H. "Neuronal and cellular oscillators." Biochimie 72, no. 5 (May 1990): 376. http://dx.doi.org/10.1016/0300-9084(90)90037-h.

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Young, Fraser I., Vsevolod Telezhkin, Sarah J. Youde, Martin S. Langley, Maria Stack, Paul J. Kemp, Rachel J. Waddington, Alastair J. Sloan, and Bing Song. "Clonal Heterogeneity in the Neuronal and Glial Differentiation of Dental Pulp Stem/Progenitor Cells." Stem Cells International 2016 (2016): 1–10. http://dx.doi.org/10.1155/2016/1290561.

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Cellular heterogeneity presents an important challenge to the development of cell-based therapies where there is a fundamental requirement for predictable and reproducible outcomes. Transplanted Dental Pulp Stem/Progenitor Cells (DPSCs) have demonstrated early promise in experimental models of spinal cord injury and stroke, despite limited evidence of neuronal and glial-like differentiation after transplantation. Here, we report, for the first time, on the ability of single cell-derived clonal cultures of murine DPSCs to differentiatein vitrointo immature neuronal-like and oligodendrocyte-like cells. Importantly, only DPSC clones with high nestin mRNA expression levels were found to successfully differentiate into Map2 and NF-positive neuronal-like cells. Neuronally differentiated DPSCs possessed a membrane capacitance comparable with primary cultured striatal neurons and small inward voltage-activated K+but not outward Na+currents were recorded suggesting a functionally immature phenotype. Similarly, only high nestin-expressing clones demonstrated the ability to adopt Olig1, Olig2, and MBP-positive immature oligodendrocyte-like phenotype. Together, these results demonstrate that appropriate markers may be used to provide an early indication of the suitability of a cell population for purposes where differentiation into a specific lineage may be beneficial and highlight that further understanding of heterogeneity within mixed cellular populations is required.
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Wylie, Steven R., and Peter D. Chantler. "Myosin IIC: A Third Molecular Motor Driving Neuronal Dynamics." Molecular Biology of the Cell 19, no. 9 (September 2008): 3956–68. http://dx.doi.org/10.1091/mbc.e07-08-0744.

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Neuronal dynamics result from the integration of forces developed by molecular motors, especially conventional myosins. Myosin IIC is a recently discovered nonsarcomeric conventional myosin motor, the function of which is poorly understood, particularly in relation to the separate but coupled activities of its close homologues, myosins IIA and IIB, which participate in neuronal adhesion, outgrowth and retraction. To determine myosin IIC function, we have applied a comparative functional knockdown approach by using isoform-specific antisense oligodeoxyribonucleotides to deplete expression within neuronally derived cells. Myosin IIC was found to be critical for driving neuronal process outgrowth, a function that it shares with myosin IIB. Additionally, myosin IIC modulates neuronal cell adhesion, a function that it shares with myosin IIA but not myosin IIB. Consistent with this role, myosin IIC knockdown caused a concomitant decrease in paxillin-phospho-Tyr118 immunofluorescence, similar to knockdown of myosin IIA but not myosin IIB. Myosin IIC depletion also created a distinctive phenotype with increased cell body diameter, increased vacuolization, and impaired responsiveness to triggered neurite collapse by lysophosphatidic acid. This novel combination of properties suggests that myosin IIC must participate in distinctive cellular roles and reinforces our view that closely related motor isoforms drive diverse functions within neuronal cells.
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Boulant, Jack A. "Cellular mechanisms of neuronal thermosensitivity." Journal of Thermal Biology 24, no. 5-6 (October 1999): 333–38. http://dx.doi.org/10.1016/s0306-4565(99)00038-8.

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Agnati, Luigi F., Diego Guidolin, Chiara Carone, Mauro Dam, Susanna Genedani, and Kjell Fuxe. "Understanding neuronal molecular networks builds on neuronal cellular network architecture." Brain Research Reviews 58, no. 2 (August 2008): 379–99. http://dx.doi.org/10.1016/j.brainresrev.2007.11.002.

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Lillycrop, K. A., Y. Z. Liu, T. Theil, T. Möröy, and D. S. Latchman. "Activation of the herpes simplex virus immediate-early gene promoters by neuronally expressed POU family transcription factors." Biochemical Journal 307, no. 2 (April 15, 1995): 581–84. http://dx.doi.org/10.1042/bj3070581.

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Herpes simplex virus immediate-early (IE) promoters contain the TAATGARAT motif which acts as a target site for the cellular POU family transcription factors Oct-1 and Oct-2. Here we show that other members of the POU family that are expressed in sensory neurons can also affect IE promoter activity. In particular, two members of the Brn-3 family of POU proteins Brn-3a and Brn-3c can activate the IE-1 and IE-3 promoters when co-transfected into fibroblasts and neuronal cells whereas a third member Brn-3b represses IE promoter activity. In contrast, Brn-3 proteins cannot overcome the inhibitory effect of neuronal Oct-2 on IE promoter activity in co-transfections nor do they prevent transactivation of the IE promoters by the Oct-1-Vmw65 complex. The potential regulation of the IE promoters by several different neuronally expressed POU proteins during the initiation, maintenance and re-activation of latent infection in sensory neurons is discussed.
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Dale, Nicholas. "Neuronal and cellular oscillators (cellular clocks series, vol. 2)." Trends in Neurosciences 12, no. 12 (January 1989): 521–22. http://dx.doi.org/10.1016/0166-2236(89)90114-8.

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Kristan,, William B. "Neuronal and Cellular Oscillators.Jon W. Jacklet." Quarterly Review of Biology 65, no. 1 (March 1990): 73–74. http://dx.doi.org/10.1086/416613.

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Dissertations / Theses on the topic "Cellule neuronali"

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CAPORALI, SIMONA. "Cellule staminali neuronali e microglia: cross - talk in modello in vitro di neuroinfiammazione." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2009. http://hdl.handle.net/10281/7547.

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Inhibition of microglia-mediated neuroinflammation is an important terapeuthic target in order to avoid cognitive and motor impairment in brain ischemia . Reportedly, neural stem cell (NSC) brain grafts have neuroprotective effecs 1. It has been proposed that these positive effects are not caused only by NSC proliferation and generation of new neurons, but also by a modulation of the brain lesion environment 2. Our primary aim was to ascertain whether NSC were capable of modifying microglial activation in vitro. We used ATP as inflammatory stimuli, since it is massively released from damaged neurons and is responsible of activation of microglia during ischemia3. We demonstrated that N9 murine microglia cells incubated with conditioned media (CM) from NSC culture have a blunted response to ATP. In fact, ATP stimulation of N9 cells preincubated with CM at different passages induced a reduced release of intracellular calcium compared to controls (Fig.1). Moreover, CM preincubation significantly inhibited the expression of inflammatory cytokines like TNF-alfa, COX-2, and IL-10 that are up-regulated after ATP stimulation (Fig.2) Reportedly, high-dose ATP (>1mM) exposure is detrimental both for neurons and microglial cells4. We tested CM action of survival of N9 microglia treated with 3mM ATP for 24 hours. CM preincubation for 24 hours was capable of significantly reducing N9 mortality induced by ATP treatment (Fig.3). In conclusion NSC release soluble factors that have an antinfiammatory action blunting N9 response to ATP stimulation.
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Fabbri, Roberta. "Dispositivi biomedici avanzati per il controllo selettivo della funzionalità di cellule cerebrali non neuronali." Master's thesis, Alma Mater Studiorum - Università di Bologna, 2019. http://amslaurea.unibo.it/19539/.

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Gli studi degli ultimi quarant’anni hanno evidenziato che gli astrociti, cellule non neuronali del Sistema Nervoso Centrale, pur essendo definite cellule non eccitabili, sono attivamente coinvolti nel mantenimento dell'omeostasi cerebrale e nel controllo della trasmissione sinaptica. I meccanismi alla base della funzionalità degli astrociti, ed in particolare i segnali mediati da variazioni della concentrazione di calcio intracellulare stanno emergendo come potenziale bersaglio per lo sviluppo di applicazioni tecnologiche in neuroscienze. Fra i materiali a base di carbonio, il grafene ed i suoi derivati hanno suscitato un notevole interesse nel campo biomedico, in virtù delle proprietà meccaniche, elettriche e di biocompatibilità. Il presente lavoro riporta lo studio dell'interazione di materiali a base di ossido di grafene con cellule astrogliali e si propone di indagare l'effetto della stimolazione elettrica operata mediante differenti dispositivi ITO-GO (ossido di indio stagno-ossido di grafene) sui segnali di [Ca2+]i in astrociti primari neocorticali di ratto. I risultati dimostrano che i substrati a base di GO e la loro funzionalizzazione con molecole alifatiche promuovono l’adesione astrogliale. Inoltre, la stimolazione elettrica extracellulare induce differenti risposte di [Ca2+]i in astrociti a seconda del dispositivo utilizzato: i)risposte oscillatorie rapide, tipiche dell’aumento di [Ca2+]i mediato dal rilascio di calcio dagli stores citoplasmatici erano osservate in astrociti su ITO e ITO-rGO. ii)Le cellule su dispositivi ITO-GO mostravano risposte a lento incremento di [Ca2+]i, caratteristiche dell’influsso di calcio extracellulare, la cui dinamica sembra dipendere dallo spessore del GO. La possibilità qui presentata di modulare selettivamente i [Ca2+]i astrogliali, utilizzando diversi dispositivi ITO-GO, pone le basi per un potenziale sviluppo di dispositivi biomedici rivolte agli astrociti e dirette alla diagnosi e terapia di disfunzioni cerebrali.
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MARACCHIONI, ALESSIA. "Il danno mitocondriale modula lo splicing alternativo in cellule neuronali: implicazioni per la neurodegenerazione." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2009. http://hdl.handle.net/2108/851.

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Il danno mitocondriale è associato a molte malattie neurodegenerative, quali: Parkinson, Alzheimer e Sclerosi Laterale Amiotrofica. Queste malattie sono associate anche a cambiamenti di isoforme tramite splicing alternativo di alcuni geni. In questo lavoro dimostriamo che il danneggiamento mitocondriale modula lo splicing alternativo in maniera generale. Cellule di neuroblastoma umano sono state incubate con l’agente chimico paraquat (una neurotossina che danneggia i mitocondri e crea stress ossidativo) e analizzate mediante RT-PCR per il pattern di splicing di 13 geni. Tutti gli mRNAs soggetti a splicing alternativo mostrano un’incremento dell’isoforma più piccola in maniera dose e tempo dipendente. Al contrario degli esoni alternativi, gli esoni costitutivi non cambiano dopo induzione con il paraquat. Dai dati ottenuti usando altre droghe, si evince che la modulazione dello splicing alternativo è correlata con il danno mitocondriale e la conseguente mancanza di ATP. Linee cellulari non neuronali non mostrano gli stessi cambiamenti nello splicing, indicando una selettiva suscettibilità delle cellule neuronali. Dato che una significativa percentuale di mRNAs di mammiferi è sottoposta a splicing alternativo, abbiamo ipotizzato che il danneggiamento mitocondriale causi uno squilibrio tra le varie isoforme dando un importante contributo alla neurodegenerazione. Con lo scopo di identificare eventuali targets farmacologici, abbiamo cercato di capire quale sia la via di trasduzione del segnale che trasmette lo stress mitocondriale al macchinario dello splicing. Due classi di proteine determinano la selezione dei siti di splicing: la famiglia delle proteine SR e la famiglia delle proteine hnRNP; entrambe regolate dalla fosforilazione, che è importante per la loro attività. Le proteine hnRNP ed SR sono state purificate da cellule di neuroblastoma umano di controllo e trattate con paraquat e studiate mediante un approccio sub-proteomico. Mentre le proteine hnRNPs non mostrano cambiamenti, le proteine SR sembrano essere down regolate e defosforilate in seguito a trattamento con il paraquat. Infine, utilizzando diversi inibitori che coinvolgono diversi pathway presenti nella cellula, abbiamo dimostrato che il calcio ha un ruolo nella via di trasduzione del segnale che stiamo osservando. I dati ottenuti non sono ancora conclusivi, ma sicuramente hanno dimostrato una correlazione fra la neurodegenerazione e lo splicing alternativo e hanno posto le basi per capire il modo in cui lo splicing alternativo è modulato nei neuroni in risposta a stimoli esterni.
Mitochondrial damage is linked to many neurodegenerative deseases, such as Parkinson, Alzheimer and Amyotrophic Lateral Sclerosis. These diseases are linked to changes in the splicing pattern of individual mRNAs. Here, we test the hypothesis that mitochondrial damage modulates alternative splicing, not only of a few mRNAs, but in a general manner. We incubated cultured human neuroblastoma cells with the chemical agent paraquat (a neurotoxin that interferes with mitochondrial function, causing energy deficit and oxidative stress) and analysed the splicing pattern of 13 genes by RT-PCR. For each alternatively spliced mRNA, we observed a dose and time dependent increase of the smaller isoforms. In contrast, splicing of all constitutive exons we monitored did not change after paraquat treatment. In addition, we prove that the modulation of alternative splicing by using different drugs correlates with ATP depletion, not with oxidative stress. Such drastic changes in alternative splicing haven’t been observed in cell lines of non-neuronal origin, suggesting a selective susceptibility of neuronal cells to modulation of splicing. Since a significant percentage of all mammalian mRNAs undergoes alternative splicing, we predict that mitochondrial failure will unbalance a large number of isoform equilibriums, thus permitting an important contribution to neurodegeneration. To identify possible drug targets, we tried to understand which is the signal trasduction trasmitting the mitochondrial damage to the splicing machinery. Two classes of proteins determine splice site selection: the hnRNP and the SR proteins. Both of them are phosphorylated and phosphorylation is important for their activity. We have purified hnRNPs and SR proteins from both paraquat-treated and human neuroblastoma control cells and we have studied them with a sub-proteomic approach. While the maps of paraquat-treated and control hnRNPs do not show up significant modifications, the SR proteins appear hypophosphorylated and downregulated by paraquat treatment. Finally, using different inhibitors involving different pathways in the cell, we demonstrate that calcium has a role in the signal trasduction that we are observing. The obtained data are not yet conclusive, but certainly have shown us a correlation between the neurodegeneration and Alternative Splicing. They have laid down the foundation for understanding the way by which the Alternative Splicing is modulated in neurons depending on external stimuli.
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Padovan, Marco. "Interfacce nanostrutturate, dispositivi ottici ed elettronici per lo studio della fisiologia di cellule cerebrali non neuronali." Bachelor's thesis, Alma Mater Studiorum - Università di Bologna, 2018. http://amslaurea.unibo.it/16293/.

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Gli astrociti, cellule non eccitabili del cervello, dapprima considerate solo cellule di supporto all’attività neuronale, hanno un ruolo centrale nella fisiologia cerebrale mantenendo l’omeostasi di ioni, acqua e neurotrasmettitori, e modulando anche l’attività neuronale, attraverso il rilascio di neurotrasmettitori. La disfunzione degli astrociti può concorrere alla patogenesi di neuropatologie acute e croniche come Ischemia o Malattia di Alzheimer. Gli astrociti svolgono li loro funzioni tramite canali ionici, trasportatori e canali per l’acqua e comunicando attraverso segnali di calcio intracellulare. Considerata l’importanza emersa degli astrociti, è fondamentale provvedere alla scoperta dei meccanismi molecolari e funzionali alla base della loro attività. Tuttavia, le metodologie allo stato dell’arte per lo studio della fisiologia astro gliale, sono state sviluppate principalmente per studiare i neuroni. Questo dato potrebbe aver limitato la capacità di comprensione dei suddetti fenomeni. In questo contesto, lo studio di cellule in vitro potrebbe avere grande rilevanza nell’avanzamento della conoscenza dei principi biofisici e molecolari che regolano l’attività degli astrociti. Tuttavia, le proprietà morfologiche e funzionali delle cellule astrogliali in vitro, sono molto diverse da quelle osservate in vivo. In quest’ottica, questo lavoro di tesi è stato focalizzato sullo studio di materiali nanostrutturati e dispositivi bioelettronici, che consentissero di differenziare gli astrociti in vitro e/o di generare strumenti innovativi per lo studio e la modulazione della funzione astrogliale. Studi di biocompatibilità tramite i test di vitalità cellulare, immunofluorescenza e Western Blot, degli astrociti su interfacce nanostrutturate, costituite da idrotalciti, nanofili di silicio e ossido di grafene o da loro derivati, sono stati ricavati dati di notevole importanza per sviluppare dispositivi utili allo studio e alla modulazione della fisiologia astrogliale.
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Torricella, Giulia. "Bioelettronica organica: Nuovi approcci tecnologici per la stimolazione e la rilevazione della comunicazione di cellule neuronali." Bachelor's thesis, Alma Mater Studiorum - Università di Bologna, 2015. http://amslaurea.unibo.it/8520/.

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Il campo della Bioelettronica si è sviluppato a partire dal 18 secolo con l’ esperimento di Luigi Galvani che, applicando uno stimolo elettrico ai muscoli di una rana dissezionata, ne osservò il movimento. Da questo esperimento si è aperta la strada che ha portato ad oggi ad un grande sviluppo tecnologico nella realizzazione di dispositivi elettronici che permettono di offrire un miglioramento generale delle condizioni di vita. Come spesso accade con le tecnologie emergenti, i materiali sono la maggiore limitazione nello sviluppo di nuove applicazioni. Questo è certamente il caso della Bioelettronica. I materiali elettronici organici, nella forma di polimeri conduttivi, hanno mostrato di poter dotare gli strumenti elettronici di grandi vantaggi rispetto a quelli tradizionali a base di silicio, in virtù delle loro proprietà meccaniche ed elettroniche, della loro biocompatibilità e dei bassi costi di produzione. E’ da questi studi che nasce più propriamente il campo della Bioelettronica Organica, che si basa sulla applicazione di semiconduttori a base di carbonio in forma di piccole molecole coniugate e di polimeri, e del loro utilizzo nei dispositivi elettronici. Con il termine di ‘Bioelettronica organica’, quindi, si descrive l’accoppiamento tra dispositivi elettronici organici e il mondo biologico, accoppiamento che si sviluppa in due direzioni: da un lato una reazione o un processo biologico può trasferire un segnale ad un dispositivo elettronico organico, dall’altro un dispositivo elettronico organico può avviare un processo biologico.
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Nizzardo, M. "UTILIZZO E CONFRONTO TRA CELLULE STAMINALI NEURONALI DI DIVERSA ORIGINE: EFFICACIA TERAPEUTICA IN UN MODELLO MURINO DI ATROFIA MUSCOLARE SPINALE." Doctoral thesis, Università degli Studi di Milano, 2009. http://hdl.handle.net/2434/157862.

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Spinal muscular atrophy (SMA), characterized by selective loss of lower motor neurons, is an incurable genetic neurodegenerative disease.and represents one of the most common genetic causes of infant mortality. Patients with SMA exhibit muscle weakness and hypotonia. Stem cell transplantation is a potential therapeutic strategy for SMA and other motor neuronal diseases. In this study, we analized the therapeutic capacity of different stem cells sources in order to improve SMA phenotype in a SMA murine model. First of all we isolated spinal cord neural stem cells (NSCs) from mice expressing green fluorescent protein (GFP) only in motor neurons and assessed their therapeutic effects on the phenotype of SMA mice. Intrathecally grafted NSCs migrated into the parenchyma and generated a small proportion of motor neurons. Treated SMA mice exhibited improved neuromuscular function, increased life span, and improved motor unit pathology NSC transplantation positively affected the SMA disease phenotype, indicating that transplantation of NSCs may be a possible treatment for SMA. However primary NSC as stem cell source have limited translational value. Thus we used alternative stem cells sources, NSC derived from wild-type embryonic stem cells (wt-ESCs) and from a drug-selectable embryonic stem cell line (OSG-ESC. This cells have promise as an unlimited source of NSCs for transplantation. We found that ESC-derived NSCs can differentiated into motor neuron in vitro, and, when intrathecally transplanted into SMA mice survived, migrated, ameliorated behavioral and life-span and may confer neuroprotection in SMA mice. NSCs obtained using a drug-selectable ESC line (positively for neuroepithelial cells and negatively for undifferentiated cells) yielded the greatest improvements. As with cells originating from primary tissue, the ESC-derived NSCs integrated appropriately into the parenchyma, expressing neuron- and motor neuron-specific markers. Our results suggest translational potential for the use of pluripotent cells in NSC-mediated therapies and highlight potential safety improvements and benefits of drug-selection for neuroepithelial cells.
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MERLO, SARA. "Effetti degli estrogeni sul differenziamento e sulla neurodegenerazione in sistemi neuronali in vitro." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2004. http://hdl.handle.net/2108/208233.

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L’obiettivo del presente lavoro è stata l’identificazione di un ruolo per il recettore degli estrogeni (ER) nel neurosviluppo e nella neurodegenerazione, con particolare attenzione al coinvolgimento delle cellule gliali. E’ noto che gli estrogeni influenzano lo sviluppo, la maturazione ed il differenziamento dei neuroni nel sistema nervoso centrale, e che i suoi recettori mostrano un picco di espressione durante le fasi precoci di neurosviluppo. La zona subventricolare del cervello di topo adulto è una ricca fonte di progenitori neurali. Questi possono essere mantenuti in coltura, in un mezzo chimicamente definito contenente il fattore di crescita epidermico (EGF), sottoforma di neurosfere, che possono differenziarsi in neuroni e glia quando piastrate su laminina in assenza di EGF. Il presente studio ha mostrato che gli ER sono espressi nelle neurosfere sia in sospensione che in adesione, ed in particolare ER mostra un picco di espressione durante le fasi più precoci del differenziamento della neurosfera (6-24 ore). Il trattamento con 17-estradiolo 10nM (17-E2) non influenza significativamente la proliferazione nelle neurosfere in sospensione, ma modifica il differenziamento già dopo 6 ore di piastratura su laminina, con un significativo aumento della percentuale di neuroblasti PSA-NCAM-positivi e, successivamente, a 3 giorni, con un aumento nel numero di neuroni MAP2-positivi. Il trattamento con 17-E2 induce inoltre un aumento nella percentuale di cellule GFAP-positive ed un aumento dei livelli proteici di GFAP, con un effetto marcato a 24 ore di piastratura. In uno studio parallelo, è stata valutata la capacità della glia di mediare gli effetti neuroprotettivi degli estrogeni. Il 17-E2 esercita infatti effetti protettivi anche verso la tossicità da beta-amiloide (AP). Al fine di valutare il coinvolgimento degli astrociti in tale fenomeno, il terreno di coltura condizionato da astroglia pre-trattata con 17-E2 per 4 ore, è stato trasferito su neuroni corticali puri trattati per 24 ore con AP25-35 25M. I risultati ottenuti hanno mostrato una aumentata vitalità dei neuroni corticali, effetto che non appare modificato dal trattamento con l’antagonista dei recettori per gli estrogeni ICI 182,780 addizionato direttamente ai neuroni. Il TGF-1 è stato identificato quale fattore solubile responsabile della neuroprotezione indotta dal 17-E2. I livelli di TGF-1 intracellulare e rilasciato aumentano infatti in seguito al trattamento con 17-E2, ed il contenuto intracellulare di TGF-1 nelle cellule positive si riduce, suggerendo che il 17-E2 stimoli prevalentemente il rilascio di tale citochina. Infine, l’incubazione con anticorpo neutralizzante anti-TGF-1 incide significativamente sulla riduzione della morte neuronale indotta dal terreno condizionato da astrociti trattati con 17-E2. Nell’insieme, i risultati ottenuti puntano verso un ruolo chiave dei recettori degli estrogeni nel neurosviluppo e nella neuroprotezione, ed identificano la glia come target primario per l’azione degli estrogeni.
The aim of the present study was the identification of a role for estrogen receptor (ER) in neurodevelopment and neurodegeneration, focusing on the involvement of glial cells. Estrogen is in fact known to affect development, maturation and differentiation of neurons in the central nervous system and its receptors exhibit a peak of expression during early phases of neurodevelopment. The subventricular zone of the adult mouse brain is a source of progenitor cells which can be grown as neurospheres in a chemically defined medium supplemented with epidermal growth factor (EGF), and are able to differentiate into neurons and glia when plated on laminin in the absence of EGF. The present study has indicated that ERs are expressed by both floating and adherent neurospheres, with ER showing a peak of expression during the earlier phases of neurosphere differentiation (6-24 hrs). Treatment with 10 nM 17-Estradiol (17-E2) did not significantly affect proliferation in floating neurospheres, but modified progenitor differentiation as early as 6 hours after plating on laminin, with a marked increase in the percentage of PSA-NCAM-positive neuroblasts, and later on at 3 days post-plating with an increase in MAP2-positive neurons. Treatment with 17-E2 also increased the number of GFAP-positive cells and the levels of GFAP protein with a major effect at 24 hours. In a parallel study, the ability of glia to mediate the neuroprotective effect of estrogen has been evaluated. 17-E2 is known to exert neuroprotective activity also against ß-amyloid (ßAP). To evaluate the involvement of astroglia in this effect, the conditioned medium from astrocytes preexposed to 17-E2 for 4 h was transferred to pure rat cortical neurons challenged with 25M AP25-35 for 24 h. The results obtained have shown an increased viability of cortical neurons. This effect is not modified by treatment with the estrogen receptor antagonist ICI 182,780 added directly to neurons. TGF-1 has been identified as the soluble factor responsible for 17-E2-induced neuroprotection. Accordingly, the intracellular and released levels of TGF-1 are increased by 17-E2 treatment, and the intracellular content of TGF-1 in immunopositive cells is reduced, suggesting that 17-E2 stimulates mainly the release of the cytokine. Finally, incubation with a neutralizing anti-TGF-1 antibody significantly modifies the decrease in neuronal death induced by 17-E2 -treated astrocyte-conditioned medium. Taken together these results point to a key role for estrogen receptor both in neurodevelopment and neurodegeneration and identify glia as a major target for estrogen action.
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Mastromauro, Michela Pia. "La Bioelettronica Organica: approcci tecnologici per la registrazione, stimolazione e la modulazione di segnali elettrofisiologici di cellule neuronali per finalità terapeutiche nell'ambito della medicina neuro-rigenerativa." Bachelor's thesis, Alma Mater Studiorum - Università di Bologna, 2019.

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La Bioelettronica organica è una disciplina sviluppatosi a partire dal XVII secolo con l’esperimento di Luigi Galvani che, applicando uno stimolo elettrico ai muscoli di una rana dissezionata, ne osservò il movimento. La Bioelettronica organica è un’evoluzione della suddetta disciplina nel quale elementi di natura biologica vengono combinati con dispositivi elettronici avanzati, basati sull’utilizzo di materiali organici, con lo scopo di realizzare dispositivi in grado di interagire con la materia vivente per sviluppare nuove metodologie diagnostiche, di analisi e terapeutiche. L’accoppiamento tra dispositivi elettronici organici e il mondo biologico si sviluppa in due direzioni: da un lato una reazione o un processo biologico può trasferire un segnale ad un dispositivo elettronico organico, dall’altro un dispositivo elettronico organico può avviare un processo biologico. In particolare, il mio studio di tesi riguarda l’interazione tra dispositivi elettronici e cellule neuronali in grado sia di riconoscere e analizzare l’attività cerebrale, sia di intervenire sul funzionamento tramite micro-stimoli elettrici localizzati. I materiali elettronici organici, quali polimeri conduttivi e piccole molecole, hanno mostrato di poter consentire la fabbricazione di strumenti elettronici che offrono numerosi vantaggi rispetto a quelli tradizionali a base di silicio, in virtù delle loro proprietà elettroniche e meccaniche, della loro biocompatibilità, dei bassi costi di produzione, così da permettere di minimizzare l’invasività e sviluppare applicazioni sempre più innovative.
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Ronsisvalle, Nicole Victoria. "Effetti protettivi del 1-(3',4'-Dichloro-2-fluoro[1,1'-biphenyl]-4-yl)-cyclo-propanecarboxylic Acid (CHF5074) su cellule neuronali sottoposte a stimoli tossici in vitro." Doctoral thesis, Università di Catania, 2012. http://hdl.handle.net/10761/1114.

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Protective effects of 1-(3',4'-Dichloro-2-fluoro[1,1'-biphenyl]-4-yl)-cyclopropanecarboxylic Acid(CHF5074) on neural cells challenged with toxic stimuli in vitro. Nicole Ronsisvalle, Renato Bernadini,Rosa Chillemi Dept of Clinical and Molecular Biomedicine, section on Pharmacology and Biochemistry, Univ of Catania Sch Med, 95125 Catania, Italy Alzheimer¡¦s disease (AD) is the most common form of dementia. The basic pathological abnormalities in AD brains are: amyloid plaques, neurofibrillary tangles and neuronal loss. Amyloid plaques are composed of £]-amyloid (A£]) peptides that are proteolytically produced from the amyloid precurson protein (APP). APP is initially cleaved by £^-secretase to generate a 99-residue carboxy-terminal fragment that is subsequently cleaved by £^-secretase to generate A£]. 1-(3 S,4 S-Dichloro-2-fluoro[1,1 S-biphenyl]-4-yl)-cyclopropanecarboxylic Acid (CHF5074) has been regarded as a modulator of £^-secretase. Thus, we evaluated the effects of CHF5074 on A£] related TRAIL toxicity in the human neuronal cell line SH-SY5Y, as well as in primary cultures of rat embryo cortical and hippocampal neurons cultured in vitro. All cells were treated 1h with CHF5074 at graded concentrations (range: 1-100 nM) and incubated for 72 h with A£] or TRAIL. Results show that CHF5074 prevented apoptotic death in all the cell types tested in a concentration-dependent fashion. The maximally active concentration was 10nM. In addition, we explored molecular mechanisms underlying the protective effect of the drug. Preliminary data suggest that either Caspases, as well as Stress and MAP kinases are among molecular mechanisms affected by the mode of action of CHF5074. Finally, treatment with CHF5074 has shown that the drug protects neural cells from apoptotic death. Therefore, it could be envisioned that CHF5074 represents a candidate potential therapeutic tool in AD.
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BOVIO, FEDERICA. "The cadmium altered oxidative homeostasis leads to energetic metabolism rearrangement, Nrf2 activation with increased GSH production and reduced SOD1 activity in neural cells." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2021. http://hdl.handle.net/10281/309982.

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Il cadmio, elemento chimico ampiamente usato in ambito industriale, è considerato un contaminante ambientale con effetti tossici sugli organismi viventi. Il suo ingresso nel corpo umano può avvenire per inalazione o ingestione di cibi ed acqua contaminati, fumo di sigaretta o impiego professionale, con tratto respiratorio e gastrointestinale principalmente coinvolti nel suo assorbimento cellulare. Anche il cervello è un bersaglio della tossicità del cadmio, che può entrare nel sistema nervoso centrale tramite una maggiore permeabilità della barriera ematoencefalica o attraverso i nervi olfattivi. Infatti, l'esposizione al cadmio è stata correlata sia ad alterazioni funzionali del sistema nervoso sia a malattie neurodegenerative, come la sclerosi laterale amiotrofica (SLA). Il 90-95% dei casi di SLA sono sporadici (sALS), mentre il restante 5-10% ha origine familiare (fALS), di cui il 15-20% è attribuito a mutazioni nel gene dell’enzima antiossidante superossido dismutasi 1 (SOD1). SOD1 è un omodimero di 32 kDa, in cui ciascun monomero presenta un ponte disulfuro e due ioni metallici, il rame con ruolo catalitico e lo zinco con funzione strutturale. Poiché uno dei principali meccanismi con cui il cadmio esercita la propria tossicità è lo stress ossidativo, responsabile di un insieme di eventi avversi che culminano nella morte cellulare, scopo di questa tesi è lo studio dell'effetto neurotossico del cadmio sul metabolismo energetico nella linea cellulare umana SH-SY5Y, sulle difese antiossidanti in cellule LUHMES differenziate e sulla funzione di SOD1 in tre modelli sperimentali (proteina ricombinante in E. coli, linea cellulare SH-SY5Y e nematode Caenorhabditis elegans). La valutazione del metabolismo energetico in cellule SH-SY5Y trattate per 24 ore con dosi sub-letali di CdCl2 ha evidenziato il passaggio ad un metabolismo anaerobico; infatti cellule trattate mostrano un aumento della glicolisi, una maggiore produzione di ATP per via glicolitica e una ridotta funzionalità mitocondriale rispetto al controllo. L’apporto bioenergetico in presenza di cadmio non altera la dipendenza da glucosio, ma aumenta quella da glutammina riducendo l’apporto derivato dagli acidi grassi. Inoltre, si osserva un aumento del GSH totale, del rapporto GSSG/GSH e della perossidazione lipidica, tutti indici di un'alterata omeostasi ossidativa. Quest’ultima è stata investigata in cellule LUHMES differenziate, in cui 24 ore di esposizione al cadmio hanno determinato, alle dosi più basse, un aumento del livello di GSH totale e un’attivazione di Nrf2 mediata da p21 e P-Akt. Gli effetti negativi del cadmio sulla vitalità cellulare possono essere annullati dall'aggiunta di GSH e dal trattamento in conditioned medium (CM) ottenuto da astrociti o microglia. Nelle LUHMES trattate in CM il livello totale di GSH rimane paragonabile a quello delle cellule non trattate anche alle concentrazioni più elevate di CdCl2. Infine, l’effetto del cadmio, combinato a dosi fisse di rame e/o zinco, sull'attività catalitica della proteina ricombinante GST-SOD1, espressa in E. coli BL21, ha mostrato una riduzione dose-dipendente dell'attività di SOD1 solo in presenza di rame, mentre il livello di espressione proteica rimane sempre costante. Risultati analoghi sono stati ottenuti nella linea cellulare SH-SY5Y, in cui l'attività enzimatica di SOD1 è diminuita in modo sia dose che tempo-dipendente dopo il trattamento con cadmio per 24 e 48 ore, così come nel nematode C. elegans, in cui si osserva una riduzione del 25% nell’attività di SOD1 dopo 16 ore di trattamento con cadmio. In entrambi i casi il livello di espressione proteica dell’enzima rimane invariato. In conclusione, il cadmio ha determinato il passaggio ad un metabolismo più anaerobico, l'attivazione di Nrf2, con conseguente aumento nella produzione di GSH e una riduzione dell'attività di SOD1.
The heavy metal cadmium is a widespread toxic pollutant, released into the environment mainly by anthropogenic activities. Human exposure can occur through different sources: occupationally or environmentally, with its uptake through inhalation of polluted air, cigarette smoking or ingestion of contaminated food and water. It mainly enters the human body through the respiratory and the gastrointestinal tract and it accumulates in liver and kidneys. Brain is also a target of cadmium toxicity, since this toxicant may enter the central nervous system by increasing blood brain barrier permeability or through the olfactory nerves. In fact, cadmium exposure has been related to impaired functions of the nervous system and to neurodegenerative diseases, like amyotrophic lateral sclerosis (ALS). ALS is a fatal motor neuron pathology with the 90-95% of ALS cases being sporadic (sALS), while the remaining 5-10% of familial onset (fALS); among fALS, the 15-20% is attributed to mutations in superoxide dismutase 1 (SOD1). SOD1 is an antioxidant protein responsible for superoxide anions disruption and it is a homodimeric metalloenzyme of 32 kDa mainly located in the cytoplasm, with each monomer binding one catalytic copper ion and one structural zinc ion within a disulfide bonded conformer. Since oxidative stress is one of the major mechanisms of cadmium induced toxicity and an alteration of oxidative homeostasis, through depletion of antioxidant defences, is responsible for a plethora of adverse outcoming mainly leading to cell death; we focused on cadmium effect (1) on the energetic metabolism in human neuroblastoma SH-SY5Y cell line, (2) on the oxidative defences responses in differentiated human LUHMES neural cell line and (3) on the function of human SOD1 in a three models approach (recombinant protein in E. coli, in SH-SY5Y cell line and in the nematode Caenorhabditis elegans). The evaluation of energetic metabolism of SH-SY5Y neural cells treated with sub-lethal CdCl2 doses for 24 hours, showed an increase in glycolysis compared to control. This shift to anaerobic metabolism has been confirmed by both glycolytic parameters and greater ATP production from glycolysis than oxidative phosphorylation, index of less mitochondrial functionality in cadmium treated cells. Regarding the fuel oxidation cadmium caused an increase in glutamine dependency and a specular reduction in the fatty acids one, without altering the glucose dependency. Moreover, we observed an increase in total GSH, in the GSSG/GSH ratio and in lipid peroxidation, all index of an altered oxidative homeostasis better investigated in LUHMES cells. In this model a 24h cadmium administration enhanced the total GSH content at the lower doses, at which also activates Nrf2 through a better protein stabilization via p21 and P-Akt. The metal adverse effects on cell viability can be rescued by GSH addition and by cadmium treatment in astrocytes- or microglia-conditioned medium. In the latter cases the total GSH level remains comparable to untreated cells even at higher CdCl2 concentrations. Finally, SOD1 catalytical activity has been investigated in the presence of cadmium. The first evaluation of this metal combined with fixed copper and/or zinc on the recombinant GST-SOD1, expressed in E. coli BL21, showed a dose-dependent reduction in SOD1 activity only when copper is added to cellular medium, while the expression remains always constant. Similar results were obtained in SH-SY5Y cell line, in which SOD1 enzymatic activity decreased in a dose- and time-dependent way after cadmium treatment for 24 and 48 hours, without altering its expression; as well as in the Caenorhabditis elegans model, where a 16 hours cadmium treatment caused a 25% reduction only in SOD1 activity. In conclusion, cadmium caused a shift to anaerobiosis, a Nrf2 activation, with increased GSH production, and a reduction in SOD1 activity.
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Books on the topic "Cellule neuronali"

1

1935-, Jacklet Jon W., ed. Neuronal and cellular oscillators. New York: Marcel Dekker, 1989.

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M, Baudry, Thompson Richard F, and Davis Joel L. 1942-, eds. Synaptic plasticity: Molecular, cellular, and functional aspects. Cambridge, Mass: MIT Press, 1993.

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Ehrlich, Yigal H., ed. Molecular and Cellular Mechanisms of Neuronal Plasticity. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-4869-0.

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Nguyen, Laurent, and Simon Hippenmeyer, eds. Cellular and Molecular Control of Neuronal Migration. Dordrecht: Springer Netherlands, 2014. http://dx.doi.org/10.1007/978-94-007-7687-6.

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Gregory, Bock, O'Connor Maeve, and Ciba Foundation, eds. Selective neuronal death. Chichester: Wiley, 1987.

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T, Roska, ed. Cellular neural networks and visual computing: Foundation and applications. Cambridge: Cambridge University Press, 2002.

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C, O'Neill, and Anderton B, eds. Neuronal signal transduction and Alzheimer's disease. London: Portland Press, 2001.

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A, Boulton A., Baker Glen B. 1947-, and Walz Wolfgang, eds. The Neuronal microenvironment. Clifton, N.J: Humana Press, 1988.

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Time to eat: Links between neuronal function and cellular phagocytosis. [New York, N.Y.?]: [publisher not identified], 2015.

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Walkinshaw, Gail. An investigation into cellular and molecular mechanisms of neurotoxin-induced neuronal celldeath. Manchester: University of Manchester, 1996.

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Book chapters on the topic "Cellule neuronali"

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Goldman, Jennifer S., and Timothy E. Kennedy. "Neuronal Domains." In Cellular Domains, 371–90. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2011. http://dx.doi.org/10.1002/9781118015759.ch22.

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Gustafsson, L. E., C. U. Wiklund, N. P. Wiklund, and L. Stelius. "Subclassification of Neuronal Adenosine Receptors." In Purines in Cellular Signaling, 200–205. New York, NY: Springer New York, 1990. http://dx.doi.org/10.1007/978-1-4612-3400-5_30.

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Bruzzone, Matteo, Enrico Chiarello, Andrea Maset, Aram Megighian, Claudia Lodovichi, and Marco dal Maschio. "Light-Based Neuronal Circuit Probing in Living Brains at High Resolution: Constraints and Layouts for Integrating Neuronal Activity Recording and Modulation in Three Dimensions." In Neuromethods, 75–100. New York, NY: Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-2764-8_3.

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AbstractUnderstanding how the brain orchestrates neuronal activity to finely produce and regulate behavior is an intriguing yet challenging task. In the last years, the progressive refinement of optical techniques and light-based molecular tools allowed to start addressing open questions in cellular and systems neuroscience with unprecedented resolution and specificity. Currently, all-optical experimental protocols for simultaneous recording of the activity of large cell populations with the concurrent modulation of the firing rate at cellular resolution represent an invaluable tool. In this scenario, it is becoming everyday more evident the importance of sampling and probing the circuit mechanisms not just in a single plane, but extending the exploration to the entire volume containing the involved circuit components. Here, we focus on the design principles and the hardware architectures of all-optical approaches allowing for studying the neuronal dynamics at cellular resolution across a volume of the brain.
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Sotelo, J. R., J. M. Verdes, A. Kun, J. C. Benech, J. R. A. Sotelo Silveira, and A. Calliari. "Regulation of Neuronal Protein Synthesis by Calcium." In Calcium and Cellular Metabolism, 125–42. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4757-9555-4_11.

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Hara, Hirokazu, and Elias Aizenman. "Oxidative Stress and Neuronal Zinc Signaling." In Zinc Signals in Cellular Functions and Disorders, 55–87. Tokyo: Springer Japan, 2014. http://dx.doi.org/10.1007/978-4-431-55114-0_4.

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Nakaishi, Hitoshi. "Functionally Distinct Oncogenes Differently Regulate Cellular Expression of Gangliosides." In Gangliosides and Modulation of Neuronal Functions, 325–26. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71932-5_30.

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Timofeev, Igor, Maxime E. Bonjean, and Maksim Bazhenov. "Cellular Mechanisms of Thalamocortical Oscillations in the Sleeping Brain." In Neuronal Oscillations of Wakefulness and Sleep, 119–70. New York, NY: Springer New York, 2020. http://dx.doi.org/10.1007/978-1-0716-0653-7_5.

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Augusti-Tocco, G., S. Biagioni, M. Plateroti, G. Scarsella, and A. L. Vignoli. "Cellular and Molecular Aspects of Neuronal Differentiation." In The Changing Visual System, 311–18. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3390-0_23.

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Neumann, H., and H. Wekerle. "Neuronal Modulation of the Immune Response in Nervous Tissue: Implications for Neurodegenerative and Autoimmune Diseases." In Cellular Therapy, 119–28. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-662-03509-2_8.

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Moorhouse, A. A., and J. Nabekura. "Cellular Mechanisms of Neuronal Cl− Homeostasis and its Modulation by Neuronal Injury." In Inhibitory Synaptic Plasticity, 123–34. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-6978-1_9.

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Conference papers on the topic "Cellule neuronali"

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Shin, Sangho, Davide Sacchetto, Yusuf Leblebici, and Sung-Mo Steve Kang. "Neuronal spike event generation by memristors." In 2012 13th International Workshop on Cellular Nanoscale Networks and their Applications (CNNA 2012). IEEE, 2012. http://dx.doi.org/10.1109/cnna.2012.6331427.

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Roukes, Michael L. "The Integrated Neurophotonics Paradigm." In CLEO: Applications and Technology. Washington, D.C.: Optica Publishing Group, 2022. http://dx.doi.org/10.1364/cleo_at.2022.ath4i.6.

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Integrated neurophotonics can surmount limitations of existing methodologies to enable fast and dense large-scale functional imaging of neuronal activity from within the brain itself. Implantable lens-less nanophotonic arrays yield cellular resolution at arbitrary brain depths.
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Li, Lulu, Alexander Davidovich, Jennifer Schloss, Uday Chippada, Rene Schloss, Noshir Langrana, and Martin Yarmush. "Control of Neural Lineage Differentiation in an Alginate Encapsulation Microenvironment via Cellular Aggregation." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206496.

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Cell replacement therapies, which utilize renewable stem cell sources, hold tremendous potential to treat a wide range of degenerative diseases. Although many studies have established techniques to successfully differentiate stem cells into different mature cell lineages, their practicality is limited by the lack of control during the differentiation process and low yields of differentiated cells. In order to address these issues, we have previously established a murine embryonic stem cell alginate-poly-L-lysine microencapsulation differentiation system [1]. We demonstrated that ES cell differentiation could be mediated by cell-cell aggregation in the encapsulation microenvironment. We have demonstrated that both cell aggregation and hepatocyte functions, such as urea and albumin secretions, as well as increased expression of cytokeratin 18 and cyp4507a, occur concomitantly with surface E-cadherin expression [2]. In the present studies, we assessed the feasibility of inducing neuronal lineage differentiation in the alginate microenvironment by incorporating soluble inducers, such as retinoic acid, into the permeable microcapsule system. We demonstrated decreased cell aggregation and enhanced neuronal lineage differentiation with the expression of various neuronal specific markers, including neurofilament, A2B5, O1 and glial fibrillary acidic protein (GFAP). In addition, we demonstrated that, by blocking the cell aggregation using anti-E-cadherin antibody, encapsulated cells increased neuronal marker expression at a later stage of the encapsulation, even in the absence of retinoic acid. In conjunction with the mechanical and physical characterizations of the alginate crosslinking network, we show that 2.2% alginate concentration is most conducive to neuronal differentiation from embryonic stem cells in the presence of retinoic acid.
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Wagner, Omer, Alexander K. Winkel, Eva Kreysing, and Kristian Franze. "Multimodal imaging using combined Optical Fourier Ptychographic Microscopy and Atomic Force Microscopy for biological measures." In CLEO: Applications and Technology. Washington, D.C.: Optica Publishing Group, 2022. http://dx.doi.org/10.1364/cleo_at.2022.atu5i.3.

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We present a platform that perform live imaging using Fourier Ptychographic Microscopy co-localised with Atomic Force Microscopy. This specially fit emerging research on cellular biological processes regulated by tissue mechanics, including neuronal growth and stem-cell differentiation.
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Me´ndez-Rojas, Miguel A., Claudia Cravioto Guzman, and Oscar Arias-Carrion. "Synthesis and Chemical Functionalization of Ferromagnetic Nanoparticles to Manipulate Stem Cells Using External Magnetic Fields." In ASME 2007 5th International Conference on Nanochannels, Microchannels, and Minichannels. ASMEDC, 2007. http://dx.doi.org/10.1115/icnmm2007-30188.

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The human brain is able to respond to several situations that promotes neural survivance, growth and neuronal cells regeneration. The potential of stem cells from the subventricular zone to be used for neuronal cell substitution has been widely studied. However, migration of endogen or transplanted cells is random, not efficient and with a very low survivance rate. The use of ferromagnetic nanoparticles may be of interest to guide the stem cells to the desired site using external fields. In this project, we have synthesized ferromagnetic nanoparticles (magnetite) with an average diameter of 10–12 nm, and functionalized with folic acid-flourosceine (with an average yield of 60–70%) in order to induce their entry into rat neuronal precursor cells in vivo and in vitro. The efficiency of cellular incorporation was low in vitro, observing clustering of the nanoparticles at the cytoplasm membrane. During the in vivo tests, no incorporation of nanoparticles was detected. Several results and perspectives are discussed in this work.
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Li, Lulu, Rene Schloss, Noshir Langrana, and Martin Yarmush. "Effects of Encapsulation Microenvironment on Embryonic Stem Cell Differentiation." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192587.

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Pluripotent embryonic stem cells represent a promising renewable cell source to generate a variety of differentiated cell types. Although many investigators have described techniques to effectively differentiate stem cells into different mature cell lineages, their practicality is limited by the absence of large scale processing consideration and low yields of differentiated cells. Previously we have established a murine embryonic stem cell alginate-poly-l-lysine microencapsulation differentiation system. The three-dimensional alginate microenvironment maintains cell viability, is conducive to ES cell differentiation to hepatocyte lineage cells, and maintains differentiated cellular function. In the present work, we demonstrate that hepatocyte differentiation is mediated by cell-cell aggregation in the encapsulation microenvironment. Both cell aggregation and hepatocyte functions, such as urea and albumin secretion, as well as increased expression of cytokaratin 18 and cyp4507a, occur concomitantly with surface E-cadherin expression. Furthermore, by incorporating soluble inducers, such as retinoic acid, into the permeable microcapsule system, we demonstrate decreased cell aggregation and enhanced neuronal lineage differentiation with the expression of various neuronal specific markers, including neurofilament, A2B5, O1 and GFAP. Therefore, as a result of capsule parameter and microenvironment manipulation, we are capable of targeting cellular differentiation to both endodermal and ectodermal cell lineages.
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Silvestri, Ludovico, Nikita Rudinskiy, Marco Paciscopi, Marie Caroline Müllenbroich, Irene Costantini, Leonardo Sacconi, Paolo Frasconi, Bradley T. hyman, and Francesco S. Pavone. "Brain-wide charting of neuronal activation maps with cellular resolution." In Bio-Optics: Design and Application. Washington, D.C.: OSA, 2015. http://dx.doi.org/10.1364/boda.2015.brm3b.6.

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Hyttinen, Jari, Barbara Genocchi, Annika Ahtiainen, Jarno M. A. Tanskanen, Kerstin Lenk, and Michael Taynnan Barros. "Astrocytes in modulating subcellular, cellular and intercellular molecular neuronal communication." In NANOCOM '21: The Eighth Annual ACM International Conference on Nanoscale Computing and Communication. New York, NY, USA: ACM, 2021. http://dx.doi.org/10.1145/3477206.3477460.

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Silvestri, Ludovico, Nikita Rudinskiy, Marco Paciscopi, Marie Caroline Müllenbroich, Irene Costantini, Leonardo Sacconi, Paolo Frasconi, Bradley T. Hyman, and Francesco S. Pavone. "Brain-wide charting of neuronal activation maps with cellular resolution." In Optics and the Brain. Washington, D.C.: OSA, 2015. http://dx.doi.org/10.1364/brain.2015.brm3b.6.

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Brattain, Laura J., Brian A. Telfer, Siddharth Samsi, Taeyun Ku, Heejin Choi, and Kwanghun Chung. "Automated dense neuronal fiber tracing and connectivity mapping at cellular level." In 2017 IEEE 14th International Symposium on Biomedical Imaging (ISBI 2017). IEEE, 2017. http://dx.doi.org/10.1109/isbi.2017.7950531.

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