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Suman, Matteo (2013) Effetti degli ormoni steroidei nell'omeostasi intracellulare del calcio e nella regolazione della crescita cellulare in cellule derivate da cervelletto di feto bovino. [Tesi di dottorato]

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Abstract (inglese)

ABSTRACT

Steroid hormones differently affect various physiological processes by genomic or non-genomic mechanisms, in both excitable and non-excitable cells. Neurosteroids play a key role in the regulation of many cellular processes, such as cell growth, cell differentiation and apoptosis, exerting their effect in different ways (i.e. promoting or inhibiting a particular event) depending on the brain region of action. In this work two different themes were investigated: 1) the slow genomic effects exerted by estradiol (E2) and testosterone (T) in the regulation of intracellular calcium (Ca2+) homeostasis in a non-excitable cellular model; 2) the trophic effects promoted by estrogens in neuronal cells and in their dendritic branches. Recent experimental evidences highlight the involvement of estrogens and androgens in the regulation of intracellular homeostasis of calcium ion (Ca2+), one of the most important second messengers mediating steroid hormones action. The effects of neurosteroids on excitable cells are well documented; however, these steroids also influence numerous physiological events in non-excitable cells, such as fibroblasts or vascular endothelial cells. In the first part of this work I have focused my attention on an immortalized endothelial-like cell line derived from fetal bovine cerebellum. E2 (10nM) and T (10nM) effects on intracellular Ca2+ homeostasis were tested by varying the exposure time to the hormones (8, 24, 48 h). Ca2+ measurements were performed with genetically encoded Ca2+ probes (Cameleons) targeted to the main subcellular compartments involved in intracellular Ca2+ homeostasis (cytosol, endoplasmic reticulum, mitochondria). While T treatment had not any effect on intracellular Ca2+ fluxes, mitochondrial Ca2+ uptake significantly decreased after 48-h exposure to E2, whereas cytosolic and endoplasmic reticulum responses were unaffected. The effect of E2 on mitochondrial Ca2+ handling was blocked by ICI 182,780 (10nM), a pure estrogen receptor antagonist, suggesting that the effect was estrogen-receptor–mediated. To investigate further the effect of E2 on mitochondria, we tested two other concentrations of E2 (1 nM and 100 nM) and we observed a similar effect on the Ca2+ peak decrease indicating that saturation was possibly reached at 1 nM. To evaluate whether the decrease of Ca2+ affected mitochondrial membrane potential (ΔΨm), cells were monitored in the presence of tetra-methyl-rhodamine-methylester (TMRM): no significant changes were seen between cells treated with E2 and controls. To investigate a mechanism of action, we assessed the possibile involvement of the permeability transition pore (PTP), an inner mitochondrial membrane channel influencing energy metabolism and cell viability. We treated cells with CyclosporinA (CsA) (0.8μM), which binds to the matrix chaperone cyclophilin-D and regulates PTP opening. CsA reversed the effects of a 48-h treatment with E2, suggesting a possible transcriptional modulation of proteins involved in the mitochondrial permeability transition process. Taken together, these data reveal that, in this immortalized endothelial-like cell line, the genomic effect exerted by E2 can affect PTP opening without causing a collapse in ΔΨm.
In the second part of this study I examined the effects of estradiol in the regulation of the growth of neuronal cells and of their dendritic branches. Dendrites are the principal cellular sites where neurons receive, process, and integrate inputs from their multiple pre-synaptic partners. It is widely known that, in early developmental stages, estrogens modulate neuronal morphology through a regulation of dendritic development. Estrogens regulate neuronal plasticity, synaptogenesis and cellular growth in many brain regions, such as cortex and hypothalamus. Few papers focused on what estrogens cause in the morphology of cerebellum, a region of the brain with a crucial role in controlling balance, posture, motor coordination as well as many other cognitive processes. To characterize the trophic effects of E2, primary neuronal cells from bovine cerebellum of both male and female fetuses were analyzed. To highlight differences in the morphological organization of neuronal cells we performed fluorescent-immunocytochemical analysis using a specific marker of immature neurons (βIII-tubulin). The whole area and the whole perimeter of neuronal cells, the number, the length and the diameter of dendritic branches were estimated and comparisons between E100nM samples and control cells were performed; differences intra sex were also considered. Results indicate that E100nM increases all the parameters in cells from females, while in males the trophic effect is restricted only to some values. Moreover, females have greater values than males in the soma dimensions, in the total number of branches and in the length of dendritic branches. On the contrary, males show superior values in the diameter of dendrites. Taken together, these preliminary data suggest that E100nM produces a trophic effect in both male and female samples; since several differences between males and females emerged, it could be supposed that neurons of the cerebellum in this embryonic stage exhibit dimorphic properties.

Abstract (italiano)

SOMMARIO

Gli ormoni steroidei possono influenzare numerosi processi fisiologici attraverso meccanismi genomici e non genomici, sia in cellule eccitabili che in cellule non eccitabili. I neurosteroidi regolano numerosi processi cellulari (come la crescita e il differenziamento cellulare, e l’apoptosi) ed esercitano il loro effetto in svariati modi, ad esempio promuovendo o inibendo un particolare evento, a seconda della regione dell’encefalo in cui stanno agendo. In questo elaborato sono state approfondite due diverse tematiche: 1) lo studio dell’effetto genomico esercitato dall’estradiolo (E2) e dal testosterone (T) nella regolazione dell’omeostasi intracellulare dello ione calcio (Ca2+) in una linea cellulare non eccitabile; 2) la caratterizzazione dell’effetto trofico dell’E2 in cellule neuronali e nelle loro arborizzazioni dendritiche. Numerose evidenze sperimentali dimostrano che estrogeni ed androgeni regolano l’omeostasi intracellulare dello ione Ca2+. Gli effetti dei neurosterodi nelle cellule eccitabili sono ben noti; tuttavia, questi ormoni influenzano in maniera significativa anche la fisiologia di cellule non eccitabili, come i fibroblasti e le cellule dell’endotelio vascolare. Per questo primo argomento di studio ho utilizzato una linea cellulare stabilizzata derivata da cellule endoteliali isolate da cervelletto di feto bovino. Per caratterizzare gli effetti genomici prodotti da E2 (10nM) e T (10nM) sull’omeostasi intracellulare di Ca2+, le cellule sono state incubate con gli ormoni a diversi intervalli di tempo (8, 24, 48 ore). Quindi sono state usate sonde fluorescenti per il Ca2+ (Cameleon) indirizzate ai principali organelli intracellulari deputati al controllo dell’omeostasi di questo ione (citoplasma, reticolo endoplasmatico, mitocondri). I risultati dimostrano che il trattamento con T non produce alcun effetto. Nelle cellule incubate con E2, non sono state riscontrate variazioni né in citoplasma né in reticolo; al contrario, l’E2 incubato per 48 ore ha prodotto una diminuzione significativa nella quantità totale di Ca2+ misurata nei mitocondri. Questo effetto è stato annullato dall’aggiunta di ICI 182,780 (10nM), un antagonista non selettivo dei recettori degli estrogeni, suggerendo che l’azione dell’E2 è mediata dai propri recettori. In seguito sono state testate altre due concentrazioni di E2 (1nM e 100nM): anch’esse hanno causato una analoga diminuzione della quantità di Ca2+ nei mitocondri, suggerendo che la saturazione del recettore può avvenire già alla concentrazione 1nM. Per verificare se le alterazioni nei flussi di Ca2+ dovute all’E2 comportassero alterazioni nel potenziale di membrana mitocondriale (ΔΨm), le cellule sono state monitorate in presenza del tetra-methyl-rhodamine-methylester (TMRM) ma non è stata riscontrata alcuna differenza tra le cellule trattate e quelle di controllo. Infine, per verificare un possibile ruolo svolto dal poro di transizione di permeabilità (PTP), un canale della membrana interna mitocondriale, le cellule sono state trattate con ciclosporina-A (CsA) (0.8μM), uno specifico inibitore del PTP che si lega alla molecola chaperone di matrice ciclofilina-D. La CsA è stata in grado di invertire l’effetto dell’E2, riportando i valori dei trattati a quelli dei controlli e suggerendo che l’ormone possa svolgere un ruolo chiave nel processo di transizione di permeabilità mitocondriale (PTPM). Riassumendo, questi dati indicano che, in questa linea stabilizzata con caratteristiche endoteliali, l’effetto genomico prodotto dall’E2 può influenzare l’apertura del PTP senza causare una perdita del potenziale di membrana. Terminata questa prima fase del lavoro, mi sono dedicato allo studio dell’effetto trofico che l’E2 produce in cellule neuronali e nelle loro arborizzazioni dendritiche. I dendriti integrano e trasportano gli stimoli nervosi dalla periferia della cellula verso il soma ed è ampiamente riconosciuto che, nelle fasi precoci dello sviluppo embrionale, l’E2 modella la morfologia delle cellule neuronali attraverso una regolazione dello sviluppo delle arborizzazioni dendritiche. Gli estrogeni regolano la plasticità neuronale, la sinaptogenesi e la crescita cellulare in diverse regioni del SNC, come ad esempio la corteccia e l’ipotalamo. Pochi lavori hanno considerato gli effetti dell’E2 nella morfologia dei neuroni del cervelletto, una regione deputata al controllo dell’equilibrio, , della coordinazione motoria e di svariati altri processi cognitivi. Per questo tipo di analisi ho utilizzato colture cellulari primarie di neuroni derivate da cervelletto di feti di bovino di entrambi i sessi. Per mettere in evidenza le alterazioni morfologiche nei neuroni ho effettuato esperimenti di immunocitochimica in fluorescenza usando uno specifico anticorpo per neuroni immaturi, la βIII-tubulina, confrontando gli effetti dell’E2 (100nM) in cellule trattate rispetto a neuroni di controllo. Come parametri morfometrici ho scelto: area e perimetro del soma, numero, lunghezza e diametro dei prolungamenti dendritici. I risultati indicano che nelle cellule da femmina, l’E2 aumenta tutti i parametri misurati, mentre nei maschi l’effetto trofico è limitato solo ad alcuni valori. Inoltre, le femmine mostrano valori maggiori rispetto ai maschi nelle dimensioni del soma, nel numero e nella lunghezza dei prolungamenti. Al contrario nei maschi si osserva un valore superiore nel diametro dei prolungamenti. Questi dati preliminari suggeriscono che l’E2 (100nM) produce un effetto trofico sia nelle cellule di maschio che in quelle di femmina; inoltre è possibile ipotizzare che, in questo stadio dello sviluppo embrionale, i neuroni di cervelletto abbiamo caratteristiche dimorfiche.

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Tipo di EPrint:Tesi di dottorato
Relatore:Ballarin, Cristina
Dottorato (corsi e scuole):Ciclo 25 > Scuole 25 > SCIENZE VETERINARIE > SCIENZE BIOMEDICHE VETERINARIE E COMPARATE
Data di deposito della tesi:29 Gennaio 2013
Anno di Pubblicazione:Gennaio 2013
Parole chiave (italiano / inglese):ormoni steroidei, estradiolo, testosterone, cervelletto, bovino, effetti genomici, omeostasi del calcio, mitocondri, poro di transizione di permeabilità, crecita cellulare, dendriti
Settori scientifico-disciplinari MIUR:Area 07 - Scienze agrarie e veterinarie > VET/01 Anatomia degli animali domestici
Struttura di riferimento:Dipartimenti > Dipartimento di Biomedicina Comparata ed Alimentazione
Codice ID:5658
Depositato il:14 Ott 2013 09:49
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