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1دورية أكاديمية
المساهمون: Olivetto, Elena, Simoni, Edi, Guaran, Valeria, Astolfi, Laura, Martini, Alessandro
مصطلحات موضوعية: ABR, Bcl-2, Cyt-c, HIF-1α, IHC, JNK, MAPK, MYH-6, NF-200, NF-kB, OHC, PJNK, ROS, TF, TM, TSH, Sensory Systems
الوصف: Hearing loss may be genetic, associated with aging or exposure to noise or ototoxic substances. Its aetiology can be attributed to vascular injury, trauma, tumours, infections or autoimmune response. All these factors could be related to alterations in cochlear microcirculation resulting in hypoxia, which in turn may damage cochlear hair cells and neurons, leading to deafness. Hypoxia could underlie the aetiology of deafness, but very few data about it are presently available. The aim of this work is to develop animal models of hypoxia and ischemia suitable for study of cochlear vascular damage, characterizing them by electrophysiology and gene/protein expression analyses. The effects of hypoxia in infarction were mimicked in rat by partial permanent occlusion of the left coronary artery, and those of ischemia in thrombosis by complete temporary carotid occlusion. In our models both hypoxia and ischemia caused a small but significant hearing loss, localized at the cochlear apex. A slight induction of the coagulation cascade and of oxidative stress pathways was detected as cell survival mechanism, and cell damages were found on the cuticular plate of outer hair cells only after carotid ischemia. Based on these data, the two developed models appear suitable for in vivo studies of cochlear vascular damage.
وصف الملف: STAMPA
العلاقة: info:eu-repo/semantics/altIdentifier/pmid/25987500; info:eu-repo/semantics/altIdentifier/wos/WOS:000361251900007; volume:327; firstpage:58; lastpage:68; numberofpages:11; journal:HEARING RESEARCH; http://hdl.handle.net/11577/3173460Test; info:eu-repo/semantics/altIdentifier/scopus/2-s2.0-84930638534; www.elsevier.com/locate/heares
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2دورية أكاديمية
المساهمون: Franchi, Nicola, Schiavon, Filippo, Michele, Betti, Laura, Canesi, Ballarin, Loriano
مصطلحات موضوعية: Phagocytosi, Botryllu, signal transduction, MAPK, NF-kB
الوصف: Tunicates are chordate invertebrates, closely related to vertebrates, which represent valuable organisms for the study of a variety of biological processes from an evolutionary point of view. As invertebrates, they rely on innate immunity to cope with foreign, potentially pathogenic material. Among tunicates, the compound ascidian Botryllus schlosseri is emerging as a reliable model organism for the study of innate immune responses. However, there is a general lack of knowledge on the signalling pathways activated during immune responses and, in particular, in phagocytosis. In the present work, we carried out a preliminary investigation of the signalling pathways involved in phagocytosis, with particular reference to MAPK activation. We studied in vitro zymosan phagocytosis in the presence of manumycin A, which inhibit the activation of Ras, PD98059, SP600125 and SB202190, inhibitors of Erk, JNK and p38, respectively, parthenolide, N-acetyl-L-cysteine (NAC) and pyrrolidine dithiocarbamate (PDTC), inhibiting NF-kB activation. In addition we carried out immunoblot and immunocytochemistry analysis with the use of anti-pErk1/2, anti-pp38, anti-pJNK, anti-NF-kB (p50) and antipan Ras antibodies. Results demonstrate that the recognition of foreign cells triggers a phosphorylation cascade leading to the activation of Ras-like small GTPases, MAPKs and NF-kB and argue in favour of a conservation, also in ascidians, of the main signalling pathways.
وصف الملف: STAMPA
العلاقة: info:eu-repo/semantics/altIdentifier/pmid/23262395; info:eu-repo/semantics/altIdentifier/wos/WOS:000315478300009; volume:112; firstpage:260; lastpage:266; numberofpages:7; journal:JOURNAL OF INVERTEBRATE PATHOLOGY; http://hdl.handle.net/11577/2551083Test; info:eu-repo/semantics/altIdentifier/scopus/2-s2.0-84872680965
