title: Acetyl-L-carnitine up-regulates expression of voltage-dependent anion channel in the rat brain.
abstract: Acetyl-L-carnitine (ALC) exerts unique neuroprotective, neuromodulatory, and neurotrophic properties, which play an important role in counteracting various pathological processes, and have antioxidative properties, protecting cells against lipid peroxidation. In this study, suppression subtractive hybridization (SSH) method was applied for the generation of subtracted cDNA libraries and the subsequent identification of differentially expressed transcripts after treatment of rats with ALC. The technique generates an equalized representation of differentially expressed genes irrespective of their relative abundance and it is based on the construction of forward and reverse cDNA libraries that allow the identification of the genes that are regulated after ALC treatment. In the present paper, we report the identification of the gene of mitochondrial voltage-dependent anion channel (VDAC) protein which is positively modulated by the ALC treatment. VDAC is a small pore-forming protein of the mitochondrial outer membrane. It represents an interesting tool for Ca(2+) homeostasis, and it plays a central role in apoptosis. In addition, VDAC seems to have a relevant role in the synaptic plasticity.
authors.affiliation: Dipartimento di Fisiologia e Biochimica G. Moruzzi, Università di Pisa, Via S. Zeno, 56127 Pisa, Italy.
authors.forename: Giovanna
authors.initials: G
authors.lastname: Traina
authors.forename: Rodolfo
authors.initials: R
authors.lastname: Bernardi
authors.forename: Milena
authors.initials: M
authors.lastname: Rizzo
authors.forename: Menotti
authors.initials: M
authors.lastname: Calvani
authors.forename: Mauro
authors.initials: M
authors.lastname: Durante
authors.forename: Marcello
authors.initials: M
authors.lastname: Brunelli
mesh_terms: D000108:Acetylcarnitine / Q000378:metabolism* / Q000494:pharmacology; D000818:Animals; D017209:Apoptosis / Q000187:drug effects / Q000502:physiology; D001921:Brain / Q000187:drug effects / Q000378:metabolism*; D020013:Calcium Signaling / Q000187:drug effects / Q000502:physiology; D016172:DNA Fingerprinting; D005786:Gene Expression Regulation / Q000187:drug effects / Q000502:physiology; D015723:Gene Library; D008297:Male; D008928:Mitochondria / Q000187:drug effects / Q000378:metabolism*; D051336:Mitochondrial Membranes / Q000187:drug effects / Q000378:metabolism*; D009473:Neuronal Plasticity / Q000187:drug effects / Q000502:physiology; D018697:Nootropic Agents / Q000378:metabolism / Q000494:pharmacology; D012333:RNA, Messenger / Q000187:drug effects / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D015854:Up-Regulation / Q000187:drug effects / Q000502:physiology*; D050995:Voltage-Dependent Anion Channel 1 / Q000235:genetics*
chemical_list: D018697:Nootropic Agents; D012333:RNA, Messenger; C494764:Vdac1 protein, rat; D000108:Acetylcarnitine; D050995:Voltage-Dependent Anion Channel 1