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001-es BibID:	BIBFORM050560
Első szerző:	Mistry, Shilpa
Cím:	Prolonged exposure to bradykinin and prostaglandin E2 increases TRPV1 mRNA but does not alter TRPV1 and TRPV1b protein expression in cultured rat primary sensory neurons / Shilpa Mistry, Cleoper C. Paule, Angelika Varga, Andy Photiou, Agnes Jenes, Antonio Avelino, Laki Buluwela, Istvan Nagy
Dátum:	2014
ISSN:	0304-3940
Megjegyzések:	Sensitisation of the capsaicin receptor, transient receptor potential vanilloid type 1 (TRPV1) ion channel in nociceptive primary sensory neurons (PSN) underlies the development of inflammatory heat hyperalgesia. Removal of the negative-dominant splice variant of the TRPV1 molecule, TRPV1b from TRPV1/TRPV1b heterotetrameric channels, which should be associated with changes in the expression of TRPV1 and TRPV1b transcripts and proteins, has been suggested to contribute to that sensitisation. Respective reverse-transcriptase polymerase chain reaction (RT-PCR) and Western-blotting revealed that both TRPV1 and TRPV1b mRNA, and their encoded proteins are expressed in rat cultured PSN. Sequencing of the RT-PCR products showed that TRPV1b mRNA lacks the entire exon 7. Further, growing PSN for 2 days in the presence of 10műM bradykinin (BK) and 10műM prostaglandin E2 (PGE2) significantly increases TRPV1 responsiveness and TRPV1 mRNA expression, without producing any changes in TRPV1b mRNA, and TRPV1 and TRPV1b protein expression. These data challenge the hypothesis that alterations in the composition of the TRPV1 ion channel contributes to the sensitisation.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	Neuroscience Letters. - 564 (2014), p. 89-93. -
További szerzők:	Paule, Cleoper C. Varga Angelika (1977-) (biológus) Photiou, Andy Jenes Ágnes (1980-) (élettanász) Avelino, Antonio Buluwela, Laki Nagy István
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM069011
Első szerző:	Sousa-Valente, Joao
Cím:	Inflammation of peripheral tissues and injury to peripheral nerves induce differing effects in the expression of the calcium-sensitive N-arachydonoylethanolamine-synthesizing enzyme and related molecules in rat primary sensory neurons / Sousa-Valente Joao, Varga Angelika, Torres-Perez Jose Vicente, Jenes Agnes, Wahba John, Mackie Ken, Cravatt Benjamin, Ueda Natsuo, Tsuboi Kazuhito, Santha Peter, Jancso Gabor, Tailor Hiren, Avelino António, Nagy Istvan
Dátum:	2017
ISSN:	0021-9967
Megjegyzések:	Elevation of intracellular Ca2+ concentration induces the synthesis of N-arachydonoylethanolamine (anandamide) in a subpopulation of primary sensory neurons. N-acylphosphatidylethanolamine phospholipase D (NAPE-PLD) is the only known enzyme that synthesizes anandamide in a Ca2+ -dependent manner. NAPE-PLD mRNA as well as anandamide's main targets, the excitatory transient receptor potential vanilloid type 1 ion channel (TRPV1), the inhibitory cannabinoid type 1 (CB1) receptor, and the main anandamide-hydrolyzing enzyme fatty acid amide hydrolase (FAAH), are all expressed by subpopulations of nociceptive primary sensory neurons. Thus, NAPE-PLD, TRPV1, the CB1 receptor, and FAAH could form an autocrine signaling system that could shape the activity of a major subpopulation of nociceptive primary sensory neurons, contributing to the development of pain. Although the expression patterns of TRPV1, the CB1 receptor, and FAAH have been comprehensively elucidated, little is known about NAPE-PLD expression in primary sensory neurons under physiological and pathological conditions. This study shows that NAPE-PLD is expressed by about one-third of primary sensory neurons, the overwhelming majority of which also express nociceptive markers as well as the CB1 receptor, TRPV1, and FAAH. Inflammation of peripheral tissues and injury to peripheral nerves induce differing but concerted changes in the expression pattern of NAPE-PLD, the CB1 receptor, TRPV1, and FAAH. Together these data indicate the existence of the anatomical basis for an autocrine signaling system in a major proportion of nociceptive primary sensory neurons and that alterations in that autocrine signaling by peripheral pathologies could contribute to the development of both inflammatory and neuropathic pain.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban cannabinoid type 1 receptor fatty acid amide hydrolase inflammation neuropathy pain transient receptor potential vanilloid type 1 ion channel
Megjelenés:	Journal Of Comparative Neurology 525 : 8 (2017), p. 1778-1796. -
További szerzők:	Varga Angelika (1977-) (biológus) Torres-Pérez, Jose Vicente Jenes Ágnes (1980-) (élettanász) Wahba, John Mackie, Ken Cravatt, Benjamin Ueda, Natsuo Tsuboi, Kazuhito Sántha Péter Jancsó Gábor Tailor, Hiren Avelino, Antonio Nagy István (orvos)
Pályázati támogatás:	TAMOP 4.1.2. E-13/1/KONV-2013-0010 TÁMOP K-101873 OTKA
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