TY  - JOUR
AU  - Nazıroğlu, M
AU  - Blum, W
AU  - Jósvay, Katalin
AU  - Çiğ, B
AU  - Henzi, T
AU  - Oláh, Zoltán
AU  - Vizler, Csaba
AU  - Schwaller, B
AU  - Pecze, László
TI  - Menthol evokes Ca2+ signals and induces oxidative stress independently of the presence of TRPM8 (menthol) receptor in cancer cells
JF  - REDOX BIOLOGY
J2  - REDOX BIOL
VL  - 14
PY  - 2018
SP  - 439
EP  - 449
PG  - 11
SN  - 2213-2317
DO  - 10.1016/j.redox.2017.10.009
UR  - https://m2.mtmt.hu/api/publication/3318960
ID  - 3318960
N1  - Cited By :18            
            Export Date: 16 September 2022
AB  - Menthol is a naturally occurring monoterpene alcohol possessing remarkable biological properties including antipruritic, analgesic, antiseptic, anti-inflammatory and cooling effects. Here, we examined the menthol-evoked Ca2+ signals in breast and prostate cancer cell lines. The effect of menthol (50–500 µM) was predicted to be mediated by the transient receptor potential ion channel melastatin subtype 8 (TRPM8). However, the intensity of menthol-evoked Ca2+ signals did not correlate with the expression levels of TRPM8 in breast and prostate cancer cells indicating a TRPM8-independent signaling pathway. Menthol-evoked Ca2+ signals were analyzed in detail in Du 145 prostate cancer cells, as well as in CRISPR/Cas9 TRPM8-knockout Du 145 cells. Menthol (500 µM) induced Ca2+ oscillations in both cell lines, thus independent of TRPM8, which were however dependent on the production of inositol trisphosphate. Results based on pharmacological tools point to an involvement of the purinergic pathway in menthol-evoked Ca2+ responses. Finally, menthol (50–500 µM) decreased cell viability and induced oxidative stress independently of the presence of TRPM8 channels, despite that temperature-evoked TRPM8-mediated inward currents were significantly decreased in TRPM8-knockout Du 145 cells compared to wild type Du 145 cells. © 2017 The Authors
LA  - English
DB  - MTMT
ER  - 

TY  - JOUR
AU  - Naziroglu, M
AU  - Cig, B
AU  - Blum, W
AU  - Vizler, Csaba
AU  - Buhala, Andrea
AU  - Marton, Annamária
AU  - Katona, Róbert László
AU  - Jósvay, Katalin
AU  - Schwaller, B
AU  - Oláh, Zoltán
AU  - Pecze, László
TI  - Targeting breast cancer cells by MRS1477, a positive allosteric modulator of TRPV1 channels
JF  - PLOS ONE
J2  - PLOS ONE
VL  - 12
PY  - 2017
IS  - 6
PG  - 19
SN  - 1932-6203
DO  - 10.1371/journal.pone.0179950
UR  - https://m2.mtmt.hu/api/publication/3250677
ID  - 3250677
N1  - OA gold
AB  - There is convincing epidemiological and experimental evidence that capsaicin, a potent natural transient receptor potential cation channel vanilloid member 1 (TRPV1) agonist, has anticancer activity. However, capsaicin cannot be given systemically in large doses, because of its induction of acute pain and neurological inflammation. MRS1477, a dihydropyridine derivative acts as a positive allosteric modulator of TRPV1, if added together with capsaicin, but is ineffective, if given alone. Addition of MRS1477 evoked Ca2+ signals in MCF7 breast cancer cells, but not in primary breast epithelial cells. This indicates that MCF7 cells not only express functional TRPV1 channels, but also produce endogenous TRPV1 agonists. We investigated the effects of MRS1477 and capsaicin on cell viability, caspase-3 and -9 activities and reactive oxygen species production in MCF7 cells. The fraction of apoptotic cells was increased after 3 days incubation with capsaicin (10 mu M) paralleled by increased reactive oxygen species production and caspase activity. These effects were even more pronounced, when cells were incubated with MRS1477 (2 mu M) either alone or together with CAPS (10 mu M). Capsazepine, a TRPV1 blocker, inhibited both the effect of capsaicin and MRS1477. Whole-cell patch clamp recordings revealed that capsaicinevoked TRPV1-mediated current density levels were increased after 3 days incubation with MRS1477 (2 mu M). However, the tumor growth in MCF7 tumor-bearing immunodeficient mice was not significantly decreased after treatment with MRS1477 (10 mg/kg body weight, i.p., injection twice a week). In conclusion, in view of a putative in vivo treatment with MRS1477 or similar compounds further optimization is required.
LA  - English
DB  - MTMT
ER  - 

TY  - JOUR
AU  - Jósvay, Katalin
AU  - Winter, Zoltán
AU  - Katona, Róbert László
AU  - Pecze, László
AU  - Marton, Annamária
AU  - Buhala, Andrea
AU  - Szakonyi, Gerda
AU  - Oláh, Zoltán
AU  - Vizler, Csaba
TI  - Besides neuro-imaging, the Thy1-YFP mouse could serve for visualizing experimental tumours, inflammation and wound-healing
JF  - SCIENTIFIC REPORTS
J2  - SCI REP
VL  - 4
PY  - 2014
SP  - 6776
PG  - 7
SN  - 2045-2322
DO  - 10.1038/srep06776
UR  - https://m2.mtmt.hu/api/publication/2763894
ID  - 2763894
AB  - The B6.Cg-Tg(Thy1-YFP)16Jrs/J transgenic mouse strain, widely used to study neuronal development and regeneration, expresses the yellow fluorescent protein (YFP) in the peripheral nerves and the central nervous system under the control of regulatory sequences of the Thy1 gene. The Thy1 (CD90) cell surface glycoprotein is present on many cell types besides neurons, and is known to be involved in cell adhesion, migration and signal transduction. We hypothesized that Thy1-activating conditions could probably activate the truncated Thy1 regulatory sequences used in the Thy1-YFP construct, resulting in YFP transgene expression outside the nervous system. We demonstrated that the stroma of subcutaneous tumours induced by the injection of 4T1 or MC26 carcinoma cells into BALB/c(Thy1-YFP) mice, carrying the same construct, indeed expressed the YFP transgene. In the tumour mass, the yellow-green fluorescent stromal cells were clearly distinguishable from 4T1 carcinoma cells stably transfected with red fluorescent protein. Local inflammation induced by subcutaneous injection of complete Freund's adjuvant, as well as the experimental wound-healing milieu, also triggered YFP fluorescence in both the BALB/c(Thy1-YFP) and B6.Cg-Tg(Thy1-YFP)16Jrs/J mice, pointing to eventual overlapping pathways of wound-healing, inflammation and tumour growth.
LA  - English
DB  - MTMT
ER  - 

TY  - JOUR
AU  - Marton, Annamária
AU  - Kolozsi, Csongor
AU  - Kusz, Erzsébet
AU  - Oláh, Zoltán
AU  - Letoha, Tamás
AU  - Vizler, Csaba
AU  - Pecze, László
TI  - Propylene-Glycol Aggravates LPS-Induced Sepsis through Production of TNF-alpha and IL-6
JF  - IRANIAN JOURNAL OF IMMUNOLOGY
J2  - IRAN J IMMUNOL
VL  - 11
PY  - 2014
IS  - 2
SP  - 113
EP  - 122
PG  - 10
SN  - 1735-1383
UR  - https://m2.mtmt.hu/api/publication/2763893
ID  - 2763893
AB  - Background: Propylene glycol (1,2-propanediol, PG) is a commonly used solvent for oral, intravenous, as well as topical pharmaceutical preparations. While PG is generally considered to be safe, it has been known that large intravenous doses given over a short period of time can be toxic. Objective: To evaluate the effect of PG in sepsis induced by the bacterial endotoxin lipopolysaccharide (LPS). Methods: Balb/c mice were treated with LPS (1 mg/kg b. w., i. p.) with or without PG (5 g/kg b. w. i. v.). The survival rate and the production of inflammatory cytokines were measured. In RAW264.7 mouse macrophages encoding NF-kappa B-luc reporter gene, the nuclear transcription factor kappaB (NF-kappa B) activation was measured. Results: We found that intravenous PG increased the mortality rate in sepsis induced by the bacterial endotoxin lipopolysaccharide (LPS) in mice. In accordance with that, PG enhanced LPS-induced production of inflammatory cytokines, including tumor necrosis factor-a (TNF-alpha) and interleukin-6 (IL-6) in vivo. PG also increased the LPS-induced macrophage activation in vitro as detected by measuring NF-kappa B activation. Conclusion: Our results indicate that drugs containing high doses of PG can pose a risk when administered to patients suffering from or prone to Gram negative bacterial infection.
LA  - English
DB  - MTMT
ER  - 

TY  - JOUR
AU  - Pecze, László
AU  - Winter, Zoltán
AU  - Jósvay, Katalin
AU  - Ötvös, Ferenc
AU  - Kolozsi, Csongor
AU  - Vizler, Csaba
AU  - Budai, D
AU  - Letoha, Tamás
AU  - Dombi, György
AU  - Szakonyi, Gerda
AU  - Oláh, Zoltán
TI  - Divalent Heavy Metal Cations Block the TRPV1 Ca2+ Channel
JF  - BIOLOGICAL TRACE ELEMENT RESEARCH
J2  - BIOL TRACE ELEM RES
VL  - 151
PY  - 2013
IS  - 3
SP  - 451
EP  - 461
PG  - 11
SN  - 0163-4984
DO  - 10.1007/s12011-012-9570-y
UR  - https://m2.mtmt.hu/api/publication/2192154
ID  - 2192154
N1  - Received: 4 May 2012 / Accepted: 3 December 2012
AB  - Transient receptor potential vanilloid 1 (TRPV1) is a non-
selective cation channel involved in pain sensation and in a 
wide range of non-pain-related physiological and pathological 
conditions. The aim of the present study was to explore the 
effects of selected heavy metal cations on the function of 
TRPV1. The cations ranked in the following sequence of pore-
blocking activity: Co(2+) [half-maximal inhibitory concentration 
(IC(50)) = 13 muM] > Cd(2+) (IC(50) = 38 muM) > Ni(2+) (IC(50) = 
62 muM) > Cu(2+) (IC(50) = 200 muM). Zn(2+) proved to be a weak 
(IC(50) = 27 muM) and only partial inhibitor of the channel 
function, whereas Mg(2+), Mn(2+) and La(3+) did not exhibit any 
substantial effect. Co(2+), the most potent channel blocker, was 
able not only to compete with Ca(2+) but also to pass with it 
through the open channel of TRPV1. In response to heat 
activation or vanilloid treatment, Co(2+) accumulation was 
verified in TRPV1-transfected cell lines and in the TRPV1+ 
dorsal root ganglion neurons. The inhibitory effect was also 
demonstrated in vivo. Co(2+) applied together with vanilloid 
agonists attenuated the nocifensive eye wipe response in mice. 
Different rat TRPV1 pore point mutants (Y627W, N628W, D646N and 
E651W) were created that can validate the binding site of 
previously used channel blockers in agonist-evoked (45)Ca(2+) 
influx assays in cells expressing TRPV1. The IC(50) of Co(2+) 
on these point mutants were determined to be reasonably 
comparable to those on the wild type, which suggests that 
divalent cations passing through the TRPV1 channel use the same 
negatively charged amino acids as Ca(2+).
LA  - English
DB  - MTMT
ER  - 

TY  - JOUR
AU  - Pecze, László
AU  - Pelsőczi, Péter
AU  - Kecskés, Miklós
AU  - Winter, Zoltán
AU  - Papp, András
AU  - Kaszas, K
AU  - Letoha, Tamás
AU  - Vizler, Csaba
AU  - Oláh, Zoltán
TI  - Resiniferatoxin mediated ablation of TRPV1+ neurons removes TRPA1 as well
JF  - CANADIAN JOURNAL OF NEUROLOGICAL SCIENCES / JOURNAL CANADIEN DES SCIENCES NEUROLOGIQUES
J2  - CAN J NEUROL SCI
VL  - 36
PY  - 2009
IS  - 2
SP  - 234
EP  - 241
PG  - 8
SN  - 0317-1671
DO  - 10.1017/S0317167100006600
UR  - https://m2.mtmt.hu/api/publication/1918262
ID  - 1918262
LA  - English
DB  - MTMT
ER  - 

TY  - JOUR
AU  - Pecze, László
AU  - Szabó, Kornélia Ágnes
AU  - Széll, Márta
AU  - Jósvay, Katalin
AU  - Kaszas, K
AU  - Kusz, Erzsébet
AU  - Letoha, Tamás
AU  - Prorok, János
AU  - Koncz, Istvan
AU  - Tóth, András
AU  - Kemény, Lajos
AU  - Vizler, Csaba
AU  - Oláh, Zoltán
TI  - Human keratinocytes are vanilloid resistant
JF  - PLOS ONE
J2  - PLOS ONE
VL  - 3
PY  - 2008
IS  - 10
PG  - 10
SN  - 1932-6203
DO  - 10.1371/journal.pone.0003419
UR  - https://m2.mtmt.hu/api/publication/1918261
ID  - 1918261
N1  - Megjegyzés-22207849
DI: 10.1371/journal.pone.0003419
Megjegyzés-22192735
DI: 10.1371/journal.pone.0003419
Megjegyzés-22193499
DI: 10.1371/journal.pone.0003419
Megjegyzés-22194631
DI: 10.1371/journal.pone.0003419
LA  - English
DB  - MTMT
ER  - 

TY  - JOUR
AU  - Oláh, Zoltán
AU  - Jósvay, Katalin
AU  - Pecze, László
AU  - Letoha, Tamás
AU  - Babai, N
AU  - Budai, D
AU  - Ötvös, Ferenc
AU  - Szalma, S
AU  - Vizler, Csaba
TI  - Anti-calmodulins and tricyclic adjuvants in pain therapy block the TRPV1 channel
JF  - PLOS ONE
J2  - PLOS ONE
VL  - 2
PY  - 2007
IS  - 6
SN  - 1932-6203
DO  - 10.1371/journal.pone.0000545
UR  - https://m2.mtmt.hu/api/publication/1915160
ID  - 1915160
LA  - English
DB  - MTMT
ER  - 

TY  - JOUR
AU  - Letoha, Tamás
AU  - Fehér, Z. Liliána
AU  - Pecze, László
AU  - Somlai, Csaba
AU  - Varga, I
AU  - Kaszaki, József
AU  - Tóth, Gábor
AU  - Vizler, Csaba
AU  - Tiszlavicz, László
AU  - Takács, Tamás
TI  - Therapeutic proteasome inhibition in experimental acute pancreatitis
JF  - WORLD JOURNAL OF GASTROENTEROLOGY
J2  - WORLD J LGASTROENTEROL
VL  - 13
PY  - 2007
IS  - 33
SP  - 4452
EP  - 4457
PG  - 6
SN  - 1007-9327
DO  - 10.3748/wjg.v13.i33.4452
UR  - https://m2.mtmt.hu/api/publication/1116110
ID  - 1116110
LA  - English
DB  - MTMT
ER  - 

TY  - THES
AU  - Pecze, László
TI  - Effects of Environmental Pollutant Heavy Metals on the Electric Activity of the Somatosensory System in Rats in Acute Application
PB  - Szegedi Tudományegyetem (SZTE)
PY  - 2004
SP  - 51
UR  - https://m2.mtmt.hu/api/publication/31156228
ID  - 31156228
LA  - English
DB  - MTMT
ER  -