@article{MTMT:3318960, title = {Menthol evokes Ca2+ signals and induces oxidative stress independently of the presence of TRPM8 (menthol) receptor in cancer cells}, url = {https://m2.mtmt.hu/api/publication/3318960}, author = {Nazıroğlu, M and Blum, W and Jósvay, Katalin and Çiğ, B and Henzi, T and Oláh, Zoltán and Vizler, Csaba and Schwaller, B and Pecze, László}, doi = {10.1016/j.redox.2017.10.009}, journal-iso = {REDOX BIOL}, journal = {REDOX BIOLOGY}, volume = {14}, unique-id = {3318960}, issn = {2213-2317}, abstract = {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}, keywords = {APOPTOSIS; TEMPERATURE; ARTICLE; MEMBRANE DEPOLARIZATION; human; priority journal; controlled study; human cell; protein expression; calcium cell level; reactive oxygen metabolite; Cell viability; Calcium Signaling; purinergic receptor; calcium transport; cancer cell; mitochondrial membrane potential; menthol; Purinergic signaling; inositol trisphosphate; ECTOPIC EXPRESSION; Prostate cancer cell line; transient receptor potential channel M8; Breast cancer cell line; CA2+ OSCILLATIONS; DU145 cell line; TRPM8; Oxidative stress}, year = {2018}, eissn = {2213-2317}, pages = {439-449} } @article{MTMT:3250677, title = {Targeting breast cancer cells by MRS1477, a positive allosteric modulator of TRPV1 channels}, url = {https://m2.mtmt.hu/api/publication/3250677}, author = {Naziroglu, M and Cig, B and Blum, W and Vizler, Csaba and Buhala, Andrea and Marton, Annamária and Katona, Róbert László and Jósvay, Katalin and Schwaller, B and Oláh, Zoltán and Pecze, László}, doi = {10.1371/journal.pone.0179950}, journal-iso = {PLOS ONE}, journal = {PLOS ONE}, volume = {12}, unique-id = {3250677}, issn = {1932-6203}, abstract = {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.}, year = {2017}, eissn = {1932-6203} } @article{MTMT:2763894, title = {Besides neuro-imaging, the Thy1-YFP mouse could serve for visualizing experimental tumours, inflammation and wound-healing}, url = {https://m2.mtmt.hu/api/publication/2763894}, author = {Jósvay, Katalin and Winter, Zoltán and Katona, Róbert László and Pecze, László and Marton, Annamária and Buhala, Andrea and Szakonyi, Gerda and Oláh, Zoltán and Vizler, Csaba}, doi = {10.1038/srep06776}, journal-iso = {SCI REP}, journal = {SCIENTIFIC REPORTS}, volume = {4}, unique-id = {2763894}, issn = {2045-2322}, abstract = {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.}, year = {2014}, eissn = {2045-2322}, pages = {6776-6783}, orcid-numbers = {Szakonyi, Gerda/0000-0002-4366-4283} } @article{MTMT:2763893, title = {Propylene-Glycol Aggravates LPS-Induced Sepsis through Production of TNF-alpha and IL-6}, url = {https://m2.mtmt.hu/api/publication/2763893}, author = {Marton, Annamária and Kolozsi, Csongor and Kusz, Erzsébet and Oláh, Zoltán and Letoha, Tamás and Vizler, Csaba and Pecze, László}, journal-iso = {IRAN J IMMUNOL}, journal = {IRANIAN JOURNAL OF IMMUNOLOGY}, volume = {11}, unique-id = {2763893}, issn = {1735-1383}, abstract = {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.}, year = {2014}, eissn = {1735-367X}, pages = {113-122} } @article{MTMT:2192154, title = {Divalent Heavy Metal Cations Block the TRPV1 Ca2+ Channel}, url = {https://m2.mtmt.hu/api/publication/2192154}, author = {Pecze, László and Winter, Zoltán and Jósvay, Katalin and Ötvös, Ferenc and Kolozsi, Csongor and Vizler, Csaba and Budai, D and Letoha, Tamás and Dombi, György and Szakonyi, Gerda and Oláh, Zoltán}, doi = {10.1007/s12011-012-9570-y}, journal-iso = {BIOL TRACE ELEM RES}, journal = {BIOLOGICAL TRACE ELEMENT RESEARCH}, volume = {151}, unique-id = {2192154}, issn = {0163-4984}, abstract = {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+).}, year = {2013}, eissn = {1559-0720}, pages = {451-461}, orcid-numbers = {Szakonyi, Gerda/0000-0002-4366-4283} } @article{MTMT:1918262, title = {Resiniferatoxin mediated ablation of TRPV1+ neurons removes TRPA1 as well}, url = {https://m2.mtmt.hu/api/publication/1918262}, author = {Pecze, László and Pelsőczi, Péter and Kecskés, Miklós and Winter, Zoltán and Papp, András and Kaszas, K and Letoha, Tamás and Vizler, Csaba and Oláh, Zoltán}, doi = {10.1017/S0317167100006600}, journal-iso = {CAN J NEUROL SCI}, journal = {CANADIAN JOURNAL OF NEUROLOGICAL SCIENCES / JOURNAL CANADIEN DES SCIENCES NEUROLOGIQUES}, volume = {36}, unique-id = {1918262}, issn = {0317-1671}, keywords = {Animals; MICE; immunohistochemistry; Cold Temperature; Hot Temperature; Blotting, Western; Pain/*physiopathology; Diterpenes/*pharmacology; Sensory Receptor Cells/*drug effects/metabolism; Trigeminal Ganglion/drug effects/metabolism; Pain Threshold/drug effects; Transient Receptor Potential Channels/*drug effects/metabolism; TRPV Cation Channels/*drug effects/metabolism}, year = {2009}, eissn = {2057-0155}, pages = {234-241}, orcid-numbers = {Papp, András/0000-0003-0485-0806} } @article{MTMT:1918261, title = {Human keratinocytes are vanilloid resistant}, url = {https://m2.mtmt.hu/api/publication/1918261}, author = {Pecze, László and Szabó, Kornélia Ágnes and Széll, Márta and Jósvay, Katalin and Kaszas, K and Kusz, Erzsébet and Letoha, Tamás and Prorok, János and Koncz, Istvan and Tóth, András and Kemény, Lajos and Vizler, Csaba and Oláh, Zoltán}, doi = {10.1371/journal.pone.0003419}, journal-iso = {PLOS ONE}, journal = {PLOS ONE}, volume = {3}, unique-id = {1918261}, issn = {1932-6203}, year = {2008}, eissn = {1932-6203}, orcid-numbers = {Szabó, Kornélia Ágnes/0000-0002-6231-3251; Széll, Márta/0000-0002-0730-714X; Prorok, János/0000-0001-8419-8859; Kemény, Lajos/0000-0002-2119-9501} } @article{MTMT:1915160, title = {Anti-calmodulins and tricyclic adjuvants in pain therapy block the TRPV1 channel}, url = {https://m2.mtmt.hu/api/publication/1915160}, author = {Oláh, Zoltán and Jósvay, Katalin and Pecze, László and Letoha, Tamás and Babai, N and Budai, D and Ötvös, Ferenc and Szalma, S and Vizler, Csaba}, doi = {10.1371/journal.pone.0000545}, journal-iso = {PLOS ONE}, journal = {PLOS ONE}, volume = {2}, unique-id = {1915160}, issn = {1932-6203}, year = {2007}, eissn = {1932-6203} } @article{MTMT:1116110, title = {Therapeutic proteasome inhibition in experimental acute pancreatitis}, url = {https://m2.mtmt.hu/api/publication/1116110}, author = {Letoha, Tamás and Fehér, Z. Liliána and Pecze, László and Somlai, Csaba and Varga, I and Kaszaki, József and Tóth, Gábor and Vizler, Csaba and Tiszlavicz, László and Takács, Tamás}, doi = {10.3748/wjg.v13.i33.4452}, journal-iso = {WORLD J LGASTROENTEROL}, journal = {WORLD JOURNAL OF GASTROENTEROLOGY}, volume = {13}, unique-id = {1116110}, issn = {1007-9327}, keywords = {ASSAY; INDUCTION; PROTEASOME INHIBITION; PROTECTS; CATHEPSIN-B; SEVERITY; myeloperoxidase; KAPPA-B; THERMOTOLERANCE; HEAT-SHOCK PROTEINS; cholecystokinin octapeptide; Acute pancreatitis; Heat shock proteins; Trypsinogen activation; nuclear factor-kappa B}, year = {2007}, eissn = {2219-2840}, pages = {4452-4457}, orcid-numbers = {Kaszaki, József/0000-0002-0750-7731; Tóth, Gábor/0000-0002-3604-4385; Tiszlavicz, László/0000-0003-1134-6587} } @mastersthesis{MTMT:31156228, title = {Effects of Environmental Pollutant Heavy Metals on the Electric Activity of the Somatosensory System in Rats in Acute Application}, url = {https://m2.mtmt.hu/api/publication/31156228}, author = {Pecze, László}, publisher = {SZTE}, unique-id = {31156228}, year = {2004} }