TY  - JOUR
AU  - Isaković, Anđelka M
AU  - Petričević, Sasa M.
AU  - Ristić, Slavica M.
AU  - Popadić, Dušan M.
AU  - Kravić-Stevović, Tamara K
AU  - Zogović, Nevena
AU  - Poljarević, Jelena M.
AU  - Živanović Radnić, Tatjana V
AU  - Sabo, Tibor J.
AU  - Isaković, Aleksandra J.
AU  - Marković, Ivanka D.
AU  - Trajković, Vladimir S.
AU  - Misirlić-Denčić, Sonja T
PY  - 2018
UR  - https://insights.ovid.com/crossref?an=00008390-201802000-00002
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3004
AB  - Melanoma, an aggressive skin tumor with high metastatic potential, is associated with high mortality and increasing morbidity. Multiple available chemotherapeutic and immunotherapeutic modalities failed to improve survival in advanced disease, and the search for new agents is ongoing. The aim of this study was to investigate antimelanoma effects of O,O-diethyl-(S,S)-ethylenediamine-N,N'di-2-(3-cyclohexyl) propanoate dihydrochloride (EE), a previously synthesized and characterized organic compound. Mouse melanoma B16 cell viability was assessed using acid phosphatase, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, sulforhodamine B, and lactate dehydrogenase assays. Apoptosis and autophagy were investigated using flow cytometry, fluorescence and electron microscopy, and western blotting. In vivo antitumor potential was assessed in subcutaneous mouse melanoma model after 14 days of treatment with EE. Tumor mass and volume were measured, and RT-PCR was used for investigating the expression of autophagy-related, proapoptotic, and antiapoptotic molecules in tumor tissue. Investigated organic compound exerts significant cytotoxic effect against B16 cells. EE induced apoptosis, as confirmed by phosphatidyl serine externalisation, caspase activation, and ultrastructural features typical for apoptosis seen on fluorescence and electron microscopes. The apoptotic mechanism included prompt disruption of mitochondrial membrane potential and oxidative stress. No autophagy was observed. Antimelanoma action and apoptosis induction were confirmed in vivo, as EE decreased mass and volume of tumors, and increased expression of several proapoptotic genes. EE possesses significant antimelanoma action and causes caspase-dependent apoptosis mediated by mitochondrial damage and reactive oxygen species production. Decrease in tumor growth and increase in expression of proapoptotic genes in tumor tissue suggest that EE warrants further investigation as a candidate agent in treating melanoma.
PB  - Melanoma Research
T2  - Melanoma Research
T2  - Melanoma Research
T1  - In vitro and in vivo antimelanoma effect of ethyl ester cyclohexyl analog of ethylenediamine dipropanoic acid.
IS  - 1
VL  - 28
DO  - 10.1097/CMR.0000000000000409
SP  - 8
EP  - 20
ER  - 

@article{
author = "Isaković, Anđelka M and Petričević, Sasa M. and Ristić, Slavica M. and Popadić, Dušan M. and Kravić-Stevović, Tamara K and Zogović, Nevena and Poljarević, Jelena M. and Živanović Radnić, Tatjana V and Sabo, Tibor J. and Isaković, Aleksandra J. and Marković, Ivanka D. and Trajković, Vladimir S. and Misirlić-Denčić, Sonja T",
year = "2018",
abstract = "Melanoma, an aggressive skin tumor with high metastatic potential, is associated with high mortality and increasing morbidity. Multiple available chemotherapeutic and immunotherapeutic modalities failed to improve survival in advanced disease, and the search for new agents is ongoing. The aim of this study was to investigate antimelanoma effects of O,O-diethyl-(S,S)-ethylenediamine-N,N'di-2-(3-cyclohexyl) propanoate dihydrochloride (EE), a previously synthesized and characterized organic compound. Mouse melanoma B16 cell viability was assessed using acid phosphatase, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, sulforhodamine B, and lactate dehydrogenase assays. Apoptosis and autophagy were investigated using flow cytometry, fluorescence and electron microscopy, and western blotting. In vivo antitumor potential was assessed in subcutaneous mouse melanoma model after 14 days of treatment with EE. Tumor mass and volume were measured, and RT-PCR was used for investigating the expression of autophagy-related, proapoptotic, and antiapoptotic molecules in tumor tissue. Investigated organic compound exerts significant cytotoxic effect against B16 cells. EE induced apoptosis, as confirmed by phosphatidyl serine externalisation, caspase activation, and ultrastructural features typical for apoptosis seen on fluorescence and electron microscopes. The apoptotic mechanism included prompt disruption of mitochondrial membrane potential and oxidative stress. No autophagy was observed. Antimelanoma action and apoptosis induction were confirmed in vivo, as EE decreased mass and volume of tumors, and increased expression of several proapoptotic genes. EE possesses significant antimelanoma action and causes caspase-dependent apoptosis mediated by mitochondrial damage and reactive oxygen species production. Decrease in tumor growth and increase in expression of proapoptotic genes in tumor tissue suggest that EE warrants further investigation as a candidate agent in treating melanoma.",
publisher = "Melanoma Research",
journal = "Melanoma Research, Melanoma Research",
title = "In vitro and in vivo antimelanoma effect of ethyl ester cyclohexyl analog of ethylenediamine dipropanoic acid.",
number = "1",
volume = "28",
doi = "10.1097/CMR.0000000000000409",
pages = "8-20"
}

Isaković, A. M., Petričević, S. M., Ristić, S. M., Popadić, D. M., Kravić-Stevović, T. K., Zogović, N., Poljarević, J. M., Živanović Radnić, T. V., Sabo, T. J., Isaković, A. J., Marković, I. D., Trajković, V. S.,& Misirlić-Denčić, S. T.. (2018). In vitro and in vivo antimelanoma effect of ethyl ester cyclohexyl analog of ethylenediamine dipropanoic acid.. in Melanoma Research
Melanoma Research., 28(1), 8-20.
https://doi.org/10.1097/CMR.0000000000000409

Isaković AM, Petričević SM, Ristić SM, Popadić DM, Kravić-Stevović TK, Zogović N, Poljarević JM, Živanović Radnić TV, Sabo TJ, Isaković AJ, Marković ID, Trajković VS, Misirlić-Denčić ST. In vitro and in vivo antimelanoma effect of ethyl ester cyclohexyl analog of ethylenediamine dipropanoic acid.. in Melanoma Research. 2018;28(1):8-20.
doi:10.1097/CMR.0000000000000409 .

Isaković, Anđelka M, Petričević, Sasa M., Ristić, Slavica M., Popadić, Dušan M., Kravić-Stevović, Tamara K, Zogović, Nevena, Poljarević, Jelena M., Živanović Radnić, Tatjana V, Sabo, Tibor J., Isaković, Aleksandra J., Marković, Ivanka D., Trajković, Vladimir S., Misirlić-Denčić, Sonja T, "In vitro and in vivo antimelanoma effect of ethyl ester cyclohexyl analog of ethylenediamine dipropanoic acid." in Melanoma Research, 28, no. 1 (2018):8-20,
https://doi.org/10.1097/CMR.0000000000000409 . .

TY  - JOUR
AU  - Marković, Zoran M.
AU  - Ristić, Biljana Z.
AU  - Arsikin, Katarina M.
AU  - Klisić, Đorđe G.
AU  - Harhaji-Trajković, Ljubica
AU  - Todorović-Marković, Biljana M.
AU  - Kepić, Dejan P.
AU  - Kravić-Stevović, Tamara K.
AU  - Jovanović, Svetlana P.
AU  - Milenković, Marina M.
AU  - Milivojević, Dusan D.
AU  - Bumbaširević, Vladimir Z.
AU  - Dramićanin, Miroslav D.
AU  - Trajković, Vladimir S.
PY  - 2012
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3587
AB  - The excellent photoluminescent properties of graphene quantum dots (GQD) makes them suitable candidates for biomedical applications, but their cytotoxicity has not been extensively studied. Here we show that electrochemically produced GQD irradiated with blue light (470. nm, 1. W) generate reactive oxygen species, including singlet oxygen, and kill U251 human glioma cells by causing oxidative stress. The cell death induced by photoexcited GQD displayed morphological and/or biochemical characteristics of both apoptosis (phosphatidylserine externalization, caspase activation, DNA fragmentation) and autophagy (formation of autophagic vesicles, LC3-I/LC3-II conversion, degradation of autophagic target p62). Moreover, a genetic inactivation of autophagy-essential LC3B protein partly abrogated the photodynamic cytotoxicity of GQD. These data indicate potential usefulness of GQD in photodynamic therapy, but also raise concerns about their possible toxicity.
PB  - Elsevier BV
T2  - Biomaterials
T1  - Graphene quantum dots as autophagy-inducing photodynamic agents
IS  - 29
VL  - 33
DO  - 10.1016/j.biomaterials.2012.06.060
SP  - 7084
EP  - 7092
ER  - 

@article{
author = "Marković, Zoran M. and Ristić, Biljana Z. and Arsikin, Katarina M. and Klisić, Đorđe G. and Harhaji-Trajković, Ljubica and Todorović-Marković, Biljana M. and Kepić, Dejan P. and Kravić-Stevović, Tamara K. and Jovanović, Svetlana P. and Milenković, Marina M. and Milivojević, Dusan D. and Bumbaširević, Vladimir Z. and Dramićanin, Miroslav D. and Trajković, Vladimir S.",
year = "2012",
abstract = "The excellent photoluminescent properties of graphene quantum dots (GQD) makes them suitable candidates for biomedical applications, but their cytotoxicity has not been extensively studied. Here we show that electrochemically produced GQD irradiated with blue light (470. nm, 1. W) generate reactive oxygen species, including singlet oxygen, and kill U251 human glioma cells by causing oxidative stress. The cell death induced by photoexcited GQD displayed morphological and/or biochemical characteristics of both apoptosis (phosphatidylserine externalization, caspase activation, DNA fragmentation) and autophagy (formation of autophagic vesicles, LC3-I/LC3-II conversion, degradation of autophagic target p62). Moreover, a genetic inactivation of autophagy-essential LC3B protein partly abrogated the photodynamic cytotoxicity of GQD. These data indicate potential usefulness of GQD in photodynamic therapy, but also raise concerns about their possible toxicity.",
publisher = "Elsevier BV",
journal = "Biomaterials",
title = "Graphene quantum dots as autophagy-inducing photodynamic agents",
number = "29",
volume = "33",
doi = "10.1016/j.biomaterials.2012.06.060",
pages = "7084-7092"
}

Marković, Z. M., Ristić, B. Z., Arsikin, K. M., Klisić, Đ. G., Harhaji-Trajković, L., Todorović-Marković, B. M., Kepić, D. P., Kravić-Stevović, T. K., Jovanović, S. P., Milenković, M. M., Milivojević, D. D., Bumbaširević, V. Z., Dramićanin, M. D.,& Trajković, V. S.. (2012). Graphene quantum dots as autophagy-inducing photodynamic agents. in Biomaterials
Elsevier BV., 33(29), 7084-7092.
https://doi.org/10.1016/j.biomaterials.2012.06.060

Marković ZM, Ristić BZ, Arsikin KM, Klisić ĐG, Harhaji-Trajković L, Todorović-Marković BM, Kepić DP, Kravić-Stevović TK, Jovanović SP, Milenković MM, Milivojević DD, Bumbaširević VZ, Dramićanin MD, Trajković VS. Graphene quantum dots as autophagy-inducing photodynamic agents. in Biomaterials. 2012;33(29):7084-7092.
doi:10.1016/j.biomaterials.2012.06.060 .

Marković, Zoran M., Ristić, Biljana Z., Arsikin, Katarina M., Klisić, Đorđe G., Harhaji-Trajković, Ljubica, Todorović-Marković, Biljana M., Kepić, Dejan P., Kravić-Stevović, Tamara K., Jovanović, Svetlana P., Milenković, Marina M., Milivojević, Dusan D., Bumbaširević, Vladimir Z., Dramićanin, Miroslav D., Trajković, Vladimir S., "Graphene quantum dots as autophagy-inducing photodynamic agents" in Biomaterials, 33, no. 29 (2012):7084-7092,
https://doi.org/10.1016/j.biomaterials.2012.06.060 . .

TY  - JOUR
AU  - Marković, Zoran M.
AU  - Harhaji-Trajković, Ljubica
AU  - Todorović-Marković, Biljana M.
AU  - Kepić, Dejan P.
AU  - Arsikin, Katarina M.
AU  - Jovanović, Svetlana P.
AU  - Pantović, Aleksandar C.
AU  - Dramićanin, Miroslav D.
AU  - Trajković, Vladimir S.
PY  - 2011
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3590
AB  - The present study compared the photothermal anticancer activity of near-infrared (NIR)-excited graphene nanoparticles and carbon nanotubes (CNT). Despite lower NIR-absorbing capacity, suspension of polyvinylpyrrolidone-coated graphene sheets exposed to NIR radiation (808nm, 2W/cm2) generated more heat than DNA or sodium dodecylbenzenesulfonate-solubilized single-wall CNT under the same conditions. Accordingly, graphene nanoparticles performed significantly better than CNT in inducing photothermal death of U251 human glioma cells in vitro. The superior photothermal sensitivity of graphene sheets could be largely explained by their better dispersivity, which has been supported by a simple calculation taking into account thermodynamic, optical and geometrical properties of the two type of carbon nanoparticles. The mechanisms of graphene-mediated photothermal killing of cancer cells apparently involved oxidative stress and mitochondrial membrane depolarization resulting in mixed apoptotic and necrotic cell death characterized by caspase activation/DNA fragmentation and cell membrane damage, respectively
PB  - Elsevier BV
T2  - Biomaterials
T1  - In vitro comparison of the photothermal anticancer activity of graphene nanoparticles and carbon nanotubes
IS  - 4
VL  - 32
DO  - 10.1016/j.biomaterials.2010.10.030
SP  - 1121
EP  - 1129
ER  - 

@article{
author = "Marković, Zoran M. and Harhaji-Trajković, Ljubica and Todorović-Marković, Biljana M. and Kepić, Dejan P. and Arsikin, Katarina M. and Jovanović, Svetlana P. and Pantović, Aleksandar C. and Dramićanin, Miroslav D. and Trajković, Vladimir S.",
year = "2011",
abstract = "The present study compared the photothermal anticancer activity of near-infrared (NIR)-excited graphene nanoparticles and carbon nanotubes (CNT). Despite lower NIR-absorbing capacity, suspension of polyvinylpyrrolidone-coated graphene sheets exposed to NIR radiation (808nm, 2W/cm2) generated more heat than DNA or sodium dodecylbenzenesulfonate-solubilized single-wall CNT under the same conditions. Accordingly, graphene nanoparticles performed significantly better than CNT in inducing photothermal death of U251 human glioma cells in vitro. The superior photothermal sensitivity of graphene sheets could be largely explained by their better dispersivity, which has been supported by a simple calculation taking into account thermodynamic, optical and geometrical properties of the two type of carbon nanoparticles. The mechanisms of graphene-mediated photothermal killing of cancer cells apparently involved oxidative stress and mitochondrial membrane depolarization resulting in mixed apoptotic and necrotic cell death characterized by caspase activation/DNA fragmentation and cell membrane damage, respectively",
publisher = "Elsevier BV",
journal = "Biomaterials",
title = "In vitro comparison of the photothermal anticancer activity of graphene nanoparticles and carbon nanotubes",
number = "4",
volume = "32",
doi = "10.1016/j.biomaterials.2010.10.030",
pages = "1121-1129"
}

Marković, Z. M., Harhaji-Trajković, L., Todorović-Marković, B. M., Kepić, D. P., Arsikin, K. M., Jovanović, S. P., Pantović, A. C., Dramićanin, M. D.,& Trajković, V. S.. (2011). In vitro comparison of the photothermal anticancer activity of graphene nanoparticles and carbon nanotubes. in Biomaterials
Elsevier BV., 32(4), 1121-1129.
https://doi.org/10.1016/j.biomaterials.2010.10.030

Marković ZM, Harhaji-Trajković L, Todorović-Marković BM, Kepić DP, Arsikin KM, Jovanović SP, Pantović AC, Dramićanin MD, Trajković VS. In vitro comparison of the photothermal anticancer activity of graphene nanoparticles and carbon nanotubes. in Biomaterials. 2011;32(4):1121-1129.
doi:10.1016/j.biomaterials.2010.10.030 .

Marković, Zoran M., Harhaji-Trajković, Ljubica, Todorović-Marković, Biljana M., Kepić, Dejan P., Arsikin, Katarina M., Jovanović, Svetlana P., Pantović, Aleksandar C., Dramićanin, Miroslav D., Trajković, Vladimir S., "In vitro comparison of the photothermal anticancer activity of graphene nanoparticles and carbon nanotubes" in Biomaterials, 32, no. 4 (2011):1121-1129,
https://doi.org/10.1016/j.biomaterials.2010.10.030 . .

TY  - JOUR
AU  - Stošić-Grujičić, Stanislava
AU  - Trajković, Vladimir S.
AU  - Maksimović-Ivanić, Danijela
AU  - Samardžić, Tatjana S.
PY  - 2002
PY  - 2002
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/532
AB  - The ability of interleukin-17 (IL-17) to induce nitric oxide (NO) synthesis in murine L929 fibroblasts was investigated. L929 cells were incubated with IL-17 and/or LPS, interferon-g (IFN-gama), interleukin-1 (IL-1), or dibutyryl-cAMP. NO production was assessed indirectly, by measuring nitrite accumulation in 24 h culture supernatants. L929 fibroblasts did not produce NO constitutively, nor IL-17 alone induced NO production. Of all other stimuli tested, only IFN-gama significantly up regulated nitrite level in L929 cell cultures. However, when IL-17 was applied simultaneously with each of the tested stimuli, NO synthesis was markedly elevated, thus indicating involvement of distinct signaling pathways of NO induction by IL-17 and other tested agents. Production of NO by IL-17+LPS-treated L929 cells was dependent on synthesis and activity of inducible NO synthase (iNOS), as indicated by abrogation of nitrite accumulation with protein synthesis inhibitor cycloheximide or selective inhibitor of iNOS, aminoguanidine. A role for protein tyrosine kinase (PTK) and transcription factor NF-kB in iNOS activation is suggested by reduction of NO synthesis with PTK inhibitor genistein and an inhibitor of NF-kB activation, pyrrolidine dithiocarbamate (PDTC). In contrast, protein kinase C inhibitor staurosporine was ineffective in blocking IL-17+LPS-induced NO production in L929 cells. Taken together, our results for the first time showed an active participation of IL-17 in co-induction of fibroblast NO synthesis with LPS, cytokines (IL-1, IFN-gama), or cAMP analogue, and suggested that IL-17 up-regulated NO synthesis in fibroblasts through mechanisms involving PTK and NF-kB activation.
AB  - Ispitan je uticaj interleukina-17 (IL-17) na produkciju azot monoksida (NO) od strane L929 fibroblasta. L929 ćelije su inkubirane sa IL-17 i/ili LPS-om, interferonom-gama (IFN-gama), interleukinom-1 (IL-1), ili dibutiril-cAMP-om. Produkcija NO ispitana je indirektno, merenjem koncentracije nitrita akumuliranih nakon 24 h u supernatantu ćelijskih kultura. Kultivisani L929 fibroblasti nisu produkovali NO konstitutivno, niti je sam IL-17 indukovao NO produkciju. Od ostalih ispitanih agenasa samo je IFN-gama značajno povećao nivo nitrita u kulturama L929 ćelija. Međutim, kada je IL-17 primenjen sa bilo kojim od testiranih agenasa, došlo je do snažnog povećanja NO sinteze, što je ukazalo da su signalni putevi indukcije NO sa IL-17 i ostalim navedenim agensima različiti. Sprečavanje akumulacije nitrita inhibitorom proteinske sinteze cikloheksimidom ili selektivnim inhibitorom iNOS aminoguanidinom u ćelijama stimulisanim sa IL-17+LPS ukazalo je da NO produkcija zavisi od sinteze i aktivnosti enzima inducibilne NO sinteze (iNOS). Inhibitor protein tirozin kinaze (PTK), genistein i inhibitor aktivacije transkripcionog faktora NF-kB, pirolidin ditiokarbamat (PDTC), takođe su redukovali sintezu NO. Nasuprot tome, inhibitor protein kinaze C, staurosporin, nije blokirao NO produkciju L929 ćelija stimulisanih sa IL-17+LPS. U celini, naši rezultati su po prvi put pokazali aktivno učešće IL-17 u koindukciji NO sinteze sa LPS-om, citokinima (IL-1, IFN-gama), ili cAMP analogom u fibroblastima i ukazali da stimulacija NO sinteze sa IL-17 uključuje mehanizme zavisne od PTK i NF-kB.
PB  - Beograd: Institut za reumatologiju
T2  - Acta rheumatologica Belgradensia
T1  - Uticaj interleukina-17 na produkciju azot monoksida (NO) od strane L929 ćelijske linije mišijih fibroblasta
T1  - Effect of interleukin-17 on nitric oxide production in murine fibroblast-like cell line L929
IS  - 1
VL  - 32
SP  - 1
EP  - 10
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_532
ER  - 

@article{
author = "Stošić-Grujičić, Stanislava and Trajković, Vladimir S. and Maksimović-Ivanić, Danijela and Samardžić, Tatjana S.",
year = "2002, 2002",
abstract = "The ability of interleukin-17 (IL-17) to induce nitric oxide (NO) synthesis in murine L929 fibroblasts was investigated. L929 cells were incubated with IL-17 and/or LPS, interferon-g (IFN-gama), interleukin-1 (IL-1), or dibutyryl-cAMP. NO production was assessed indirectly, by measuring nitrite accumulation in 24 h culture supernatants. L929 fibroblasts did not produce NO constitutively, nor IL-17 alone induced NO production. Of all other stimuli tested, only IFN-gama significantly up regulated nitrite level in L929 cell cultures. However, when IL-17 was applied simultaneously with each of the tested stimuli, NO synthesis was markedly elevated, thus indicating involvement of distinct signaling pathways of NO induction by IL-17 and other tested agents. Production of NO by IL-17+LPS-treated L929 cells was dependent on synthesis and activity of inducible NO synthase (iNOS), as indicated by abrogation of nitrite accumulation with protein synthesis inhibitor cycloheximide or selective inhibitor of iNOS, aminoguanidine. A role for protein tyrosine kinase (PTK) and transcription factor NF-kB in iNOS activation is suggested by reduction of NO synthesis with PTK inhibitor genistein and an inhibitor of NF-kB activation, pyrrolidine dithiocarbamate (PDTC). In contrast, protein kinase C inhibitor staurosporine was ineffective in blocking IL-17+LPS-induced NO production in L929 cells. Taken together, our results for the first time showed an active participation of IL-17 in co-induction of fibroblast NO synthesis with LPS, cytokines (IL-1, IFN-gama), or cAMP analogue, and suggested that IL-17 up-regulated NO synthesis in fibroblasts through mechanisms involving PTK and NF-kB activation., Ispitan je uticaj interleukina-17 (IL-17) na produkciju azot monoksida (NO) od strane L929 fibroblasta. L929 ćelije su inkubirane sa IL-17 i/ili LPS-om, interferonom-gama (IFN-gama), interleukinom-1 (IL-1), ili dibutiril-cAMP-om. Produkcija NO ispitana je indirektno, merenjem koncentracije nitrita akumuliranih nakon 24 h u supernatantu ćelijskih kultura. Kultivisani L929 fibroblasti nisu produkovali NO konstitutivno, niti je sam IL-17 indukovao NO produkciju. Od ostalih ispitanih agenasa samo je IFN-gama značajno povećao nivo nitrita u kulturama L929 ćelija. Međutim, kada je IL-17 primenjen sa bilo kojim od testiranih agenasa, došlo je do snažnog povećanja NO sinteze, što je ukazalo da su signalni putevi indukcije NO sa IL-17 i ostalim navedenim agensima različiti. Sprečavanje akumulacije nitrita inhibitorom proteinske sinteze cikloheksimidom ili selektivnim inhibitorom iNOS aminoguanidinom u ćelijama stimulisanim sa IL-17+LPS ukazalo je da NO produkcija zavisi od sinteze i aktivnosti enzima inducibilne NO sinteze (iNOS). Inhibitor protein tirozin kinaze (PTK), genistein i inhibitor aktivacije transkripcionog faktora NF-kB, pirolidin ditiokarbamat (PDTC), takođe su redukovali sintezu NO. Nasuprot tome, inhibitor protein kinaze C, staurosporin, nije blokirao NO produkciju L929 ćelija stimulisanih sa IL-17+LPS. U celini, naši rezultati su po prvi put pokazali aktivno učešće IL-17 u koindukciji NO sinteze sa LPS-om, citokinima (IL-1, IFN-gama), ili cAMP analogom u fibroblastima i ukazali da stimulacija NO sinteze sa IL-17 uključuje mehanizme zavisne od PTK i NF-kB.",
publisher = "Beograd: Institut za reumatologiju",
journal = "Acta rheumatologica Belgradensia",
title = "Uticaj interleukina-17 na produkciju azot monoksida (NO) od strane L929 ćelijske linije mišijih fibroblasta, Effect of interleukin-17 on nitric oxide production in murine fibroblast-like cell line L929",
number = "1",
volume = "32",
pages = "1-10",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_532"
}

Stošić-Grujičić, S., Trajković, V. S., Maksimović-Ivanić, D.,& Samardžić, T. S.. (2002). Uticaj interleukina-17 na produkciju azot monoksida (NO) od strane L929 ćelijske linije mišijih fibroblasta. in Acta rheumatologica Belgradensia
Beograd: Institut za reumatologiju., 32(1), 1-10.
https://hdl.handle.net/21.15107/rcub_ibiss_532

Stošić-Grujičić S, Trajković VS, Maksimović-Ivanić D, Samardžić TS. Uticaj interleukina-17 na produkciju azot monoksida (NO) od strane L929 ćelijske linije mišijih fibroblasta. in Acta rheumatologica Belgradensia. 2002;32(1):1-10.
https://hdl.handle.net/21.15107/rcub_ibiss_532 .

Stošić-Grujičić, Stanislava, Trajković, Vladimir S., Maksimović-Ivanić, Danijela, Samardžić, Tatjana S., "Uticaj interleukina-17 na produkciju azot monoksida (NO) od strane L929 ćelijske linije mišijih fibroblasta" in Acta rheumatologica Belgradensia, 32, no. 1 (2002):1-10,
https://hdl.handle.net/21.15107/rcub_ibiss_532 .