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133 results on '"Tilan, Jason"'

1. Hypoxia-activated neuropeptide Y/Y5 receptor/RhoA pathway triggers chromosomal instability and bone metastasis in Ewing sarcoma

Author

Lu, Congyi, Mahajan, Akanksha, Hong, Sung-Hyeok, Galli, Susana, Zhu, Shiya, Tilan, Jason U., Abualsaud, Nouran, Adnani, Mina, Chung, Stacey, Elmansy, Nada, Rodgers, Jasmine, Rodriguez, Olga, Albanese, Christopher, Wang, Hongkun, Regan, Maureen, Zgonc, Valerie, Blancato, Jan, Krawczyk, Ewa, Gallicano, G. Ian, Girgis, Michael, Cheema, Amrita, Iżycka-Świeszewska, Ewa, Cavalli, Luciane R., Pack, Svetlana D., and Kitlinska, Joanna

Published
2022
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2. Publisher Correction: Hypoxia-activated neuropeptide Y/Y5 receptor/RhoA pathway triggers chromosomal instability and bone metastasis in Ewing sarcoma

Author

Lu, Congyi, Mahajan, Akanksha, Hong, Sung-Hyeok, Galli, Susana, Zhu, Shiya, Tilan, Jason U., Abualsaud, Nouran, Adnani, Mina, Chung, Stacey, Elmansy, Nada, Rodgers, Jasmine, Rodriguez, Olga, Albanese, Christopher, Wang, Hongkun, Regan, Maureen, Zgonc, Valerie, Blancato, Jan, Krawczyk, Ewa, Gallicano, G. Ian, Girgis, Michael, Cheema, Amrita, Iżycka-Świeszewska, Ewa, Cavalli, Luciane R., Pack, Svetlana D., and Kitlinska, Joanna

Published
2022
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8. Abstract PR018: Neuropeptide Y as a metastatic factor

Author

Adnani, Mina, primary, Hong, Sung-Hyeok, additional, Galli, Susana, additional, Mahajan, Akanksha, additional, Abualsaud, Nouran, additional, Caprio, Lindsay, additional, Tilan, Jason U., additional, Rodriguez, Olga, additional, Wang, Hingkun, additional, Albanese, Christopher, additional, Cavalli, Luciane R., additional, and Kitlinska, Joanna, additional

Published
2023
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13. Renal and cardiac neuropeptide Y and NPY receptors in a rat model of congestive heart failure

Author

Callanan, Ean Y., Lee, Edward W., Tilan, Jason U., Winaver, Joseph, Haramati, Aviad, Mulroney, Susan E., and Zukowska, Zofia

Subjects
Vasoconstriction -- Physiological aspects, Vasoconstriction -- Research, Biological sciences
Abstract

Neuropeptide Y (NPY) is coreleased with norepinephrine and stimulates vasoconstriction, vascular and cardiomyocyte hypertrophy via Y1 receptors (R) and angiogenesis via Y2R. Although circulating NPY is elevated in heart failure, NPY's role remains unclear. Activation of the NPY system was determined in Wistar rats with the aortocaval (A-V) fistula model of high-output heart failure. Plasma NPY levels were elevated in A-V fistula animals (115.7 [+ or -] 15.3 vs. 63.1 [+ or -] 17.4 pM in sham, P < 0.04). Animals either compensated [urinary [Na.sup.+] excretion returning to normal with moderate disease (COMP)] or remained decompensated with severe cardiac and renal failure (urinary [Na.sup.+] excretion Y1 receptor; Y2 receptor; renal blood flow; cardiac hypertrophy

Published
2007

14. Neuropeptide Y acts directly in the periphery on fat tissue and mediates stress-induced obesity and metabolic syndrome

Author

Kuo, Lydia E, Kitlinska, Joanna B, Tilan, Jason U, Li, Lijun, Baker, Stephen B, Johnson, Michael D, Lee, Edward W, Burnett, Mary Susan, Fricke, Stanley T, Kvetnansky, Richard, Herzog, Herbert, and Zukowska, Zofia

Abstract

The relationship between stress and obesity remains elusive. In response to stress, some people lose weight, whereas others gain. Here we report that stress exaggerates diet-induced obesity through a peripheral mechanism in the abdominal white adipose tissue that is mediated by neuropeptide Y (NPY). Stressors such as exposure to cold or aggression lead to the release of NPY from sympathetic nerves, which in turn upregulates NPY and its Y2 receptors (NPY2R) in a glucocorticoid-dependent manner in the abdominal fat. This positive feedback response by NPY leads to the growth of abdominal fat. Release of NPY and activation of NPY2R stimulates fat angiogenesis, macrophage infiltration, and the proliferation and differentiation of new adipocytes, resulting in abdominal obesity and a metabolic syndrome-like condition. NPY, like stress, stimulates mouse and human fat growth, whereas pharmacological inhibition or fat-targeted knockdown of NPY2R is anti-angiogenic and anti-adipogenic, while reducing abdominal obesity and metabolic abnormalities. Thus, manipulations of NPY2R activity within fat tissue offer new ways to remodel fat and treat obesity and metabolic syndrome., Author(s): Lydia E Kuo [1]; Joanna B Kitlinska [1]; Jason U Tilan [1]; Lijun Li [1]; Stephen B Baker [2]; Michael D Johnson [3]; Edward W Lee [1, 8]; Mary [...]

Published
2007
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21. In vivo model for testing effect of hypoxia on tumor metastasis

Author

Hong, Sung-Hyeok, Tilan, Jason U., Galli, Susana, Acree, Rachel, Connors, Katherine, Mahajan, Akanksha, Wietlisbach, Larissa, Polk, Taylor, Izycka-Swieszewska, Ewa, Lee, Yi-Chien, Cavalli, Luciane R., Rodriguez, Olga C., Albanese, Chris, and Kitlinska, Joanna B.

Subjects
Disease Models, Animal, Mice, Animals, Humans, Mice, SCID, Sarcoma, Ewing, Neoplasm Metastasis, Hypoxia, Article, Neoplasm Transplantation
Abstract

Hypoxia has been implicated in the metastasis of Ewing sarcoma (ES) by clinical observations and in vitro data, yet direct evidence for its pro-metastatic effect is lacking and the exact mechanisms of its action are unclear. Here, we report an animal model that allows for direct testing of the effects of tumor hypoxia on ES dissemination and investigation into the underlying pathways involved. This approach combines two well-established experimental strategies, orthotopic xenografting of ES cells and femoral artery ligation (FAL), which induces hindlimb ischemia. Human ES cells were injected into the gastrocnemius muscles of SCID/beige mice and the primary tumors were allowed to grow to a size of 250 mm3. At this stage either the tumors were excised (control group) or the animals were subjected to FAL to create tumor hypoxia, followed by tumor excision 3 days later. The efficiency of FAL was confirmed by a significant increase in binding of hypoxyprobe-1 in the tumor tissue, severe tumor necrosis and complete inhibition of primary tumor growth. Importantly, despite these direct effects of ischemia, an enhanced dissemination of tumor cells from the hypoxic tumors was observed. This experimental strategy enables comparative analysis of the metastatic properties of primary tumors of the same size, yet significantly different levels of hypoxia. It also provides a new platform to further assess the mechanistic basis for the hypoxia-induced alterations that occur during metastatic tumor progression in vivo. In addition, while this model was established using ES cells, we anticipate that this experimental strategy can be used to test the effect of hypoxia in other sarcomas, as well as tumors orthotopically implanted in sites with a well-defined blood supply route.

Published
2016

26. In Vivo Model for Testing Effect of Hypoxia on Tumor Metastasis

Author

Hong, Sung-Hyeok, primary, Tilan, Jason U., primary, Galli, Susana, primary, Acree, Rachel, primary, Connors, Katherine, primary, Mahajan, Akanksha, primary, Wietlisbach, Larissa, primary, Polk, Taylor, primary, Izycka-Swieszewska, Ewa, primary, Lee, Yi-Chien, primary, Cavalli, Luciane R., primary, Rodriguez, Olga C., primary, Albanese, Chris, primary, and Kitlinska, Joanna B., primary

Published
2016
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27. Abstract 2478: Tumor hypoxia promotes Ewing sarcoma metastases in a mouse xenograft model

Author

Tilan, Jason U., primary, Hong, Sung-Hyeok, additional, Galli, Susana, additional, Acree, Rachel, additional, Connors, Katherine, additional, Horton, Meredith, additional, Mahajan, Akanksha, additional, Wietlisbach, Larissa, additional, Lee, Yi-Chien, additional, Rodriguez, Olga, additional, Albanese, Christopher, additional, and Kitlinska, Joanna, additional

Published
2016
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30. Dipeptidyl Peptidases as Survival Factors in Ewing Sarcoma Family of Tumors: IMPLICATIONS FOR TUMOR BIOLOGY AND THERAPY*

Author

Lu, Congyi, Tilan, Jason U., Everhart, Lindsay, Czarnecka, Magdalena, Soldin, Steven J., Mendu, Damodara R., Jeha, Dima, Hanafy, Jailan, Lee, Christina K., Sun, Junfeng, Izycka-Swieszewska, Ewa, Toretsky, Jeffrey A., and Kitlinska, Joanna

Subjects
Reverse Transcriptase Polymerase Chain Reaction, Cell Line, Tumor, mental disorders, Humans, Molecular Bases of Disease, Sarcoma, Ewing, RNA, Small Interfering, Dipeptidyl-Peptidases and Tripeptidyl-Peptidases, humanities
Abstract

Ewing sarcoma family of tumors (ESFT) is a group of aggressive pediatric malignancies driven by the EWS-FLI1 fusion protein, an aberrant transcription factor up-regulating specific target genes, such as neuropeptide Y (NPY) and its Y1 and Y5 receptors (Y5Rs). Previously, we have shown that both exogenous NPY and endogenous NPY stimulate ESFT cell death via its Y1 and Y5Rs. Here, we demonstrate that this effect is prevented by dipeptidyl peptidases (DPPs), which cleave NPY to its shorter form, NPY(3-36), not active at Y1Rs. We have shown that NPY-induced cell death can be abolished by overexpression of DPPs and enhanced by their down-regulation. Both NPY treatment and DPP blockade activated the same cell death pathway mediated by poly(ADP-ribose) polymerase (PARP-1) and apoptosis-inducing factor (AIF). Moreover, the decrease in cell survival induced by DPP inhibition was blocked by Y1 and Y5R antagonists, confirming its dependence on endogenous NPY. Interestingly, similar levels of NPY-driven cell death were achieved by blocking membrane DPPIV and cytosolic DPP8 and DPP9. Thus, this is the first evidence of these intracellular DPPs cleaving releasable peptides, such as NPY, in live cells. In contrast, another membrane DPP, fibroblast activation protein (FAP), did not affect NPY actions. In conclusion, DPPs act as survival factors for ESFT cells and protect them from cell death induced by endogenous NPY. This is the first demonstration that intracellular DPPs are involved in regulation of ESFT growth and may become potential therapeutic targets for these tumors.

Published
2011

33. High neuropeptide Y release associates with Ewing sarcoma bone dissemination -in vivomodel of site-specific metastases

Author

Hong, Sung-Hyeok, primary, Tilan, Jason U., additional, Galli, Susana, additional, Izycka-Swieszewska, Ewa, additional, Polk, Taylor, additional, Horton, Meredith, additional, Mahajan, Akanksha, additional, Christian, David, additional, Jenkins, Shari, additional, Acree, Rachel, additional, Connors, Katherine, additional, Ledo, Phuong, additional, Lu, Congyi, additional, Lee, Yi-Chien, additional, Rodriguez, Olga, additional, Toretsky, Jeffrey A., additional, Albanese, Chris, additional, and Kitlinska, Joanna, additional

Published
2015
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36. Systemic levels of neuropeptide Y and dipeptidyl peptidase activity in patients with Ewing sarcoma—Associations with tumor phenotype and survival

Author

Tilan, Jason U., primary, Krailo, Mark, additional, Barkauskas, Donald A., additional, Galli, Susana, additional, Mtaweh, Haifa, additional, Long, Jessica, additional, Wang, Hongkun, additional, Hawkins, Kirsten, additional, Lu, Congyi, additional, Jeha, Dima, additional, Izycka‐Swieszewska, Ewa, additional, Lawlor, Elizabeth R., additional, Toretsky, Jeffrey A., additional, and Kitlinska, Joanna B., additional

Published
2014
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38. Abstract 3105: Neuropeptide Y Y5 receptor in neuroblastoma chemoresistance

Author

Trinh, Emily, primary, Czarnecka, Magdalena, additional, Hong, Sung-Hyeok, additional, Lu, Congyi, additional, Martin, Samantha, additional, Galli, Susana, additional, Izycka-Swieszewska, Ewa, additional, Kuan-Celarier, Anna, additional, Christian, David, additional, Horton, Meredith, additional, Tilan, Jason U., additional, and Kitlinska, Joanna B., additional

Published
2014
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39. Endogenous Neuropeptide Y and ischemic revascularization in rodents : sources and receptors

Author

Tilan, Jason Ulip. and Tilan, Jason Ulip.

Abstract

Therapeutic revascularization of ischemic tissue in Peripheral Arterial Disease (PAD) is presently inadequate, leaving many of those affected with advancing limb ischemia and/or loss of limb function. In order to examine processes of vascular development in PAD, we built upon our previous work which established a role for the sympathetic neurotransmitter, Neuropeptide Y (NPY), in ischemic angiogenesis. NPY is potently angiogenic via its Y2 receptor (R) and is also a mitogen for vascular smooth muscle cells via Y1R. The purpose of this study was to further characterize the role of NPY in arteriogenesis and angiogenesis in hindlimb ischemia following femoral artery ligation (FAL) in rodents. We sought to determine the role of endogenous NPY and the time course in activation of the NPY system - the peptide, its receptors, and a serine protease, DPPIV. We also investigated the contribution of platelet-derived NPY to ischemic revascularization in 129Sv mice. In NPY+/+ Wistar rats, NPY-immunoreactivity ( -ir) of platelet-poor plasma, reflective of sympathetic nerve release of the peptide, was increased by 24 hours post-FAL. This was followed by a rise in Y2R mRNA levels in gastrocnemius muscle, which remained ischemic within the first week. However, spontaneous recovery was observed via immunohistochemistry by 14 days, in parallel with increased platelet-rich plasma NPY-ir, which reflect platelet levels of the peptide. Simultaneously, Y1R mRNA expression in adductor muscle was upregulated. Recovery in ischemic NPY-/- mice was delayed within the first week and by 14 days, marked impairment in capillary angiogenesis was observed (P<0.01). Angiogenic response to FAL was similarly inhibited in NPY-/- and thrombocytopenic NPY+/+ mice. However, transfer of NPY+/+ platelets into NPY-/- mice fully restored the capillarity in ischemic tissue indicating that platelets are a complete angiogenic source of the peptide. These data suggest that endogenous NPY is important early in ischemic recovery and that there is temporal coordination in the NPY system between circulating NPY and local receptor expression. Furthermore, this is the first study to demonstrate platelet-derived NPY is critical for ischemic capillary angiogenesis in 129Sv mice, in part, due to enhanced proliferation of endothelial cells.

Published
2009

40. Hypoxia shifts activity of neuropeptide Y in Ewing sarcoma from growth-inhibitory to growth-promoting effects

Author

Tilan, Jason U., primary, Lu, Congyi, additional, Galli, Susana, additional, Izycka-Swieszewska, Ewa, additional, Earnest, Joshua Patrick, additional, Shabbir, Asim, additional, Everhart, Lindsay M., additional, Wang, Shuo, additional, Martin, Samantha, additional, Horton, Meredith, additional, Mahajan, Akanksha, additional, Christian, David, additional, O’Neill, Alison, additional, Wang, Hongkun, additional, Zhuang, Tingting, additional, Czarnecka, Magdalena, additional, Johnson, Michael D., additional, Toretsky, Jeffrey A., additional, and Kitlinska, Joanna, additional

Published
2013
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45. Dipeptidyl Peptidases as Survival Factors in Ewing Sarcoma Family of Tumors

Author

Lu, Congyi, primary, Tilan, Jason U., additional, Everhart, Lindsay, additional, Czarnecka, Magdalena, additional, Soldin, Steven J., additional, Mendu, Damodara R., additional, Jeha, Dima, additional, Hanafy, Jailan, additional, Lee, Christina K., additional, Sun, Junfeng, additional, Izycka-Swieszewska, Ewa, additional, Toretsky, Jeffrey A., additional, and Kitlinska, Joanna, additional

Published
2011
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50. Corrigenda: Neuropeptide Y acts directly in the periphery on fat tissue and mediates stress-induced obesity and metabolic syndrome

Author

Kuo, Lydia E, Kitlinska, Joanna B, Tilan, Jason U, Li, Lijun, Baker, Stephen B, Johnson, Michael D, Lee, Edward W, Burnett, Mary Susan, Fricke, Stanley T, Kvetnansky, Richard, Herzog, Herbert, and Zukowska, Zofia

Abstract

Author(s): Lydia E Kuo; Joanna B Kitlinska; Jason U Tilan; Lijun Li; Stephen B Baker; Michael D Johnson; Edward W Lee; Mary Susan Burnett; Stanley T Fricke; Richard Kvetnansky; Herbert [...]

Published
2007
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