Effects of catecholamines on thymocyte apoptosis and proliferation depend on thymocyte microenvironment
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2014
Authors
Radojević, KatarinaRakin, Ana
Pilipović, Ivan
Kosec, Duško
Đikić, Jasmina
Bufan, Biljana
Vujnović, Ivana
Leposavić, Gordana
Article (Published version)
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The present study, through quantification of tyrosine hydroxylase (TH) expression and catecholamine (CA) content in the presence and in the absence of alpha-methyl-p-tyrosine (AMPT), a TH inhibitor, in adult thymic organ (ATOC) and thymocyte culture, demonstrated that thymic cells produce CAs. In addition, in ATOC an increase in beta(2)-adrenoceptor (AR) mRNA expression and beta(2)-AR thymocyte surface density was registered. Furthermore, AMPT (10(-4) M), as propranolol (10(-4) M), augmented thymocyte apoptosis and diminished thymocyte proliferation in ATOC. Propranolol exerted these effects acting on CD3(high) thymocytes. However, in thymocyte cultures, propranolol (10(-6) M) acting on the same-thymocyte subset exerted the opposing effect on thymocyte apoptosis and ConA-stimulated proliferation. This suggested that, depending on thymocyte microenvironment, differential effects can be induced through the same type of AR. Additionally, arterenol (10(-8) to 10(-6) M), similar to proprano...lol, diminished apoptosis, but increased ConA-stimulated thymocyte proliferation in thymocyte culture. However, differently from propranolol, arterenol affected manly CD3- thymocyte subset, which harbors majority of alpha(1)-AR+ thymocytes. Additionally, arterenol showed a dose-dependent decrease in efficiency of thymocyte apoptosis and proliferation modulation with the rise in its concentration. Considering greater affinity of arterenol for alpha(1)-ARs than for beta(2)-ARs, the previous findings could be attributable to increased engagement of beta(2)-ARs with the rise of arterenol concentration. Consistently, in the presence of propranolol (10(-6) M), a beta-AR blacker, the arterenol (10(-8) M) effects on thymocytes were augmented. In conclusion, thymic endogenous CAs, acting through distinct AR types and, possible, the same AR type (but in different cell microenvironment) may exert the opposing effects on thymocyte apoptosis/proliferation. (C) 2014 Elsevier B.V. All rights reserved.
Keywords:
Adult thymus organ culture / Thymocyte culture / Propranolol / Arterenol / Thymocyte apoptosis / Thymocyte proliferationSource:
Journal of Neuroimmunology, 2014, 272, 1-2, 16-28Publisher:
- Elsevier, Amsterdam
Funding / projects:
- Immune system plasticity during aging: Immunomodulatory capacity of oestrogens (RS-MESTD-Basic Research (BR or ON)-175050)
DOI: 10.1016/j.jneuroim.2014.04.010
ISSN: 0165-5728
PubMed: 24837703
WoS: 000338613500003
Scopus: 2-s2.0-84902002547
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TorlakTY - JOUR AU - Radojević, Katarina AU - Rakin, Ana AU - Pilipović, Ivan AU - Kosec, Duško AU - Đikić, Jasmina AU - Bufan, Biljana AU - Vujnović, Ivana AU - Leposavić, Gordana PY - 2014 UR - http://intor.torlakinstitut.com/handle/123456789/409 AB - The present study, through quantification of tyrosine hydroxylase (TH) expression and catecholamine (CA) content in the presence and in the absence of alpha-methyl-p-tyrosine (AMPT), a TH inhibitor, in adult thymic organ (ATOC) and thymocyte culture, demonstrated that thymic cells produce CAs. In addition, in ATOC an increase in beta(2)-adrenoceptor (AR) mRNA expression and beta(2)-AR thymocyte surface density was registered. Furthermore, AMPT (10(-4) M), as propranolol (10(-4) M), augmented thymocyte apoptosis and diminished thymocyte proliferation in ATOC. Propranolol exerted these effects acting on CD3(high) thymocytes. However, in thymocyte cultures, propranolol (10(-6) M) acting on the same-thymocyte subset exerted the opposing effect on thymocyte apoptosis and ConA-stimulated proliferation. This suggested that, depending on thymocyte microenvironment, differential effects can be induced through the same type of AR. Additionally, arterenol (10(-8) to 10(-6) M), similar to propranolol, diminished apoptosis, but increased ConA-stimulated thymocyte proliferation in thymocyte culture. However, differently from propranolol, arterenol affected manly CD3- thymocyte subset, which harbors majority of alpha(1)-AR+ thymocytes. Additionally, arterenol showed a dose-dependent decrease in efficiency of thymocyte apoptosis and proliferation modulation with the rise in its concentration. Considering greater affinity of arterenol for alpha(1)-ARs than for beta(2)-ARs, the previous findings could be attributable to increased engagement of beta(2)-ARs with the rise of arterenol concentration. Consistently, in the presence of propranolol (10(-6) M), a beta-AR blacker, the arterenol (10(-8) M) effects on thymocytes were augmented. In conclusion, thymic endogenous CAs, acting through distinct AR types and, possible, the same AR type (but in different cell microenvironment) may exert the opposing effects on thymocyte apoptosis/proliferation. (C) 2014 Elsevier B.V. All rights reserved. PB - Elsevier, Amsterdam T2 - Journal of Neuroimmunology T1 - Effects of catecholamines on thymocyte apoptosis and proliferation depend on thymocyte microenvironment EP - 28 IS - 1-2 SP - 16 VL - 272 DO - 10.1016/j.jneuroim.2014.04.010 ER -
@article{ author = "Radojević, Katarina and Rakin, Ana and Pilipović, Ivan and Kosec, Duško and Đikić, Jasmina and Bufan, Biljana and Vujnović, Ivana and Leposavić, Gordana", year = "2014", abstract = "The present study, through quantification of tyrosine hydroxylase (TH) expression and catecholamine (CA) content in the presence and in the absence of alpha-methyl-p-tyrosine (AMPT), a TH inhibitor, in adult thymic organ (ATOC) and thymocyte culture, demonstrated that thymic cells produce CAs. In addition, in ATOC an increase in beta(2)-adrenoceptor (AR) mRNA expression and beta(2)-AR thymocyte surface density was registered. Furthermore, AMPT (10(-4) M), as propranolol (10(-4) M), augmented thymocyte apoptosis and diminished thymocyte proliferation in ATOC. Propranolol exerted these effects acting on CD3(high) thymocytes. However, in thymocyte cultures, propranolol (10(-6) M) acting on the same-thymocyte subset exerted the opposing effect on thymocyte apoptosis and ConA-stimulated proliferation. This suggested that, depending on thymocyte microenvironment, differential effects can be induced through the same type of AR. Additionally, arterenol (10(-8) to 10(-6) M), similar to propranolol, diminished apoptosis, but increased ConA-stimulated thymocyte proliferation in thymocyte culture. However, differently from propranolol, arterenol affected manly CD3- thymocyte subset, which harbors majority of alpha(1)-AR+ thymocytes. Additionally, arterenol showed a dose-dependent decrease in efficiency of thymocyte apoptosis and proliferation modulation with the rise in its concentration. Considering greater affinity of arterenol for alpha(1)-ARs than for beta(2)-ARs, the previous findings could be attributable to increased engagement of beta(2)-ARs with the rise of arterenol concentration. Consistently, in the presence of propranolol (10(-6) M), a beta-AR blacker, the arterenol (10(-8) M) effects on thymocytes were augmented. In conclusion, thymic endogenous CAs, acting through distinct AR types and, possible, the same AR type (but in different cell microenvironment) may exert the opposing effects on thymocyte apoptosis/proliferation. (C) 2014 Elsevier B.V. All rights reserved.", publisher = "Elsevier, Amsterdam", journal = "Journal of Neuroimmunology", title = "Effects of catecholamines on thymocyte apoptosis and proliferation depend on thymocyte microenvironment", pages = "28-16", number = "1-2", volume = "272", doi = "10.1016/j.jneuroim.2014.04.010" }
Radojević, K., Rakin, A., Pilipović, I., Kosec, D., Đikić, J., Bufan, B., Vujnović, I.,& Leposavić, G.. (2014). Effects of catecholamines on thymocyte apoptosis and proliferation depend on thymocyte microenvironment. in Journal of Neuroimmunology Elsevier, Amsterdam., 272(1-2), 16-28. https://doi.org/10.1016/j.jneuroim.2014.04.010
Radojević K, Rakin A, Pilipović I, Kosec D, Đikić J, Bufan B, Vujnović I, Leposavić G. Effects of catecholamines on thymocyte apoptosis and proliferation depend on thymocyte microenvironment. in Journal of Neuroimmunology. 2014;272(1-2):16-28. doi:10.1016/j.jneuroim.2014.04.010 .
Radojević, Katarina, Rakin, Ana, Pilipović, Ivan, Kosec, Duško, Đikić, Jasmina, Bufan, Biljana, Vujnović, Ivana, Leposavić, Gordana, "Effects of catecholamines on thymocyte apoptosis and proliferation depend on thymocyte microenvironment" in Journal of Neuroimmunology, 272, no. 1-2 (2014):16-28, https://doi.org/10.1016/j.jneuroim.2014.04.010 . .
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