Jovčić, Gordana

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Macrophage migration inhibitory factor is an endogenous regulator of stress-induced extramedullary erythropoiesis

Vignjević Petrinović, Sanja; Budeč, Mirela; Marković, Dragana; Gotić, Mirjana; Mitrović Ajtić, Olivera; Mojsilović, Slavko; Stošić-Grujičić, Stanislava; Ivanov, Milan; Jovčić, Gordana; Čokić, Vladan

(Springer Verlag, 2016)

TY  - JOUR
AU  - Vignjević Petrinović, Sanja
AU  - Budeč, Mirela
AU  - Marković, Dragana
AU  - Gotić, Mirjana
AU  - Mitrović Ajtić, Olivera
AU  - Mojsilović, Slavko
AU  - Stošić-Grujičić, Stanislava
AU  - Ivanov, Milan
AU  - Jovčić, Gordana
AU  - Čokić, Vladan
PY  - 2016
UR  - https://link.springer.com/article/10.1007%2Fs00418-016-1442-7#aboutcontent
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2986
AB  - Macrophage migration inhibitory factor is a well-known proinflammatory cytokine that is released during systemic stress response. Although MIF can affect erythrocyte production, the role of this cytokine in stress-induced erythropoiesis is completely unknown. To extend our previous findings showing that chronic psychological stress stimulates extramedullary erythropoiesis, here we examined whether MIF is involved in the control of stress-induced erythropoietic response. Adult male C57BL/6 wild-type (WT) and MIF-KO (knock-out) mice were subjected to 2-h daily restraint stress for either 7 or 14 consecutive days. The number of erythroid progenitors and CD71/Ter119 profile of erythroid precursors were analyzed in the bone marrow and spleen. Additionally, MIF protein expression was assessed in WT mice. Our results demonstrated that chronic restraint stress enhanced the number of both erythroid progenitors and precursors in the spleen. Stress-induced increase in the number of splenic late erythroid progenitors as well as in the percentage of CD71(+)Ter119(+)-double-positive precursors was significantly more pronounced in MIF-KO mice compared to WT animals. Furthermore, repeatedly stressed WT animals demonstrated an augmented MIF expression in the spleen. Unlike the spleen, the bone marrow of chronically stressed WT mice exhibited less prominent changes in erythropoietic stress response and no significant alteration in MIF expression. In addition, MIF deficiency did not influence the bone marrow erythropoiesis in stressed animals. These findings suggest that MIF regulates extramedullary erythropoiesis by inhibiting an overexpansion of splenic immature erythroid cells during chronic stress and indicate a novel role for this cytokine under chronic stress conditions.
PB  - Springer Verlag
T2  - Histochemistry and cell biology
T1  - Macrophage migration inhibitory factor is an endogenous regulator of stress-induced extramedullary erythropoiesis
DO  - 10.1007/s00418-016-1442-7
SP  - 1
EP  - 14
ER  - 
@article{
author = "Vignjević Petrinović, Sanja and Budeč, Mirela and Marković, Dragana and Gotić, Mirjana and Mitrović Ajtić, Olivera and Mojsilović, Slavko and Stošić-Grujičić, Stanislava and Ivanov, Milan and Jovčić, Gordana and Čokić, Vladan",
year = "2016",
abstract = "Macrophage migration inhibitory factor is a well-known proinflammatory cytokine that is released during systemic stress response. Although MIF can affect erythrocyte production, the role of this cytokine in stress-induced erythropoiesis is completely unknown. To extend our previous findings showing that chronic psychological stress stimulates extramedullary erythropoiesis, here we examined whether MIF is involved in the control of stress-induced erythropoietic response. Adult male C57BL/6 wild-type (WT) and MIF-KO (knock-out) mice were subjected to 2-h daily restraint stress for either 7 or 14 consecutive days. The number of erythroid progenitors and CD71/Ter119 profile of erythroid precursors were analyzed in the bone marrow and spleen. Additionally, MIF protein expression was assessed in WT mice. Our results demonstrated that chronic restraint stress enhanced the number of both erythroid progenitors and precursors in the spleen. Stress-induced increase in the number of splenic late erythroid progenitors as well as in the percentage of CD71(+)Ter119(+)-double-positive precursors was significantly more pronounced in MIF-KO mice compared to WT animals. Furthermore, repeatedly stressed WT animals demonstrated an augmented MIF expression in the spleen. Unlike the spleen, the bone marrow of chronically stressed WT mice exhibited less prominent changes in erythropoietic stress response and no significant alteration in MIF expression. In addition, MIF deficiency did not influence the bone marrow erythropoiesis in stressed animals. These findings suggest that MIF regulates extramedullary erythropoiesis by inhibiting an overexpansion of splenic immature erythroid cells during chronic stress and indicate a novel role for this cytokine under chronic stress conditions.",
publisher = "Springer Verlag",
journal = "Histochemistry and cell biology",
title = "Macrophage migration inhibitory factor is an endogenous regulator of stress-induced extramedullary erythropoiesis",
doi = "10.1007/s00418-016-1442-7",
pages = "1-14"
}
Vignjević Petrinović, S., Budeč, M., Marković, D., Gotić, M., Mitrović Ajtić, O., Mojsilović, S., Stošić-Grujičić, S., Ivanov, M., Jovčić, G.,& Čokić, V.. (2016). Macrophage migration inhibitory factor is an endogenous regulator of stress-induced extramedullary erythropoiesis. in Histochemistry and cell biology
Springer Verlag., 1-14.
https://doi.org/10.1007/s00418-016-1442-7
Vignjević Petrinović S, Budeč M, Marković D, Gotić M, Mitrović Ajtić O, Mojsilović S, Stošić-Grujičić S, Ivanov M, Jovčić G, Čokić V. Macrophage migration inhibitory factor is an endogenous regulator of stress-induced extramedullary erythropoiesis. in Histochemistry and cell biology. 2016;:1-14.
doi:10.1007/s00418-016-1442-7 .
Vignjević Petrinović, Sanja, Budeč, Mirela, Marković, Dragana, Gotić, Mirjana, Mitrović Ajtić, Olivera, Mojsilović, Slavko, Stošić-Grujičić, Stanislava, Ivanov, Milan, Jovčić, Gordana, Čokić, Vladan, "Macrophage migration inhibitory factor is an endogenous regulator of stress-induced extramedullary erythropoiesis" in Histochemistry and cell biology (2016):1-14,
https://doi.org/10.1007/s00418-016-1442-7 . .
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