TY  - JOUR
AU  - Trifunovic, Dragana
AU  - Nikolovski, Neda
AU  - Lavrnja, Irena
AU  - SophieWendrich, Katrin
AU  - Paquet-Durand, Francois
AU  - Miljković, Đorđe
PY  - 2015
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1915
AB  - Infiltration of macrophages into the central nervous system and
   activation of microglia are hallmarks of multiple sclerosis and its
   animal model-experimental autoimmune encephalomyelitis (EAE). Cell death
   in EAE has been demonstrated as an essential mechanism in the local
   regulation of the inflammatory reaction, but also as one of the major
   factors contributing to the destruction of the nervous tissue. The focus
   of this study was on detection of cell death among ED1(+) cells
   (macrophages/activated microglia) in the spinal cord of Dark Agouti rats
   at the peak of EAE. Cell death was assessed using the TUNEL assay and
   immunostaining for cleaved caspase 3, as markers for cell death in
   general and ``classical{''} apoptosis, respectively. Major infiltrates
   of immune cells were detected both in white matter and gray matter of
   spinal cords in rats at the disease peak. ED1, TUNEL, and caspase 3
   positive cells were detected within, but also outside the infiltrates.
   There were more dying ED1+ cells in white matter than in gray matter,
   both in the general population and in infiltrated regions. The observed
   discrepancy in the proportion of dying ED1+ cells in spinal cord gray
   and white matter indicated that in EAE rat macrophages/microglia within
   gray matter are less prone to cell death induction. This is of special
   interest in the context of the increasingly appreciated contribution of
   spinal cord gray matter inflammation to multiple sclerosis pathogenesis.
   Our findings suggest that activated macrophages/microglia of gray matter
   are less susceptible to cell death induction. Alternatively, it can be
   assumed that intrinsic cell death-inductive mechanisms of nervous tissue
   differ in white and gray matter. Thus, further research on the gray
   matter macrophages/microglia cell death during EAE is warranted. They
   should be aimed at identification of the reasons for the observed
   differences and finding suitable ways to stimulate gray matter activated
   macrophages/microglia death.
T2  - Peerj
T1  - Cell death of spinal cord ED1(+) cells in a rat model of multiple
 sclerosis
IS  - 3:e1189
VL  - 3
DO  - 10.7717/peerj.1189
ER  - 

@article{
author = "Trifunovic, Dragana and Nikolovski, Neda and Lavrnja, Irena and SophieWendrich, Katrin and Paquet-Durand, Francois and Miljković, Đorđe",
year = "2015",
abstract = "Infiltration of macrophages into the central nervous system and
   activation of microglia are hallmarks of multiple sclerosis and its
   animal model-experimental autoimmune encephalomyelitis (EAE). Cell death
   in EAE has been demonstrated as an essential mechanism in the local
   regulation of the inflammatory reaction, but also as one of the major
   factors contributing to the destruction of the nervous tissue. The focus
   of this study was on detection of cell death among ED1(+) cells
   (macrophages/activated microglia) in the spinal cord of Dark Agouti rats
   at the peak of EAE. Cell death was assessed using the TUNEL assay and
   immunostaining for cleaved caspase 3, as markers for cell death in
   general and ``classical{''} apoptosis, respectively. Major infiltrates
   of immune cells were detected both in white matter and gray matter of
   spinal cords in rats at the disease peak. ED1, TUNEL, and caspase 3
   positive cells were detected within, but also outside the infiltrates.
   There were more dying ED1+ cells in white matter than in gray matter,
   both in the general population and in infiltrated regions. The observed
   discrepancy in the proportion of dying ED1+ cells in spinal cord gray
   and white matter indicated that in EAE rat macrophages/microglia within
   gray matter are less prone to cell death induction. This is of special
   interest in the context of the increasingly appreciated contribution of
   spinal cord gray matter inflammation to multiple sclerosis pathogenesis.
   Our findings suggest that activated macrophages/microglia of gray matter
   are less susceptible to cell death induction. Alternatively, it can be
   assumed that intrinsic cell death-inductive mechanisms of nervous tissue
   differ in white and gray matter. Thus, further research on the gray
   matter macrophages/microglia cell death during EAE is warranted. They
   should be aimed at identification of the reasons for the observed
   differences and finding suitable ways to stimulate gray matter activated
   macrophages/microglia death.",
journal = "Peerj",
title = "Cell death of spinal cord ED1(+) cells in a rat model of multiple
 sclerosis",
number = "3:e1189",
volume = "3",
doi = "10.7717/peerj.1189"
}

Trifunovic, D., Nikolovski, N., Lavrnja, I., SophieWendrich, K., Paquet-Durand, F.,& Miljković, Đ.. (2015). Cell death of spinal cord ED1(+) cells in a rat model of multiple
 sclerosis. in Peerj, 3(3:e1189).
https://doi.org/10.7717/peerj.1189

Trifunovic D, Nikolovski N, Lavrnja I, SophieWendrich K, Paquet-Durand F, Miljković Đ. Cell death of spinal cord ED1(+) cells in a rat model of multiple
 sclerosis. in Peerj. 2015;3(3:e1189).
doi:10.7717/peerj.1189 .

Trifunovic, Dragana, Nikolovski, Neda, Lavrnja, Irena, SophieWendrich, Katrin, Paquet-Durand, Francois, Miljković, Đorđe, "Cell death of spinal cord ED1(+) cells in a rat model of multiple
 sclerosis" in Peerj, 3, no. 3:e1189 (2015),
https://doi.org/10.7717/peerj.1189 . .

TY  - CONF
AU  - Nikolovski, Neda
AU  - Lavrnja, Irena
AU  - Wendrich, Katrin
AU  - Momčilović, Miljana
AU  - Paquet-Durand, François
AU  - Trifunović, Dragana
AU  - Miljković, Đorđe
PY  - 2015
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/6061
AB  - Infiltration of macrophages into the central nervous system (CNS), as well
as activation of microglia is a hallmark of multiple sclerosis and its animal
model - experimental autoimmune encephalomyelitis (EAE). Cell death in
EAE has been demonstrated as an essential mechanism in the local
regulation of the inflammatory reaction, but also as one of the major factors
contributing to the destruction of the CNS tissue. Here, cell death of ED1+
cells (macrophages/microglia) in the spinal cord of EAE rats was
investigated. Cell death in general was assessed using the TUNEL assay,
while cleaved caspase-3 immunostaining was employed as the marker of
“classical” apoptosis. Dark Agouti (DA) rats were immunized with spinal
cord homogenate emulsified in complete Freund's adjuvant. Infiltrates of
immune cells were detected both in white matter (WM) and grey matter
(GM) of spinal cords in DA rats at the peak of EAE. ED1+, TUNEL+ and
caspase-3+ cells were detected within, but also outside the infiltrates. While
there were no differences in the proportion of TUNEL+ ED1+ cells between
infiltrates and non-infiltrated areas in WM, there were more ED1+TUNEL+
cells in GM in infiltrates than in non–infiltrated areas. A similar distribution
was observed for ED1+caspase-3+ cells. The observed discrepancy in
distribution of dead ED1+ cells in infiltrates and non-infiltrated areas in GM
and WM of spinal cord indicated that differential spatial regulation of
macrophage/microglia cell death occurred in DA rats. These findings
contribute to the understanding of pathogenesis of EAE in DA rats. It also
opens new perspectives for a research aiming at more efficient treatment of
multiple sclerosis.
PB  - Belgrade: Immunological Society of Serbia
C3  - 3rd Belgrade EFIS symposium on Immunoregulation: Immunity, Infection, Autoimmunity and Aging; 2015 May 24-27; Arandjelovac, Serbia
T1  - Cell death of ED1+ cells in the central nervous system of Dark Agouti rats at the peak of experimental autoimmune encephalitis
SP  - 67
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_6061
ER  - 

@conference{
author = "Nikolovski, Neda and Lavrnja, Irena and Wendrich, Katrin and Momčilović, Miljana and Paquet-Durand, François and Trifunović, Dragana and Miljković, Đorđe",
year = "2015",
abstract = "Infiltration of macrophages into the central nervous system (CNS), as well
as activation of microglia is a hallmark of multiple sclerosis and its animal
model - experimental autoimmune encephalomyelitis (EAE). Cell death in
EAE has been demonstrated as an essential mechanism in the local
regulation of the inflammatory reaction, but also as one of the major factors
contributing to the destruction of the CNS tissue. Here, cell death of ED1+
cells (macrophages/microglia) in the spinal cord of EAE rats was
investigated. Cell death in general was assessed using the TUNEL assay,
while cleaved caspase-3 immunostaining was employed as the marker of
“classical” apoptosis. Dark Agouti (DA) rats were immunized with spinal
cord homogenate emulsified in complete Freund's adjuvant. Infiltrates of
immune cells were detected both in white matter (WM) and grey matter
(GM) of spinal cords in DA rats at the peak of EAE. ED1+, TUNEL+ and
caspase-3+ cells were detected within, but also outside the infiltrates. While
there were no differences in the proportion of TUNEL+ ED1+ cells between
infiltrates and non-infiltrated areas in WM, there were more ED1+TUNEL+
cells in GM in infiltrates than in non–infiltrated areas. A similar distribution
was observed for ED1+caspase-3+ cells. The observed discrepancy in
distribution of dead ED1+ cells in infiltrates and non-infiltrated areas in GM
and WM of spinal cord indicated that differential spatial regulation of
macrophage/microglia cell death occurred in DA rats. These findings
contribute to the understanding of pathogenesis of EAE in DA rats. It also
opens new perspectives for a research aiming at more efficient treatment of
multiple sclerosis.",
publisher = "Belgrade: Immunological Society of Serbia",
journal = "3rd Belgrade EFIS symposium on Immunoregulation: Immunity, Infection, Autoimmunity and Aging; 2015 May 24-27; Arandjelovac, Serbia",
title = "Cell death of ED1+ cells in the central nervous system of Dark Agouti rats at the peak of experimental autoimmune encephalitis",
pages = "67",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_6061"
}

Nikolovski, N., Lavrnja, I., Wendrich, K., Momčilović, M., Paquet-Durand, F., Trifunović, D.,& Miljković, Đ.. (2015). Cell death of ED1+ cells in the central nervous system of Dark Agouti rats at the peak of experimental autoimmune encephalitis. in 3rd Belgrade EFIS symposium on Immunoregulation: Immunity, Infection, Autoimmunity and Aging; 2015 May 24-27; Arandjelovac, Serbia
Belgrade: Immunological Society of Serbia., 67.
https://hdl.handle.net/21.15107/rcub_ibiss_6061

Nikolovski N, Lavrnja I, Wendrich K, Momčilović M, Paquet-Durand F, Trifunović D, Miljković Đ. Cell death of ED1+ cells in the central nervous system of Dark Agouti rats at the peak of experimental autoimmune encephalitis. in 3rd Belgrade EFIS symposium on Immunoregulation: Immunity, Infection, Autoimmunity and Aging; 2015 May 24-27; Arandjelovac, Serbia. 2015;:67.
https://hdl.handle.net/21.15107/rcub_ibiss_6061 .

Nikolovski, Neda, Lavrnja, Irena, Wendrich, Katrin, Momčilović, Miljana, Paquet-Durand, François, Trifunović, Dragana, Miljković, Đorđe, "Cell death of ED1+ cells in the central nervous system of Dark Agouti rats at the peak of experimental autoimmune encephalitis" in 3rd Belgrade EFIS symposium on Immunoregulation: Immunity, Infection, Autoimmunity and Aging; 2015 May 24-27; Arandjelovac, Serbia (2015):67,
https://hdl.handle.net/21.15107/rcub_ibiss_6061 .