TY  - CONF
AU  - Kojić, Snežana
AU  - Bošković, Srđan
AU  - Milovanović, Mina
AU  - Stainie, Didier
AU  - Juez, Rubén Marín
AU  - Jasnić, Jovana
AU  - Novković, Mirjana
AU  - Milošević, Emilija
PY  - 2024
UR  - https://www.izfs.org/education/10sczi
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/2309
AB  - In contrast to humans, zebrafish have a remarkable ability to regenerate their hearts after injury, while both humans and zebrafish efficiently repair the wounded skeletal muscle. Common players in these two processes might represent potential targets for the development of efficient therapies to stimulate human heart to regenerate after injury. We identified ankrd1a expression to be upregulated in both regenerating zebrafish hearts and in repairing skeletal muscle. Its mammalian homolog ANKRD1/CARP encodes a stress responsive cardiac ankyrin repeat protein involved in transcriptional regulation, sarcomere assembly and mechanosensing. Using a TgBAC(ankrd1a:EGFP) line, we showed that activation of ankrd1a in cryoinjured heart is restricted to border zone cardiomyocytes, implicating this gene in dedifferentiation and proliferation of regenerating cardiomyocytes. After stab wound injury of skeletal muscle expression of the fluorescent reporter was observed from 3 dpi, when new EGFP-positive muscle cells emerged inside the injury zone. At later time points, EGFP-positive myofibers were visible in the deeper tissue layers, concomitant with active repair of the injured tissue. In cryoinjured skeletal muscle, strong activation of ankrd1a was also observed in myofibers adjacent to the injury, and in those on uninjured side. Detection of the transgene in both newly formed myofibers that invade the wound and in the apparently uninjured tissue surrounding the injury suggests the role of ankrd1a in skeletal muscle tissue repair and adaptive processes in uninjured myofibers surrounding the injury site. Our results implicate ankrd1a in zebrafish muscle regeneration, repair and remodeling, promoting it as an attractive target for translational studies, as a player in muscle healing and as a sensor of stressed muscle.
PB  - Society for Zebrafish Research
C3  - 10th Strategic Conference of Zebrafish Investigators
T1  - Zebrafish ankrd1a as a common player  in heart regeneration and skeletal muscle repair
UR  - https://hdl.handle.net/21.15107/rcub_imagine_2309
ER  - 

@conference{
author = "Kojić, Snežana and Bošković, Srđan and Milovanović, Mina and Stainie, Didier and Juez, Rubén Marín and Jasnić, Jovana and Novković, Mirjana and Milošević, Emilija",
year = "2024",
abstract = "In contrast to humans, zebrafish have a remarkable ability to regenerate their hearts after injury, while both humans and zebrafish efficiently repair the wounded skeletal muscle. Common players in these two processes might represent potential targets for the development of efficient therapies to stimulate human heart to regenerate after injury. We identified ankrd1a expression to be upregulated in both regenerating zebrafish hearts and in repairing skeletal muscle. Its mammalian homolog ANKRD1/CARP encodes a stress responsive cardiac ankyrin repeat protein involved in transcriptional regulation, sarcomere assembly and mechanosensing. Using a TgBAC(ankrd1a:EGFP) line, we showed that activation of ankrd1a in cryoinjured heart is restricted to border zone cardiomyocytes, implicating this gene in dedifferentiation and proliferation of regenerating cardiomyocytes. After stab wound injury of skeletal muscle expression of the fluorescent reporter was observed from 3 dpi, when new EGFP-positive muscle cells emerged inside the injury zone. At later time points, EGFP-positive myofibers were visible in the deeper tissue layers, concomitant with active repair of the injured tissue. In cryoinjured skeletal muscle, strong activation of ankrd1a was also observed in myofibers adjacent to the injury, and in those on uninjured side. Detection of the transgene in both newly formed myofibers that invade the wound and in the apparently uninjured tissue surrounding the injury suggests the role of ankrd1a in skeletal muscle tissue repair and adaptive processes in uninjured myofibers surrounding the injury site. Our results implicate ankrd1a in zebrafish muscle regeneration, repair and remodeling, promoting it as an attractive target for translational studies, as a player in muscle healing and as a sensor of stressed muscle.",
publisher = "Society for Zebrafish Research",
journal = "10th Strategic Conference of Zebrafish Investigators",
title = "Zebrafish ankrd1a as a common player  in heart regeneration and skeletal muscle repair",
url = "https://hdl.handle.net/21.15107/rcub_imagine_2309"
}

Kojić, S., Bošković, S., Milovanović, M., Stainie, D., Juez, R. M., Jasnić, J., Novković, M.,& Milošević, E.. (2024). Zebrafish ankrd1a as a common player  in heart regeneration and skeletal muscle repair. in 10th Strategic Conference of Zebrafish Investigators
Society for Zebrafish Research..
https://hdl.handle.net/21.15107/rcub_imagine_2309

Kojić S, Bošković S, Milovanović M, Stainie D, Juez RM, Jasnić J, Novković M, Milošević E. Zebrafish ankrd1a as a common player  in heart regeneration and skeletal muscle repair. in 10th Strategic Conference of Zebrafish Investigators. 2024;.
https://hdl.handle.net/21.15107/rcub_imagine_2309 .

Kojić, Snežana, Bošković, Srđan, Milovanović, Mina, Stainie, Didier, Juez, Rubén Marín, Jasnić, Jovana, Novković, Mirjana, Milošević, Emilija, "Zebrafish ankrd1a as a common player  in heart regeneration and skeletal muscle repair" in 10th Strategic Conference of Zebrafish Investigators (2024),
https://hdl.handle.net/21.15107/rcub_imagine_2309 .

TY  - CONF
AU  - Milovanović, Mina
AU  - Bošković, Srđan
AU  - Jasnić, Jovana
AU  - Novković, Mirjana
AU  - Milošević, Emilija
AU  - Kojić, Snežana
PY  - 2023
UR  - https://zebrafish2023.org/
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/2023
AB  - In our previous work, using transgenic zebrafish line TgBAC(ankrd1a:EGFP), we showed activation
of the zebrafish ankrd1a gene in border zone cardiomyocytes of cryoinjured heart and in close
proximity of needle-stab wounds in skeletal muscle, indicating its involvement in muscle
regeneration. Our results implicated ankrd1a in zebrafish skeletal muscle tissue repair and
remodeling, as a sensor of stressed muscle. Here we take a closer look at the spatio-temporal
expression profile of the ankrd1a gene in injured zebrafish skeletal muscle by analyzing cryosections
prepared from wounded tissue of TgBAC(ankrd1a:EGFP) adults at 1, 3, 5, 7 and 10 days post-injury
(dpi). The expression of the fluorescent reporter was observed from 3 dpi and remained until 10 dpi.
At 3dpi, new GFP-positive muscle cells emerged inside the injury zone, at the site of needle entry,
while in the later days (5, 7 and 10 dpi), newly formed GFP-positive myofibers were visible in the
deeper tissue layers within the injury, indicating active repair of the injured tissue. To identify cells
in which ankrd1a is activated after injury, we stained the sections for markers of satellite-like cells,
undifferentiated and differentiated muscle cells, and mature myofibers. Since the reporter was
detected both in the newly formed myofibers that invade the wound and in the apparently uninjured
tissue surrounding the injury, we hypothesize that ankrd1a is not only involved in satellite celldependent tissue repair, but its expression might be a hallmark of adaptive process in undamaged
myofibers surrounding the physical injury.
C3  - 12th European Zebrafish Meeting
T1  - Expression profile of ankrd1a during repair of injured zebrafish skeletal muscle
EP  - 276
SP  - 276
SP  - 0254
VL  - 14
VL  - 12
UR  - https://hdl.handle.net/21.15107/rcub_imagine_2023
ER  - 

@conference{
author = "Milovanović, Mina and Bošković, Srđan and Jasnić, Jovana and Novković, Mirjana and Milošević, Emilija and Kojić, Snežana",
year = "2023",
abstract = "In our previous work, using transgenic zebrafish line TgBAC(ankrd1a:EGFP), we showed activation
of the zebrafish ankrd1a gene in border zone cardiomyocytes of cryoinjured heart and in close
proximity of needle-stab wounds in skeletal muscle, indicating its involvement in muscle
regeneration. Our results implicated ankrd1a in zebrafish skeletal muscle tissue repair and
remodeling, as a sensor of stressed muscle. Here we take a closer look at the spatio-temporal
expression profile of the ankrd1a gene in injured zebrafish skeletal muscle by analyzing cryosections
prepared from wounded tissue of TgBAC(ankrd1a:EGFP) adults at 1, 3, 5, 7 and 10 days post-injury
(dpi). The expression of the fluorescent reporter was observed from 3 dpi and remained until 10 dpi.
At 3dpi, new GFP-positive muscle cells emerged inside the injury zone, at the site of needle entry,
while in the later days (5, 7 and 10 dpi), newly formed GFP-positive myofibers were visible in the
deeper tissue layers within the injury, indicating active repair of the injured tissue. To identify cells
in which ankrd1a is activated after injury, we stained the sections for markers of satellite-like cells,
undifferentiated and differentiated muscle cells, and mature myofibers. Since the reporter was
detected both in the newly formed myofibers that invade the wound and in the apparently uninjured
tissue surrounding the injury, we hypothesize that ankrd1a is not only involved in satellite celldependent tissue repair, but its expression might be a hallmark of adaptive process in undamaged
myofibers surrounding the physical injury.",
journal = "12th European Zebrafish Meeting",
title = "Expression profile of ankrd1a during repair of injured zebrafish skeletal muscle",
pages = "276-276-0254",
volume = "14, 12",
url = "https://hdl.handle.net/21.15107/rcub_imagine_2023"
}

Milovanović, M., Bošković, S., Jasnić, J., Novković, M., Milošević, E.,& Kojić, S.. (2023). Expression profile of ankrd1a during repair of injured zebrafish skeletal muscle. in 12th European Zebrafish Meeting, 14, 276-276.
https://hdl.handle.net/21.15107/rcub_imagine_2023

Milovanović M, Bošković S, Jasnić J, Novković M, Milošević E, Kojić S. Expression profile of ankrd1a during repair of injured zebrafish skeletal muscle. in 12th European Zebrafish Meeting. 2023;14:276-276.
https://hdl.handle.net/21.15107/rcub_imagine_2023 .

Milovanović, Mina, Bošković, Srđan, Jasnić, Jovana, Novković, Mirjana, Milošević, Emilija, Kojić, Snežana, "Expression profile of ankrd1a during repair of injured zebrafish skeletal muscle" in 12th European Zebrafish Meeting, 14 (2023):276-276,
https://hdl.handle.net/21.15107/rcub_imagine_2023 .

TY  - CONF
AU  - Milovanović, Mina
AU  - Bošković, Srđan
AU  - Jasnić, Jovana
AU  - Novković, Mirjana
AU  - Milošević, Emilija
AU  - Kojić, Snežana
PY  - 2023
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/2132
AB  - Introduction: In contrast to humans, zebrafish have a remarkable ability to regenerate injured heart
through a complex and highly orchestrated processinvolving all cardiac structures. The majorsource of
new myocardial cells are resident cardiomyocytes, which dedifferentiate and reinitiate proliferation, invading the area of injury to replace the lost myocardium. The response of the myocardium and coronary
vasculature is preceded by activation of epi- and endocardium, which form active scaffolds to guide regeneration. The aim of thisstudy wasto identify cardiac structuresin which ankrd1a gene is activated during zebrafish heart regeneration.
Methods: We crossed several zebrafish reporter lines: TgBAC(ankrd1a:EGFP) (to identify cells expressing
ankrd1a), Tg(myl7:nls-dsRedExpress) (for labeling cardiomyocyte nuclei) and Tg(kdrl:RAS-mCherry) (for labeling endocardial/endothelial cells). Zebrafish hearts were cryoinjured and left to regenerate for 3 and
7 days. Dedifferentiating cardiomyocytes and epicardial cells were immunostained with anti-MYH7 and
anti-caveolin1 antibody, respectively. Cells labeled with transgenes and immunostaining were visualized on tissue cryosections by fluorescent microscopy.
Results: Zebrafish ankrd1a was activated in the injury border zone cardiomyocytes, located between
the injured and remote myocardium. Its expression preceded that of a dedifferentiation marker, MYH7.
The TgBAC(ankrd1a:EGFP) transgene was not detected in epicardial or endocardial cells of regenerating
zebrafish heart.
Conclusion: Activation of ankrd1a during regeneration of zebrafish heart is restricted to borderzone
cardiomyocytes, implicating this gene in dedifferentiation and proliferation of cardiomyocytes. The absence of ankrd1a expression in epicardium and endocardium indicatesthat this gene does not contribute
to the regeneration process occuring in these layers of the heart.
PB  - Institute of Molecular Genetics and Genetic Engineering (IMGGE), University of Belgrade
C3  - CoMBoS2 – the Second Congress of Molecular Biologists of Serbia, Abstract Book – Trends in Molecular Biology, Special issue 06-08 October 2023, Belgrade, Serbia
T1  - Spatial profile of ankrd1a activation during regeneration of zebrafish heart
EP  - 141
SP  - 141
UR  - https://hdl.handle.net/21.15107/rcub_imagine_2132
ER  - 

@conference{
author = "Milovanović, Mina and Bošković, Srđan and Jasnić, Jovana and Novković, Mirjana and Milošević, Emilija and Kojić, Snežana",
year = "2023",
abstract = "Introduction: In contrast to humans, zebrafish have a remarkable ability to regenerate injured heart
through a complex and highly orchestrated processinvolving all cardiac structures. The majorsource of
new myocardial cells are resident cardiomyocytes, which dedifferentiate and reinitiate proliferation, invading the area of injury to replace the lost myocardium. The response of the myocardium and coronary
vasculature is preceded by activation of epi- and endocardium, which form active scaffolds to guide regeneration. The aim of thisstudy wasto identify cardiac structuresin which ankrd1a gene is activated during zebrafish heart regeneration.
Methods: We crossed several zebrafish reporter lines: TgBAC(ankrd1a:EGFP) (to identify cells expressing
ankrd1a), Tg(myl7:nls-dsRedExpress) (for labeling cardiomyocyte nuclei) and Tg(kdrl:RAS-mCherry) (for labeling endocardial/endothelial cells). Zebrafish hearts were cryoinjured and left to regenerate for 3 and
7 days. Dedifferentiating cardiomyocytes and epicardial cells were immunostained with anti-MYH7 and
anti-caveolin1 antibody, respectively. Cells labeled with transgenes and immunostaining were visualized on tissue cryosections by fluorescent microscopy.
Results: Zebrafish ankrd1a was activated in the injury border zone cardiomyocytes, located between
the injured and remote myocardium. Its expression preceded that of a dedifferentiation marker, MYH7.
The TgBAC(ankrd1a:EGFP) transgene was not detected in epicardial or endocardial cells of regenerating
zebrafish heart.
Conclusion: Activation of ankrd1a during regeneration of zebrafish heart is restricted to borderzone
cardiomyocytes, implicating this gene in dedifferentiation and proliferation of cardiomyocytes. The absence of ankrd1a expression in epicardium and endocardium indicatesthat this gene does not contribute
to the regeneration process occuring in these layers of the heart.",
publisher = "Institute of Molecular Genetics and Genetic Engineering (IMGGE), University of Belgrade",
journal = "CoMBoS2 – the Second Congress of Molecular Biologists of Serbia, Abstract Book – Trends in Molecular Biology, Special issue 06-08 October 2023, Belgrade, Serbia",
title = "Spatial profile of ankrd1a activation during regeneration of zebrafish heart",
pages = "141-141",
url = "https://hdl.handle.net/21.15107/rcub_imagine_2132"
}

Milovanović, M., Bošković, S., Jasnić, J., Novković, M., Milošević, E.,& Kojić, S.. (2023). Spatial profile of ankrd1a activation during regeneration of zebrafish heart. in CoMBoS2 – the Second Congress of Molecular Biologists of Serbia, Abstract Book – Trends in Molecular Biology, Special issue 06-08 October 2023, Belgrade, Serbia
Institute of Molecular Genetics and Genetic Engineering (IMGGE), University of Belgrade., 141-141.
https://hdl.handle.net/21.15107/rcub_imagine_2132

Milovanović M, Bošković S, Jasnić J, Novković M, Milošević E, Kojić S. Spatial profile of ankrd1a activation during regeneration of zebrafish heart. in CoMBoS2 – the Second Congress of Molecular Biologists of Serbia, Abstract Book – Trends in Molecular Biology, Special issue 06-08 October 2023, Belgrade, Serbia. 2023;:141-141.
https://hdl.handle.net/21.15107/rcub_imagine_2132 .

Milovanović, Mina, Bošković, Srđan, Jasnić, Jovana, Novković, Mirjana, Milošević, Emilija, Kojić, Snežana, "Spatial profile of ankrd1a activation during regeneration of zebrafish heart" in CoMBoS2 – the Second Congress of Molecular Biologists of Serbia, Abstract Book – Trends in Molecular Biology, Special issue 06-08 October 2023, Belgrade, Serbia (2023):141-141,
https://hdl.handle.net/21.15107/rcub_imagine_2132 .

TY  - CONF
AU  - Novković, Mirjana
AU  - Vasić, Marko
AU  - Jasnić, Jovana
AU  - Milošević, Emilija
AU  - Milovanović, Mina
AU  - Savić, Slobodan
AU  - Kojić, Snežana
PY  - 2023
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/2114
AB  - Introduction: Ankyrin Repeat Domain 2 (ANKRD2) is expressed in skeletal muscle, where plays a role in
muscle development, differentiation and adaptation to stress. Human skeletal muscle consists of three
major fiber types: type 1 (slow-twitch, oxidative), type 2A (fast-twitch, oxidative) and type 2X (fast-twitch,
glycolytic). ANKRD2 is reported to be primarily expressed in type 1 myofibers. However, recent findings
on human single myofibers and our study of chicken muscles have shown that this protein may also be
expressed in type 2A fibers. Hence, our objective was to examine whether ANKRD2 is present in human
fast, type 2A muscle fibers using immunohistochemistry.
Methods: Samples of large leg musclessoleus, gastrocnemius, vastusintermedius and vastuslateralis were
obtained from human cadaveric tissue. Serial cryosections were independently stained with anti-ANKRD2
and antibodies for different myosin heavy chain isoforms (6H1 for type 2X, BF35 for type 1 and 2A, antiMHCs for type 1 and anti-MHCf for type 2A and 2X fibers). Immunostained tissues were analyzed by fluorescent microscopy.
Results: In addition to slow, type 1, ANKRD2 wasfound expressed in fast, type 2A myofibers, which both
have oxidative metabolism. Further, we did not observe ANDRD2 expression in glycolytic, type 2X
myiofibers. This pattern of ANKRD2 expression was consistent across all examined muscles.
Conclusion: Our resultsimplicate that the regulatory mechanism of ANKRD2 expression in human skeletal muscle is associated with oxidative metabolism, rather than muscle contraction speed.
PB  - Institute of Molecular Genetics and Genetic Engineering (IMGGE), University of Belgrade
C3  - CoMBoS2 – the Second Congress of Molecular Biologists of Serbia, Abstract Book – Trends in Molecular Biology, Special issue 06-08 October 2023, Belgrade, Serbia
T1  - Determination of muscle fiber types expressing ANKRD2
EP  - 155
SP  - 155
UR  - https://hdl.handle.net/21.15107/rcub_imagine_2114
ER  - 

@conference{
author = "Novković, Mirjana and Vasić, Marko and Jasnić, Jovana and Milošević, Emilija and Milovanović, Mina and Savić, Slobodan and Kojić, Snežana",
year = "2023",
abstract = "Introduction: Ankyrin Repeat Domain 2 (ANKRD2) is expressed in skeletal muscle, where plays a role in
muscle development, differentiation and adaptation to stress. Human skeletal muscle consists of three
major fiber types: type 1 (slow-twitch, oxidative), type 2A (fast-twitch, oxidative) and type 2X (fast-twitch,
glycolytic). ANKRD2 is reported to be primarily expressed in type 1 myofibers. However, recent findings
on human single myofibers and our study of chicken muscles have shown that this protein may also be
expressed in type 2A fibers. Hence, our objective was to examine whether ANKRD2 is present in human
fast, type 2A muscle fibers using immunohistochemistry.
Methods: Samples of large leg musclessoleus, gastrocnemius, vastusintermedius and vastuslateralis were
obtained from human cadaveric tissue. Serial cryosections were independently stained with anti-ANKRD2
and antibodies for different myosin heavy chain isoforms (6H1 for type 2X, BF35 for type 1 and 2A, antiMHCs for type 1 and anti-MHCf for type 2A and 2X fibers). Immunostained tissues were analyzed by fluorescent microscopy.
Results: In addition to slow, type 1, ANKRD2 wasfound expressed in fast, type 2A myofibers, which both
have oxidative metabolism. Further, we did not observe ANDRD2 expression in glycolytic, type 2X
myiofibers. This pattern of ANKRD2 expression was consistent across all examined muscles.
Conclusion: Our resultsimplicate that the regulatory mechanism of ANKRD2 expression in human skeletal muscle is associated with oxidative metabolism, rather than muscle contraction speed.",
publisher = "Institute of Molecular Genetics and Genetic Engineering (IMGGE), University of Belgrade",
journal = "CoMBoS2 – the Second Congress of Molecular Biologists of Serbia, Abstract Book – Trends in Molecular Biology, Special issue 06-08 October 2023, Belgrade, Serbia",
title = "Determination of muscle fiber types expressing ANKRD2",
pages = "155-155",
url = "https://hdl.handle.net/21.15107/rcub_imagine_2114"
}

Novković, M., Vasić, M., Jasnić, J., Milošević, E., Milovanović, M., Savić, S.,& Kojić, S.. (2023). Determination of muscle fiber types expressing ANKRD2. in CoMBoS2 – the Second Congress of Molecular Biologists of Serbia, Abstract Book – Trends in Molecular Biology, Special issue 06-08 October 2023, Belgrade, Serbia
Institute of Molecular Genetics and Genetic Engineering (IMGGE), University of Belgrade., 155-155.
https://hdl.handle.net/21.15107/rcub_imagine_2114

Novković M, Vasić M, Jasnić J, Milošević E, Milovanović M, Savić S, Kojić S. Determination of muscle fiber types expressing ANKRD2. in CoMBoS2 – the Second Congress of Molecular Biologists of Serbia, Abstract Book – Trends in Molecular Biology, Special issue 06-08 October 2023, Belgrade, Serbia. 2023;:155-155.
https://hdl.handle.net/21.15107/rcub_imagine_2114 .

Novković, Mirjana, Vasić, Marko, Jasnić, Jovana, Milošević, Emilija, Milovanović, Mina, Savić, Slobodan, Kojić, Snežana, "Determination of muscle fiber types expressing ANKRD2" in CoMBoS2 – the Second Congress of Molecular Biologists of Serbia, Abstract Book – Trends in Molecular Biology, Special issue 06-08 October 2023, Belgrade, Serbia (2023):155-155,
https://hdl.handle.net/21.15107/rcub_imagine_2114 .

TY  - CONF
AU  - Kojić, Snežana
AU  - Bošković, Srđan
AU  - Milovanović, Mina
PY  - 2022
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1746
AB  - Nakon infarkta miokarda povređeno srce čoveka ne može da se regeneriše, već
reaguje formiranjem fibrotičnog ožiljka i remodelovanjem miokarda, koji dovode
do slabljenja njegove funkcije. Miokard sisara je dugo vremena smatran
postmitotičkim i terminalno diferenciranim tkivom. Međutim, kardiomiociti
sisara poseduju ograničenu sposobnost proliferacije. Njihova deoba je redak
događaj i odvija se po veoma niskoj stopi, što svakako nije dovoljno da nadoknadi
milione kardiomiocita trajno izgubljenih usled infarkta miokarda. Trenutno se
u svetu razvijaju dve strategije za podsticanje regeneracije povređenog srca
čoveka kako bi se povratile njegova struktura i funkcija. Jedna strategija
podrazumeva naseljavanje oštećenog tkiva zdravim kardiomiocitima poreklom od
indukovanih pluripotentnih ćelija, dok je cilj druge strategije aktivacija
endogenih mehanizama regeneracije. Za razliku od čoveka, neki kičmenjaci imaju
sposobnost regeneracije povređenih organa, uključujući srce. Životinja koja se
najčešće koristi za proučavanje regeneracije srca je riba zebrica (Danio rerio).
Pionirska studija o izuzetnom regenerativnom kapacitetu srca zebrice nakon
amputacije dela komore objavljena je 2002. godine, nakon koje je usledilo mnoštvo
publikacija o ćelijskim i molekularnim mehanizmima koji doprinose
regenerativnom odgovoru. Regeneracija srca zebrice je rezultat strogo regulisane
interakcije većeg broja procesa, uključujući inflamatorni odgovor,
dediferencijaciju i proliferaciju kardiomiocita, neovaskularizaciju i
reorganizaciju ekstraćelijskog matriksa. Regeneracija se može posmatrati kao
uspavan proces u organima koji ne regenerišu i manipulacijom ovog procesa bi
se mogla postići reaktivacija proliferacije u tim organima nakon povrede.
Ispitivanje interakcije između pro-regenerišućih mehanizama i procesa koji
utiču na regenerativni kapacitet treba da dovede do identifikacije faktora
potrebnih za prevazilaženje blokade regeneracije. Na taj način bi se razvile nove
strategije za indukciju proliferacije kardiomiocita i regeneraciju srca čoveka.
AB  - Након инфаркта миокарда повређено срце човека не може да се регенерише, већ
реагује формирањем фибротичног ожиљка и ремоделовањем миокарда, који доводе
до слабљења његове функције. Миокард сисара је дуго времена сматран
постмитотичким и терминално диференцираним ткивом. Међутим, кардиомиоцити
сисара поседују ограничену способност пролиферације. Њихова деоба је редак
догађај и одвија се по веома ниској стопи, што свакако није довољно да надокнади
милионе кардиомиоцита трајно изгубљених услед инфаркта миокарда. Тренутно се
у свету развијају две стратегије за подстицање регенерације повређеног срца
човека како би се повратиле његова структура и функција. Једна стратегија
подразумева насељавање оштећеног ткива здравим кардиомиоцитима пореклом од
индукованих плурипотентних ћелија, док је циљ друге стратегије активација
ендогених механизама регенерације. За разлику од човека, неки кичмењаци имају
способност регенерације повређених органа, укључујући срце. Животиња која се
најчешће користи за проучавање регенерације срца је риба зебрица (Danio rerio).
Пионирска студија о изузетном регенеративном капацитету срца зебрице након
ампутације дела коморе објављена је 2002. године, након које је уследило мноштво
публикација о ћелијским и молекуларним механизмима који доприносе
регенеративном одговору. Регенерација срца зебрице је резултат строго регулисане
интеракције већег броја процеса, укључујући инфламаторни одговор,
дедиференцијацију и пролиферацију кардиомиоцита, неоваскуларизацију и
реорганизацију екстраћелијског матрикса. Регенерација се може посматрати као
успаван процес у органима који не регенеришу и манипулацијом овог процеса би
се могла постићи реактивација пролиферације у тим органима након повреде.
Испитивање интеракције између про-регенеришућих механизама и процеса који
утичу на регенеративни капацитет треба да доведе до идентификације фактора
потребних за превазилажење блокаде регенерације. На тај начин би се развиле нове
стратегије за индукцију пролиферације кардиомиоцита и регенерацију срца човека.
PB  - Beograd : Srpsko biološko društvo
C3  - Treći kongres biologa Srbije
T1  - Mehanizmi regeneracije srca – šta možemo naučiti od zebrice
T1  - Механизми регенерације срца – шта можемо научити од зебрице
SP  - 288
UR  - https://hdl.handle.net/21.15107/rcub_imagine_1746
ER  - 

@conference{
author = "Kojić, Snežana and Bošković, Srđan and Milovanović, Mina",
year = "2022",
abstract = "Nakon infarkta miokarda povređeno srce čoveka ne može da se regeneriše, već
reaguje formiranjem fibrotičnog ožiljka i remodelovanjem miokarda, koji dovode
do slabljenja njegove funkcije. Miokard sisara je dugo vremena smatran
postmitotičkim i terminalno diferenciranim tkivom. Međutim, kardiomiociti
sisara poseduju ograničenu sposobnost proliferacije. Njihova deoba je redak
događaj i odvija se po veoma niskoj stopi, što svakako nije dovoljno da nadoknadi
milione kardiomiocita trajno izgubljenih usled infarkta miokarda. Trenutno se
u svetu razvijaju dve strategije za podsticanje regeneracije povređenog srca
čoveka kako bi se povratile njegova struktura i funkcija. Jedna strategija
podrazumeva naseljavanje oštećenog tkiva zdravim kardiomiocitima poreklom od
indukovanih pluripotentnih ćelija, dok je cilj druge strategije aktivacija
endogenih mehanizama regeneracije. Za razliku od čoveka, neki kičmenjaci imaju
sposobnost regeneracije povređenih organa, uključujući srce. Životinja koja se
najčešće koristi za proučavanje regeneracije srca je riba zebrica (Danio rerio).
Pionirska studija o izuzetnom regenerativnom kapacitetu srca zebrice nakon
amputacije dela komore objavljena je 2002. godine, nakon koje je usledilo mnoštvo
publikacija o ćelijskim i molekularnim mehanizmima koji doprinose
regenerativnom odgovoru. Regeneracija srca zebrice je rezultat strogo regulisane
interakcije većeg broja procesa, uključujući inflamatorni odgovor,
dediferencijaciju i proliferaciju kardiomiocita, neovaskularizaciju i
reorganizaciju ekstraćelijskog matriksa. Regeneracija se može posmatrati kao
uspavan proces u organima koji ne regenerišu i manipulacijom ovog procesa bi
se mogla postići reaktivacija proliferacije u tim organima nakon povrede.
Ispitivanje interakcije između pro-regenerišućih mehanizama i procesa koji
utiču na regenerativni kapacitet treba da dovede do identifikacije faktora
potrebnih za prevazilaženje blokade regeneracije. Na taj način bi se razvile nove
strategije za indukciju proliferacije kardiomiocita i regeneraciju srca čoveka., Након инфаркта миокарда повређено срце човека не може да се регенерише, већ
реагује формирањем фибротичног ожиљка и ремоделовањем миокарда, који доводе
до слабљења његове функције. Миокард сисара је дуго времена сматран
постмитотичким и терминално диференцираним ткивом. Међутим, кардиомиоцити
сисара поседују ограничену способност пролиферације. Њихова деоба је редак
догађај и одвија се по веома ниској стопи, што свакако није довољно да надокнади
милионе кардиомиоцита трајно изгубљених услед инфаркта миокарда. Тренутно се
у свету развијају две стратегије за подстицање регенерације повређеног срца
човека како би се повратиле његова структура и функција. Једна стратегија
подразумева насељавање оштећеног ткива здравим кардиомиоцитима пореклом од
индукованих плурипотентних ћелија, док је циљ друге стратегије активација
ендогених механизама регенерације. За разлику од човека, неки кичмењаци имају
способност регенерације повређених органа, укључујући срце. Животиња која се
најчешће користи за проучавање регенерације срца је риба зебрица (Danio rerio).
Пионирска студија о изузетном регенеративном капацитету срца зебрице након
ампутације дела коморе објављена је 2002. године, након које је уследило мноштво
публикација о ћелијским и молекуларним механизмима који доприносе
регенеративном одговору. Регенерација срца зебрице је резултат строго регулисане
интеракције већег броја процеса, укључујући инфламаторни одговор,
дедиференцијацију и пролиферацију кардиомиоцита, неоваскуларизацију и
реорганизацију екстраћелијског матрикса. Регенерација се може посматрати као
успаван процес у органима који не регенеришу и манипулацијом овог процеса би
се могла постићи реактивација пролиферације у тим органима након повреде.
Испитивање интеракције између про-регенеришућих механизама и процеса који
утичу на регенеративни капацитет треба да доведе до идентификације фактора
потребних за превазилажење блокаде регенерације. На тај начин би се развиле нове
стратегије за индукцију пролиферације кардиомиоцита и регенерацију срца човека.",
publisher = "Beograd : Srpsko biološko društvo",
journal = "Treći kongres biologa Srbije",
title = "Mehanizmi regeneracije srca – šta možemo naučiti od zebrice, Механизми регенерације срца – шта можемо научити од зебрице",
pages = "288",
url = "https://hdl.handle.net/21.15107/rcub_imagine_1746"
}

Kojić, S., Bošković, S.,& Milovanović, M.. (2022). Mehanizmi regeneracije srca – šta možemo naučiti od zebrice. in Treći kongres biologa Srbije
Beograd : Srpsko biološko društvo., 288.
https://hdl.handle.net/21.15107/rcub_imagine_1746

Kojić S, Bošković S, Milovanović M. Mehanizmi regeneracije srca – šta možemo naučiti od zebrice. in Treći kongres biologa Srbije. 2022;:288.
https://hdl.handle.net/21.15107/rcub_imagine_1746 .

Kojić, Snežana, Bošković, Srđan, Milovanović, Mina, "Mehanizmi regeneracije srca – šta možemo naučiti od zebrice" in Treći kongres biologa Srbije (2022):288,
https://hdl.handle.net/21.15107/rcub_imagine_1746 .