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://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  - 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 .

TY  - GEN
PY  - 2021
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/2272
AB  - ZEBARR project aims to contribute to better understanding of cellular and molecular
mechanisms of healing injured cardiac and skeletal muscles by investigating a common player
that participates in both processes. As a model organism competent in both regeneration of the
heart and repair of skeletal muscle after injury we will use adult zebrafish. Injured zebrafish
heart gets fully regenerated in 60 days by proliferation of unaffected cardiomyocytes, while
skeletal muscle replace injured tissue by activation of dedicated pool of stem cells called
satellite-like cells, that pass thought transformation to form myofibers. Do these processes
have common players and if they do in which particular molecular event(s) they participate?
Are there any points of intersection? We hypothesized that these players and associated
pathways do exist and might help to unlock endogenous regenerative mechanism of human
heart. In our preliminary experiments, ankrd1a gene, homologue of mammalian pleiotropic
transcriptional regulator ANKRD1, stood out as a common player in these processes, since it
was found activated in both muscle tissues after the injury (cryoinjury of ventricle wall and stab
wound of skeletal muscle). Deciphering precise role of ankrd1a in different pathways involved
in regeneration of zebrafish heart and repair of skeletal muscle and its contribution to the
regenerative potential of different zebrafish muscles will help us to understand these very
important processes in depth. Moreover, ankrd1a might become strong candidate for
consideration when designing novel strategies for healing human heart after myocardial
infraction.
Experimental work will be organized in five work packages:
WP1. Determination of spatio-temporal profile of ankrd1a expression after injury of adult
zebrafish heart and skeletal muscle.
WP2. Investigation of ankrd1a function in regeneration of adult zebrafish heart.
WP3. Investigation of ankrd1a function in repair of adult zebrafish skeletal muscle.
WP4. Identification of ankrd1a downstream targets and associated pathways involved in
regeneration of heart and repair of skeletal muscle of adult zebrafish
WP5. Testing the mediator role of ankrd1a in the beneficial effect of exercise on regeneration
of heart and repair of skeletal muscle.
T2  - Science Fund of the Republic of Serbia, Program IDEAS
T1  - Zebrafish ankrd1a as a common player in heart regeneration and skeletal muscle repair - a new prospect for unlocking regenerative potential of human heart (ZEBARR)
UR  - https://hdl.handle.net/21.15107/rcub_imagine_2272
ER  - 

@misc{
year = "2021",
abstract = "ZEBARR project aims to contribute to better understanding of cellular and molecular
mechanisms of healing injured cardiac and skeletal muscles by investigating a common player
that participates in both processes. As a model organism competent in both regeneration of the
heart and repair of skeletal muscle after injury we will use adult zebrafish. Injured zebrafish
heart gets fully regenerated in 60 days by proliferation of unaffected cardiomyocytes, while
skeletal muscle replace injured tissue by activation of dedicated pool of stem cells called
satellite-like cells, that pass thought transformation to form myofibers. Do these processes
have common players and if they do in which particular molecular event(s) they participate?
Are there any points of intersection? We hypothesized that these players and associated
pathways do exist and might help to unlock endogenous regenerative mechanism of human
heart. In our preliminary experiments, ankrd1a gene, homologue of mammalian pleiotropic
transcriptional regulator ANKRD1, stood out as a common player in these processes, since it
was found activated in both muscle tissues after the injury (cryoinjury of ventricle wall and stab
wound of skeletal muscle). Deciphering precise role of ankrd1a in different pathways involved
in regeneration of zebrafish heart and repair of skeletal muscle and its contribution to the
regenerative potential of different zebrafish muscles will help us to understand these very
important processes in depth. Moreover, ankrd1a might become strong candidate for
consideration when designing novel strategies for healing human heart after myocardial
infraction.
Experimental work will be organized in five work packages:
WP1. Determination of spatio-temporal profile of ankrd1a expression after injury of adult
zebrafish heart and skeletal muscle.
WP2. Investigation of ankrd1a function in regeneration of adult zebrafish heart.
WP3. Investigation of ankrd1a function in repair of adult zebrafish skeletal muscle.
WP4. Identification of ankrd1a downstream targets and associated pathways involved in
regeneration of heart and repair of skeletal muscle of adult zebrafish
WP5. Testing the mediator role of ankrd1a in the beneficial effect of exercise on regeneration
of heart and repair of skeletal muscle.",
journal = "Science Fund of the Republic of Serbia, Program IDEAS",
title = "Zebrafish ankrd1a as a common player in heart regeneration and skeletal muscle repair - a new prospect for unlocking regenerative potential of human heart (ZEBARR)",
url = "https://hdl.handle.net/21.15107/rcub_imagine_2272"
}

(2021). Zebrafish ankrd1a as a common player in heart regeneration and skeletal muscle repair - a new prospect for unlocking regenerative potential of human heart (ZEBARR). in Science Fund of the Republic of Serbia, Program IDEAS.
https://hdl.handle.net/21.15107/rcub_imagine_2272

Zebrafish ankrd1a as a common player in heart regeneration and skeletal muscle repair - a new prospect for unlocking regenerative potential of human heart (ZEBARR). in Science Fund of the Republic of Serbia, Program IDEAS. 2021;.
https://hdl.handle.net/21.15107/rcub_imagine_2272 .

"Zebrafish ankrd1a as a common player in heart regeneration and skeletal muscle repair - a new prospect for unlocking regenerative potential of human heart (ZEBARR)" in Science Fund of the Republic of Serbia, Program IDEAS (2021),
https://hdl.handle.net/21.15107/rcub_imagine_2272 .