The protective role of GATA6

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00023001%3A_____%2F24%3A00084972" target="_blank" >RIV/00023001:_____/24:00084972 - isvavai.cz</a>

Výsledek na webu

<a href="https://www.sciencedirect.com/science/article/pii/S258900422401469X?via%3Dihub" target="_blank" >https://www.sciencedirect.com/science/article/pii/S258900422401469X?via%3Dihub</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1016/j.isci.2024.110244" target="_blank" >10.1016/j.isci.2024.110244</a>

Jazyk výsledku

angličtina

Název v původním jazyce

The protective role of GATA6

Popis výsledku v původním jazyce

Prior research has suggested that GATA6 + pericardial macrophages may traffic to the myocardium to prevent interstitial fibrosis after myocardial infarction (MI), while subsequent literature claims that they do not. We demonstrate that GATA6 + pericardial macrophages are critical for preventing IL -33 induced pericarditis and attenuate trafficking of inflammatory monocytes and granulocytes to the pericardial cavity after MI. However, absence of GATA6 + macrophages did not affect myocardial inflammation due to MI or coxsackievirus-B3 induced myocarditis, or late -stage cardiac fibrosis and cardiac function post MI. GATA6 + macrophages are significantly less transcriptionally active following stimulation in vitro compared to bone marrow -derived macrophages and do not induce upregulation of inflammatory markers in fibroblasts. This suggests that GATA6 + pericardial macrophages attenuate inflammation through their interactions with surrounding cells. We therefore conclude that GATA6 + pericardial macrophages are critical in modulating pericardial inflammation, but do not play a significant role in controlling myocardial inflammation or fibrosis.

Název v anglickém jazyce

The protective role of GATA6

Popis výsledku anglicky

Prior research has suggested that GATA6 + pericardial macrophages may traffic to the myocardium to prevent interstitial fibrosis after myocardial infarction (MI), while subsequent literature claims that they do not. We demonstrate that GATA6 + pericardial macrophages are critical for preventing IL -33 induced pericarditis and attenuate trafficking of inflammatory monocytes and granulocytes to the pericardial cavity after MI. However, absence of GATA6 + macrophages did not affect myocardial inflammation due to MI or coxsackievirus-B3 induced myocarditis, or late -stage cardiac fibrosis and cardiac function post MI. GATA6 + macrophages are significantly less transcriptionally active following stimulation in vitro compared to bone marrow -derived macrophages and do not induce upregulation of inflammatory markers in fibroblasts. This suggests that GATA6 + pericardial macrophages attenuate inflammation through their interactions with surrounding cells. We therefore conclude that GATA6 + pericardial macrophages are critical in modulating pericardial inflammation, but do not play a significant role in controlling myocardial inflammation or fibrosis.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

30201 - Cardiac and Cardiovascular systems

Projekt

Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Rok uplatnění

2024

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

iScience

ISSN

2589-0042

e-ISSN

2589-0042

Svazek periodika

27

Číslo periodika v rámci svazku

7

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

21

Strana od-do

"art. no. 110244"

Kód UT WoS článku

001261512200001

EID výsledku v databázi Scopus

2-s2.0-85196840578