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Midkine-a regulates the formation of a fibrotic scar during zebrafish heart regeneration
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AbstractThe adult zebrafish heart regenerates after injury, unlike the hearts of mammals. Heart cryoinjury triggers the formation of a fibrotic scar that gradually degrades, leading to regeneration. Midkine-a (Mdka) is a multifunctional cytokine that is activated after cardiac injury. Here, we investigated the role ofmdkain zebrafish heart regeneration. We show thatmdkaexpression is strongly induced at 1-day post cryoinjury (dpci) throughout the epicardium, whereas by 7 dpci expression has become restricted to epicardial cells covering the injured area. To study the role ofmdkain heart regeneration, we generatedmdka-knock out (KO) zebrafish strains. Analysis of injured hearts showed that loss ofmdkadecreased endothelial cell proliferation and resulted in a blockade of heart regeneration characterized by retention of a collagenous scar. Transcriptional analysis revealed increases in collagen transcription and TGFβ signalling activity. These results reveal a critical role formdkain fibrosis regulation during heart regeneration.
Title: Midkine-a regulates the formation of a fibrotic scar during zebrafish heart regeneration
Description:
AbstractThe adult zebrafish heart regenerates after injury, unlike the hearts of mammals.
Heart cryoinjury triggers the formation of a fibrotic scar that gradually degrades, leading to regeneration.
Midkine-a (Mdka) is a multifunctional cytokine that is activated after cardiac injury.
Here, we investigated the role ofmdkain zebrafish heart regeneration.
We show thatmdkaexpression is strongly induced at 1-day post cryoinjury (dpci) throughout the epicardium, whereas by 7 dpci expression has become restricted to epicardial cells covering the injured area.
To study the role ofmdkain heart regeneration, we generatedmdka-knock out (KO) zebrafish strains.
Analysis of injured hearts showed that loss ofmdkadecreased endothelial cell proliferation and resulted in a blockade of heart regeneration characterized by retention of a collagenous scar.
Transcriptional analysis revealed increases in collagen transcription and TGFβ signalling activity.
These results reveal a critical role formdkain fibrosis regulation during heart regeneration.
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