Hepatic cell mobilization for protection against ischemic myocardial injury

Abstract The heart is capable of activating protective mechanisms in response to ischemic injury to support myocardial survival and performance. These mechanisms have been recognized primarily in the ischemic heart, involving paracrine signaling processes. Here, we report a distant cardioprotective...

Descripción completa

Guardado en:

Detalles Bibliográficos
Autores principales:	Shu Q. Liu, John B. Troy, Chi-Hao Luan, Roger J. Guillory
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/cc24b5925a3e480d9684db15bc56349a
Etiquetas:	Agregar Etiqueta Sin Etiquetas, Sea el primero en etiquetar este registro!

id	oai:doaj.org-article:cc24b5925a3e480d9684db15bc56349a
record_format	dspace
spelling	oai:doaj.org-article:cc24b5925a3e480d9684db15bc56349a2021-12-02T18:49:27ZHepatic cell mobilization for protection against ischemic myocardial injury10.1038/s41598-021-94170-z2045-2322https://doaj.org/article/cc24b5925a3e480d9684db15bc56349a2021-08-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-94170-zhttps://doaj.org/toc/2045-2322Abstract The heart is capable of activating protective mechanisms in response to ischemic injury to support myocardial survival and performance. These mechanisms have been recognized primarily in the ischemic heart, involving paracrine signaling processes. Here, we report a distant cardioprotective mechanism involving hepatic cell mobilization to the ischemic myocardium in response to experimental myocardial ischemia–reperfusion (MI-R) injury. A parabiotic mouse model was generated by surgical skin-union of two mice and used to induce bilateral MI-R injury with unilateral hepatectomy, establishing concurrent gain- and loss-of-hepatic cell mobilization conditions. Hepatic cells, identified based on the cell-specific expression of enhanced YFP, were found in the ischemic myocardium of parabiotic mice with intact liver (0.2 ± 0.1%, 1.1 ± 0.3%, 2.7 ± 0.6, and 0.7 ± 0.4% at 1, 3, 5, and 10 days, respectively, in reference to the total cell nuclei), but not significantly in the ischemic myocardium of parabiotic mice with hepatectomy (0 ± 0%, 0.1 ± 0.1%, 0.3 ± 0.2%, and 0.08 ± 0.08% at the same time points). The mobilized hepatic cells were able to express and release trefoil factor 3 (TFF3), a protein mitigating MI-R injury as demonstrated in TFF3−/− mice (myocardium infarcts 17.6 ± 2.3%, 20.7 ± 2.6%, and 15.3 ± 3.8% at 1, 5, and 10 days, respectively) in reference to wildtype mice (11.7 ± 1.9%, 13.8 ± 2.3%, and 11.0 ± 1.8% at the same time points). These observations suggest that MI-R injury can induce hepatic cell mobilization to support myocardial survival by releasing TFF3.Shu Q. LiuJohn B. TroyChi-Hao LuanRoger J. GuilloryNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-14 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Shu Q. Liu John B. Troy Chi-Hao Luan Roger J. Guillory Hepatic cell mobilization for protection against ischemic myocardial injury
description	Abstract The heart is capable of activating protective mechanisms in response to ischemic injury to support myocardial survival and performance. These mechanisms have been recognized primarily in the ischemic heart, involving paracrine signaling processes. Here, we report a distant cardioprotective mechanism involving hepatic cell mobilization to the ischemic myocardium in response to experimental myocardial ischemia–reperfusion (MI-R) injury. A parabiotic mouse model was generated by surgical skin-union of two mice and used to induce bilateral MI-R injury with unilateral hepatectomy, establishing concurrent gain- and loss-of-hepatic cell mobilization conditions. Hepatic cells, identified based on the cell-specific expression of enhanced YFP, were found in the ischemic myocardium of parabiotic mice with intact liver (0.2 ± 0.1%, 1.1 ± 0.3%, 2.7 ± 0.6, and 0.7 ± 0.4% at 1, 3, 5, and 10 days, respectively, in reference to the total cell nuclei), but not significantly in the ischemic myocardium of parabiotic mice with hepatectomy (0 ± 0%, 0.1 ± 0.1%, 0.3 ± 0.2%, and 0.08 ± 0.08% at the same time points). The mobilized hepatic cells were able to express and release trefoil factor 3 (TFF3), a protein mitigating MI-R injury as demonstrated in TFF3−/− mice (myocardium infarcts 17.6 ± 2.3%, 20.7 ± 2.6%, and 15.3 ± 3.8% at 1, 5, and 10 days, respectively) in reference to wildtype mice (11.7 ± 1.9%, 13.8 ± 2.3%, and 11.0 ± 1.8% at the same time points). These observations suggest that MI-R injury can induce hepatic cell mobilization to support myocardial survival by releasing TFF3.
format	article
author	Shu Q. Liu John B. Troy Chi-Hao Luan Roger J. Guillory
author_facet	Shu Q. Liu John B. Troy Chi-Hao Luan Roger J. Guillory
author_sort	Shu Q. Liu
title	Hepatic cell mobilization for protection against ischemic myocardial injury
title_short	Hepatic cell mobilization for protection against ischemic myocardial injury
title_full	Hepatic cell mobilization for protection against ischemic myocardial injury
title_fullStr	Hepatic cell mobilization for protection against ischemic myocardial injury
title_full_unstemmed	Hepatic cell mobilization for protection against ischemic myocardial injury
title_sort	hepatic cell mobilization for protection against ischemic myocardial injury
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/cc24b5925a3e480d9684db15bc56349a
work_keys_str_mv	AT shuqliu hepaticcellmobilizationforprotectionagainstischemicmyocardialinjury AT johnbtroy hepaticcellmobilizationforprotectionagainstischemicmyocardialinjury AT chihaoluan hepaticcellmobilizationforprotectionagainstischemicmyocardialinjury AT rogerjguillory hepaticcellmobilizationforprotectionagainstischemicmyocardialinjury
_version_	1718377590226419712

Hepatic cell mobilization for protection against ischemic myocardial injury

Ejemplares similares