Hepatic cell mobilization for protection against ischemic myocardial injury.
Hepatic cell mobilization for protection against ischemic myocardial injury.
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DOI：
10.1038/s41598-021-94170-z
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发表时间：
2021-08-04
影响因子：
4.6
通讯作者：
Guillory RJ
中科院分区：
文献类型：
--
作者：
Liu SQ;Troy JB;Luan CH;Guillory RJ
心脏能够激活保护机制以响应缺血性损伤，从而支持心肌存活和性能。这些机制主要在缺血性心脏中被认识到，涉及旁分泌信号传导过程。在这里，我们报告了一个遥远的心脏保护机制，涉及肝细胞动员缺血心肌在实验性心肌缺血再灌注（MI-R）损伤。通过两只小鼠的手术皮肤愈合产生联体小鼠模型，并用于通过单侧肝切除术诱导双侧MI-R损伤，建立同时获得和丧失肝细胞动员条件。基于增强的YFP的细胞特异性表达鉴定的肝细胞在具有完整肝脏的联体小鼠的缺血心肌中被发现（第1、3、5和10天分别为0.2 ± 0.1%、1.1 ± 0.3%、2.7 ± 0.6和0.7 ± 0.4%，相对于总细胞核），而在同种异体肝切除小鼠的缺血心肌中无显著性差异（0 ± 0%，0.1 ± 0.1%，0.3 ± 0.2%，0.08 ± 0.08%）。动员的肝细胞能够表达和释放三叶因子3（TFF 3），这是一种减轻MI-R损伤的蛋白质，在TFF 3 −/−小鼠中得到证实（1、5和10天时心肌梗死率分别为17.6 ± 2.3%、20.7 ± 2.6%和15.3 ± 3.8%）（在相同时间点为11.7 ± 1.9%、13.8 ± 2.3%和11.0 ± 1.8%）。这些观察结果表明，MI-R损伤可以诱导肝细胞动员，通过释放TFF 3来支持心肌存活。
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.
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影响因子：
4.8
作者：
Jackerott, Malene;Lee, Ying C.;Nielsen, Jens H.
通讯作者：
Nielsen, Jens H.
DOI：
10.1016/s0022-2828(02)00310-3
发表时间：
2003-02-01
影响因子：
5
作者：
Bell, RM;Yellon, DM
通讯作者：
Yellon, DM
影响因子：
14.8
作者：
通讯作者：
--
影响因子：
7.3
作者：
Leung, WK;Yu, J;Sung, JJY
通讯作者：
Sung, JJY
影响因子：
20.1
作者：
Kucia, M;Dawn, B;Ratajczak, MZ
通讯作者：
Ratajczak, MZ