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首页> 外文期刊>Circulation research: a journal of the American Heart Association >Induction of the CXC chemokine interferon-gamma-inducible protein 10 regulates the reparative response following myocardial infarction.
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Induction of the CXC chemokine interferon-gamma-inducible protein 10 regulates the reparative response following myocardial infarction.

机译：CXC趋化因子干扰素-γ-诱导蛋白10的诱导调节心肌梗塞后的修复反应。

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RATIONALE: Interferon-gamma-inducible protein (IP)-10/CXCL10, an angiostatic and antifibrotic chemokine with an important role in T-cell trafficking, is markedly induced in myocardial infarcts, and may regulate the reparative response. OBJECTIVE: To study the role of IP-10 in cardiac repair and remodeling. METHODS AND RESULTS: We studied cardiac repair in IP-10-null and wild-type (WT) mice undergoing reperfused infarction protocols and examined the effects of IP-10 on cardiac fibroblast function. IP-10-deficient and WT animals had comparable acute infarct size. However, the absence of IP-10 resulted in a hypercellular early reparative response and delayed contraction of the scar. Infarcted IP-10(-/-) hearts exhibited accentuated early dilation, followed by rapid wall thinning during infarct maturation associated with systolic dysfunction. Although IP-10-null and WT mice had comparable cytokine expression, the absence of IP-10 was associated with marked alterations in the cellular content of the infarct. IP-10(-/-) infarcts had more intense infiltration with CD45(+) leukocytes, Mac-2(+) macrophages, and alpha-smooth muscle actin (alpha-SMA)(+) myofibroblasts than WT infarcts but exhibited reduced recruitment of the subpopulations of leukocytes, T lymphocytes and alpha-SMA(+) cells that expressed CXCR3, the IP-10 receptor. IP-10 did not modulate cardiac fibroblast proliferation and apoptosis but significantly inhibited basic fibroblast growth factor-induced fibroblast migration. In addition, IP-10 enhanced growth factor-mediated wound contraction in fibroblast-populated collagen lattices. CONCLUSIONS: Endogenous IP-10 is an essential inhibitory signal that regulates the cellular composition of the healing infarct and promotes wound contraction, attenuating adverse remodeling. IP-10-mediated actions may be due, at least in part, to direct effects on fibroblast migration and function.
机译：理由：干扰素-γ诱导蛋白（IP）-10 / CXCL10是一种在T细胞运输中起重要作用的血管抑制和抗纤维化趋化因子，在心肌梗塞中被明显诱导，并可能调节修复反应。目的：研究IP-10在心脏修复和重塑中的作用。方法和结果：我们研究了IP-10无效和野生型（WT）小鼠的心脏修复过程，该小鼠接受了再灌注梗塞方案，并检查了IP-10对心脏成纤维细胞功能的影响。 IP-10-缺陷和野生型动物的急性梗死面积相当。但是，缺乏IP-10会导致细胞过度修复早期反应和瘢痕收缩延迟。梗塞的IP-10（-/-）心脏表现出较早的扩张，随后在与收缩功能障碍相关的梗塞成熟过程中壁迅速变薄。尽管IP-10-null和WT小鼠具有可比的细胞因子表达，但IP-10的缺失与梗死细胞含量的显着改变有关。与WT梗死相比，IP-10（-/-）梗死具有更强的CD45（+）白细胞，Mac-2（+）巨噬细胞和α-平滑肌肌动蛋白（alpha-SMA）（+）成纤维细胞浸润能力，但募集减少表达CXCR3（IP-10受体）的白细胞，T淋巴细胞和α-SMA（+）细胞亚群。 IP-10不能调节心脏成纤维细胞的增殖和凋亡，但可以显着抑制碱性成纤维细胞生长因子诱导的成纤维细胞迁移。另外，IP-10增强了成纤维细胞填充胶原蛋白晶格中生长因子介导的伤口收缩。结论：内源性IP-10是一种重要的抑制信号，可调节愈合性梗塞的细胞组成并促进伤口收缩，从而减轻不良重塑。 IP-10介导的作用可能至少部分是由于对成纤维细胞迁移和功能的直接影响。

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