Limb functional recovery is impaired in fibroblast growth factor-2 (FGF2) deficient mice despite chronic ischaemia-induced vascular growth.
Limb functional recovery is impaired in fibroblast growth factor-2 (FGF2) deficient mice despite chronic ischaemia-induced vascular growth.
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DOI：
10.1080/08977194.2020.1767612
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发表时间：
2020-03
期刊：
影响因子：
--
通讯作者：
Schultz JEJ
中科院分区：
文献类型：
--
作者：
Adeyemo A;Johnson C;Stiene A;LaSance K;Qi Z;Lemen L;Schultz JEJ
FGF2是一种有效的血管生长刺激物；然而，即使缺乏FGF2 (FGF2−/−)，发育性血管生长或缺血诱导的血运重建仍然发生。至于FGF2在缺血性损伤中有什么功能，如果有的话，还有待阐明。野生型（WT）或Fgf2−/−小鼠后肢缺血长达42天。在不同时间点评估假手术和缺血肢体的肢体功能、血管生长、炎症和血管生成相关蛋白以及炎症细胞浸润。Fgf2−/−小鼠缺血肢体功能恢复延迟。然而，血管生长对缺血的反应在WT和Fgf2−/−后肢之间是相似的。几种血管生成和炎症相关蛋白（MCP-1、CXCL16、MMPs和PAI-1）在Fgf2−/−缺血肌肉中升高。中性粒细胞或单核细胞募集/浸润在Fgf2−/−缺血肌肉中升高。总之，我们的研究表明，FGF2的缺失会在骨骼肌中诱导促炎微环境，从而加剧缺血性损伤并延迟肢体功能的使用。
FGF2 is a potent stimulator of vascular growth; however, even with a deficiency of FGF2 (Fgf2−/−), developmental vessel growth or ischemia-induced revascularization still transpires. It remains to be elucidated as to what function, if any, FGF2 has during ischemic injury. Wildtype (WT) or Fgf2−/− mice were subjected to hindlimb ischemia for up to 42-days. Limb function, vascular growth, inflammatory- and angiogenesis-related proteins, and inflammatory cell infiltration were assessed in sham and ischemic limbs at various timepoints. Recovery of ischemic limb function was delayed in Fgf2−/− mice. Yet, vascular growth response to ischemia was similar between WT and Fgf2−/− hindlimbs. Several angiogenesis- and inflammatory-related proteins (MCP-1, CXCL16, MMPs and PAI-1) were increased in Fgf2−/− ischemic muscle. Neutrophil or monocyte recruitment/infiltration was elevated in Fgf2−/− ischemic muscle. In summary, our study indicates that loss of FGF2 induces a pro-inflammatory microenvironment in skeletal muscle which exacerbates ischemic injury and delays functional limb use.
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影响因子：
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作者：
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DOI：
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发表时间：
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