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周细胞在狭窄后充血诱导的毛细血管去募集过程中的作用。

The role of pericytes in hyperemia-induced capillary de-recruitment following stenosis.

作者信息

Kaul Sanjiv, Methner Carmen, Mishra Anusha

机构信息

Knight Cardiovascular Institute Oregon Health & Science University, Portland, Oregon, USA.

Jungers Center for Neurosciences Research, Department of Neurology, Oregon Health & Science University, Portland, Oregon, USA.

出版信息

Curr Tissue Microenviron Rep. 2020 Dec;1(4):163-169. doi: 10.1007/s43152-020-00017-6. Epub 2020 Oct 30.

DOI:10.1007/s43152-020-00017-6
PMID:33778770
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7992506/
Abstract

PURPOSE

The microvascular capillary network is ensheathed by cells called pericytes - a heterogeneous population of mural cells derived from multiple lineages. Pericytes play a multifaceted role in the body, including in vascular structure and permeability, regulation of local blood flow, immune and wound healing functions, induction of angiogenesis, and generation of various progenitor cells. Here, we consider the role of pericytes in capillary de-recruitment, a pathophysiologic phenomenon that is observed following hyperemic stimuli in the presence of a stenosis and attenuates the hyperemic response.

RECENT FINDINGS

We discuss recent observations that conclusively demonstrate pericytes to be the cellular structures that contract in response to hyperemic stimuli when an upstream arterial stenosis is present. This response constricts capillaries, which is likely aimed at maintaining capillary hydrostatic pressure, an important factor in tissue homeostasis. Nonetheless, the ensuing attenuation of the hyperemic response can lead to a decrease in energy supply and negatively impact tissue health.

SUMMARY

Therapeutics aimed at preventing pericyte-mediated capillary de-recruitment may prove beneficial in conditions such as coronary stenosis and peripheral arterial disease by reducing restriction in hyperemic flow. Identification of the pericyte subtypes involved in this de-recruitment and the underlying molecular mechanisms regulating this process will greatly assist this purpose.

摘要

目的

微血管毛细血管网络由称为周细胞的细胞包裹,周细胞是源自多个谱系的异质性壁细胞群体。周细胞在体内发挥多方面作用,包括在血管结构和通透性、局部血流调节、免疫和伤口愈合功能、血管生成诱导以及各种祖细胞生成等方面。在此,我们探讨周细胞在毛细血管去募集过程中的作用,毛细血管去募集是一种病理生理现象,在存在狭窄的情况下,充血刺激后会出现这种现象,并减弱充血反应。

最新发现

我们讨论了最近的观察结果,这些结果确凿地表明,当存在上游动脉狭窄时,周细胞是对充血刺激产生收缩反应的细胞结构。这种反应会收缩毛细血管,这可能旨在维持毛细血管静水压,这是组织稳态中的一个重要因素。尽管如此,随后充血反应的减弱会导致能量供应减少,并对组织健康产生负面影响。

总结

旨在预防周细胞介导的毛细血管去募集的治疗方法,可能通过减少充血血流的限制,在冠状动脉狭窄和外周动脉疾病等病症中证明是有益的。确定参与这种去募集的周细胞亚型以及调节这一过程的潜在分子机制,将极大地有助于实现这一目标。

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本文引用的文献

1
Brain capillary pericytes exert a substantial but slow influence on blood flow.脑毛细血管周细胞对血流有显著但缓慢的影响。
Nat Neurosci. 2021 May;24(5):633-645. doi: 10.1038/s41593-020-00793-2. Epub 2021 Feb 18.
2
Platelet-derived growth factor receptor-β (PDGFRβ) lineage tracing highlights perivascular cell to myofibroblast transdifferentiation during post-traumatic osteoarthritis.血小板衍生生长因子受体-β(PDGFRβ)谱系示踪表明,创伤后骨关节炎发生时,血管周细胞向肌成纤维细胞的转分化。
J Orthop Res. 2020 Nov;38(11):2484-2494. doi: 10.1002/jor.24648. Epub 2020 Mar 9.
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A High Output Method to Isolate Cerebral Pericytes from Mouse.
J Vis Exp. 2020 Jan 14(155). doi: 10.3791/60588.
4
Precapillary sphincters maintain perfusion in the cerebral cortex.前毛细血管括约肌维持大脑皮层的灌注。
Nat Commun. 2020 Jan 20;11(1):395. doi: 10.1038/s41467-020-14330-z.
5
The impact of skeletal muscle contraction on CD146Lin pericytes.骨骼肌收缩对 CD146Lin 周细胞的影响。
Am J Physiol Cell Physiol. 2019 Nov 1;317(5):C1011-C1024. doi: 10.1152/ajpcell.00156.2019. Epub 2019 Aug 21.
6
Retinal ischemia induces α-SMA-mediated capillary pericyte contraction coincident with perivascular glycogen depletion.视网膜缺血诱导 α-SMA 介导的毛细血管周细胞收缩,同时伴有血管周细胞糖原耗竭。
Acta Neuropathol Commun. 2019 Aug 20;7(1):134. doi: 10.1186/s40478-019-0761-z.
7
Pericyte constriction underlies capillary derecruitment during hyperemia in the setting of arterial stenosis.在动脉狭窄的情况下,充血期间的血管内皮细胞收缩是毛细血管再募集的基础。
Am J Physiol Heart Circ Physiol. 2019 Aug 1;317(2):H255-H263. doi: 10.1152/ajpheart.00097.2019. Epub 2019 May 24.
8
Pericytes in the Heart.心脏中的周细胞。
Adv Exp Med Biol. 2019;1122:187-210. doi: 10.1007/978-3-030-11093-2_11.
9
Blood-brain barrier-associated pericytes internalize and clear aggregated amyloid-β42 by LRP1-dependent apolipoprotein E isoform-specific mechanism.血脑屏障相关周细胞通过 LRP1 依赖性载脂蛋白 E 异构体特异性机制内化和清除聚集的淀粉样蛋白-β42。
Mol Neurodegener. 2018 Oct 19;13(1):57. doi: 10.1186/s13024-018-0286-0.
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