小柯机器人

美国国立卫生研究院Dorian B. McGavern小组发现，不同的髓样细胞反应介导脑血管损伤后的损伤和修复。该研究于2021年1月18日在线发表于国际一流学术期刊《自然—神经科学》。

研究人员观察成功进行急性大血管闭塞的血管内血栓切除术后再通与发生出血性转化患者的脑水肿和不良的临床预后有关。为了理解这一过程，研究人员使用经颅超声开发了脑血管损伤模型，该模型能够对驻留和周围的髓样细胞进行时空性评估。研究人员发现伤害性和修复性反应根据时间和细胞起源而有所不同。驻留型小胶质细胞最初以嘌呤能受体依赖性的方式稳定受损血管，随后大量骨髓单核细胞大量涌入。

用抗粘连分子疗法长时间阻止髓样细胞募集可以预防严重的水肿，但通过干扰随后由促炎性单核细胞和促血管生成修复相关的小胶质细胞（RAM）进行的血管修复则会促进神经元破坏和纤维化。这些数据证明了在时间上不同的髓样细胞反应如何能够控制、加剧并最终修复脑血管损伤。

据悉，脑血管损伤可导致严重的水肿和炎症，对人体健康产生不利影响。

附：英文原文

Title: Temporally distinct myeloid cell responses mediate damage and repair after cerebrovascular injury

Author: Panagiotis Mastorakos, Nicole Mihelson, Marie Luby, Scott R. Burks, Kory Johnson, Amie W. Hsia, Jaclyn Witko, Joseph A. Frank, Lawrence Latour, Dorian B. McGavern

Issue&Volume: 2021-01-18

Abstract: Cerebrovascular injuries can cause severe edema and inflammation that adversely affect human health. Here, we observed that recanalization after successful endovascular thrombectomy for acute large vessel occlusion was associated with cerebral edema and poor clinical outcomes in patients who experienced hemorrhagic transformation. To understand this process, we developed a cerebrovascular injury model using transcranial ultrasound that enabled spatiotemporal evaluation of resident and peripheral myeloid cells. We discovered that injurious and reparative responses diverged based on time and cellular origin. Resident microglia initially stabilized damaged vessels in a purinergic receptor–dependent manner, which was followed by an influx of myelomonocytic cells that caused severe edema. Prolonged blockade of myeloid cell recruitment with anti-adhesion molecule therapy prevented severe edema but also promoted neuronal destruction and fibrosis by interfering with vascular repair subsequently orchestrated by proinflammatory monocytes and proangiogenic repair-associated microglia (RAM). These data demonstrate how temporally distinct myeloid cell responses can contain, exacerbate and ultimately repair a cerebrovascular injury.

DOI: 10.1038/s41593-020-00773-6

Source: https://www.nature.com/articles/s41593-020-00773-6

Nature Neuroscience：《自然—神经科学》，创刊于1998年。隶属于施普林格·自然出版集团，最新IF：28.771
官方网址：https://www.nature.com/neuro/
投稿链接：https://mts-nn.nature.com/cgi-bin/main.plex