美国德克萨斯大学西南医学中心Sean J. Morrison等研究人员合作发现，瘦素受体⁺细胞通过合成神经生长因子促进骨髓神经支配和再生。相关论文于2023年11月27日在线发表在《自然—细胞生物学》杂志上。

研究人员发现瘦素受体（LepR⁺）基质细胞产生的神经生长因子（NGF）是维持成人骨髓中神经纤维所需的。在无神经的骨髓中，稳态造血是正常的，但在骨髓去除后，造血和血管再生功能受损。LepR⁺细胞及其产生的脂肪细胞在骨髓缺血后增加了NGF的分泌，从而促进了骨髓中的神经萌发以及造血和血管再生。神经通过激活LepR⁺细胞中的β2和β3肾上腺素能受体信号来促进再生，也可能激活脂肪细胞，从而增加它们产生多种造血和血管再生生长因子。因此，周围神经和LepR⁺细胞通过一种互惠关系促进骨髓再生，在这种关系中，LepR⁺细胞通过合成NGF来维持神经，而神经则通过促进LepR⁺细胞产生生长因子来增加再生。

研究人员表示，骨髓中含有促进照射或化疗（骨髓消融）后造血再生的外周神经，但人们对其如何调节知之甚少。

附：英文原文

Title: Leptin receptor+ cells promote bone marrow innervation and regeneration by synthesizing nerve growth factor

Author: Gao, Xiang, Murphy, Malea M., Peyer, James G., Ni, Yuehan, Yang, Min, Zhang, Yixuan, Guo, Jiaming, Kara, Nergis, Embree, Claire, Tasdogan, Alpaslan, Ubellacker, Jessalyn M., Crane, Genevieve M., Fang, Shentong, Zhao, Zhiyu, Shen, Bo, Morrison, Sean J.

Issue&Volume: 2023-11-27

Abstract: The bone marrow contains peripheral nerves that promote haematopoietic regeneration after irradiation or chemotherapy (myeloablation), but little is known about how this is regulated. Here we found that nerve growth factor (NGF) produced by leptin receptor-expressing (LepR+) stromal cells is required to maintain nerve fibres in adult bone marrow. In nerveless bone marrow, steady-state haematopoiesis was normal but haematopoietic and vascular regeneration were impaired after myeloablation. LepR+ cells, and the adipocytes they gave rise to, increased NGF production after myeloablation, promoting nerve sprouting in the bone marrow and haematopoietic and vascular regeneration. Nerves promoted regeneration by activating β2 and β3 adrenergic receptor signalling in LepR+ cells, and potentially in adipocytes, increasing their production of multiple haematopoietic and vascular regeneration growth factors. Peripheral nerves and LepR+ cells thus promote bone marrow regeneration through a reciprocal relationship in which LepR+ cells sustain nerves by synthesizing NGF and nerves increase regeneration by promoting the production of growth factors by LepR+ cells.

DOI: 10.1038/s41556-023-01284-9

Source: https://www.nature.com/articles/s41556-023-01284-9