Liu Huan-Di, Zhang Ai-Jie, Xu Jing-Jing, Chen Ying, Zhu Yi-Chun
Shanghai Key Laboratory of Bioactive Small Molecules and Research Center on Aging and Medicine, Department of Physiology and Pathophysiology, Fudan University Shanghai Medical College, 138 Yi Xue Yuan Road, Shanghai, 200032, China.
Collaborative Innovation Center of Molecular Diagnosis and Laboratory Medicine in Henan Province, School of Laboratory Medicine, Xinxiang Medical University, Xinxiang, China.
J Hematol Oncol. 2016 Feb 24;9:13. doi: 10.1186/s13045-016-0244-7.
Our previous pilot studies aimed to examine the role of hydrogen sulfide (H2S) in the generation of endothelial progenitor cells led to an unexpected result, i.e., H2S promoted the differentiation of certain hematopoietic stem/progenitor cells in the bone marrow. This gave rise to an idea that H2S might promote hematopoiesis.
To test this idea, a mice model of myelosuppression and cultured fetal liver cells were used to examine the role of H2S in hematopoiesis.
H2S promoted the generation of megakaryocytes, increased platelet levels, ameliorate entorrhagia, and improved survival. These H2S effects were blocked in both in vivo and in vitro models with thrombopoietin (TPO) receptor knockout mice (c-mpl(-/-) mice). In contrast, H2S promoted megakaryocytes/platelets generation in both in vivo and in vitro models with TPO knockout mice (TPO(-/-) mice).
H2S is a novel promoter for megakaryopoiesis by acting on the TPO receptors but not TPO to generate megakaryocytes/platelets.
我们之前的初步研究旨在探讨硫化氢（H2S）在内皮祖细胞生成中的作用，却得到了一个意外的结果，即H2S促进了骨髓中某些造血干/祖细胞的分化。这引发了一个想法，即H2S可能促进造血作用。
为了验证这一想法，使用了骨髓抑制小鼠模型和培养的胎肝细胞来研究H2S在造血作用中的角色。
H2S促进了巨核细胞的生成，提高了血小板水平，改善了出血情况，并提高了生存率。在体内和体外模型中，血小板生成素（TPO）受体敲除小鼠（c-mpl(-/-)小鼠）阻断了这些H2S效应。相反，在体内和体外模型中，TPO敲除小鼠（TPO(-/-)小鼠）中H2S促进了巨核细胞/血小板的生成。
H2S是一种通过作用于TPO受体而非TPO来生成巨核细胞/血小板的新型巨核细胞生成促进剂。
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