National Engineering Laboratory for Druggable Gene and Protein Screening, Northeast Normal University, Changchun 130024, China.
NMPA Key Laboratory for Quality of Cell and Gene Therapy Medicinal Products, Northeast Normal University, Changchun 130024, China.
Int J Mol Sci. 2023 Feb 3;24(3):2987. doi: 10.3390/ijms24032987.
STS1 and STS2, as the protein phosphatases that dephosphorylate FLT3 and cKIT, negatively regulate the self-renewal and differentiation of hematopoietic stem and progenitor cells (HSPCs). To obtain the small molecule inhibitors of STS1/STS2 phosphatase activity used to expand HSPCs both in vitro and in vivo, we establish an in vitro phosphatase assay using the recombinant proteins of the STS1/STS2 histidine phosphatase (HP) domain, by which we screened out baicalein (BC) as one of the effective inhibitors targeting STS1 and STS2. Then, we further demonstrate the direct binding of BC with STS1/STS2 using molecular docking and capillary electrophoresis and verify that BC can restore the phosphorylation of FLT3 and cKIT from STS1/STS2 inhibition. In a short-term in vitro culture, BC promotes profound expansion and enhances the colony-forming capacity of both human and mouse HSPCs along with the elevation of phospho-FLT3 and phospho-cKIT levels. Likewise, in vivo administration with BC significantly increases the proportions of short-term hematopoietic stem cells (ST-HSCs), multipotent progenitors (MPPs) and especially long-term HSCs (LT-HSCs) in healthy mouse bone marrow and increases the numbers of colony-forming units (CFU) formed by HSPCs as well. More importantly, pre-administration of BC significantly enhances the survival of mice with lethal 5-fluorouracil (5-FU) injection due to the alleviation of 5-FU-induced myelosuppression, as evidenced by the recovery of bone marrow histologic injury, the increased proportions of LT-HSCs, ST-HSCs and MPPs, and enhanced colony-forming capacity. Collectively, our study not only suggests BC as one of the small molecule candidates to stimulate HSPC expansion both in vitro and in vivo when needed in either physiologic or pathologic conditions, but also supports STS1/STS2 as potential therapeutic drug targets for HSPC expansion and hematopoietic injury recovery.
STS1 和 STS2 是去磷酸化 FLT3 和 cKIT 的蛋白磷酸酶,负调控造血干/祖细胞(HSPCs)的自我更新和分化。为了获得 STS1/STS2 磷酸酶活性的小分子抑制剂,用于在体外和体内扩增 HSPCs,我们使用 STS1/STS2 组氨酸磷酸酶(HP)结构域的重组蛋白建立了体外磷酸酶测定法,通过该方法筛选出黄芩素(BC)作为有效抑制剂之一,靶向 STS1 和 STS2。然后,我们进一步通过分子对接和毛细管电泳证明 BC 与 STS1/STS2 的直接结合,并验证 BC 可以从 STS1/STS2 抑制中恢复 FLT3 和 cKIT 的磷酸化。在短期体外培养中,BC 促进了人源和鼠源 HSPCs 的深刻扩增,并增强了集落形成能力,同时提高了磷酸化 FLT3 和磷酸化 cKIT 的水平。同样,体内给予 BC 可显著增加健康小鼠骨髓中短期造血干细胞(ST-HSCs)、多能祖细胞(MPPs),特别是长期造血干细胞(LT-HSCs)的比例,并增加 HSPCs 形成的集落形成单位(CFU)的数量。更重要的是,BC 的预先给药可显著提高因 5-氟尿嘧啶(5-FU)注射引起的致命性骨髓抑制的小鼠的存活率,这可从骨髓组织学损伤的恢复、LT-HSCs、ST-HSCs 和 MPPs 比例的增加以及集落形成能力的增强得到证明。总之,我们的研究不仅表明 BC 是在生理或病理条件下需要时在体外和体内刺激 HSPC 扩增的小分子候选物之一,还支持 STS1/STS2 作为 HSPC 扩增和造血损伤恢复的潜在治疗药物靶点。