肺血管重构是低氧性肺动脉高压（HPAH）持续进展的关键，其主要特征是肺动脉平滑肌细胞(PASMC)异常增生，如何在体确认这些异常增生PASMC的来源以及这些PASMC究竟源于何种细胞是困扰HPAH研究的基本问题。成体干细胞是维持所居器官细胞稳态和更新的基础，最新发现肺脏存在成体肺干细胞（LSC），从稳态角度分析，肺血管重构时PASMC异常增生是PASMC稳态失衡的结果，我们推测：LSC可能参与HPAH肺血管重构且是异常增生PASMC的重要来源。课题组根据干细胞归巢特性建立了"自体部分LSC永久标记大鼠"的制备方法，能够在体确认异常增生PASMC是否源于LSC分化。本项目拟在此基础上，研究LSC是否通过迁移分化为PASMC和/或旁分泌作用参与肺血管重构，以验证上述推测并探讨其可能机制。研究结果可能为HPAH肺血管重构的细胞机制提供新知识、为以LSC为靶点开发治疗HPAH的药物提供新线索。

Lung vascular remodeling characterized by the aberrant proliferation of pulmonary artery smooth muscle cells ( PASMCs ) is the key of hypoxic pulmonary artery hypertension ( HPAH ). However, it is still difficult to identify the origin of the increased PASMCs in vivo and the origin of PASMCs is an enigma for the research of HPAH. Adult stem cell is the base of cell homeostasis and regeneration in their resident organ. Recently, adult lung stem cells ( LSCs ) is found to exist in adult lung and be involved in the regeneration and homeostasis of lung cells. The aberrant proliferation of PASMCs is the result of imbalance of PASMCs homeostasis in pulmonary vascular remodeling in HPHA, so we hypothesize that LSCs take part in the pulmonary vascular remodeling via migration and differentiation into PASMCs and / or paracine factors and may be one of the origins of increased PASMCs in HPAH. According to the homing character of adult stem cell, we established an experiment method by which we can permanently mark a part of LSCs in rats and in vivo identify whether some of the increased PASMCc in pulmonary vascular wall in HPAH origin from LSCs. This project will use the established method to further explore whether LSCs are involved in pulmonary vascular remodeling in HPAH via differentiating into PASMC and / or paracrine factor and its possible mechanism. The aim is to test our hypothesis. The results of the project will provide novel information for the cellular mechanism of pulmonary vascular remodeling in HPAH and new clue for development of drugs for the treatment of HPAH.