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Published on: March 24, 2015
CD34+ cell atlas of main organs implicates its impact on fibrosis
Xiangyuan Pu1, Pengwei Zhu1, Xuhao Zhou1
1Department of Cardiology, the First Affiliated Hospital, Zhejiang University School of Medicine, 79 Qingchun Road, Hangzhou, 310003, Hangzhou, China.
Insights
CD34+ cells are diverse progenitors. These cells contribute to blood vessel repair and may transform into myofibroblasts, playing a role in organ fibrosis and wound healing.
Area of Science:
- Cardiovascular Biology
- Regenerative Medicine
- Cell Biology
Background:
- CD34+ cells are considered progenitor cells with potential therapeutic applications in cardiovascular disease.
- The precise identity and functional roles of CD34+ cells in normal physiology and disease states are not fully understood.
Purpose of the Study:
- To elucidate the heterogeneity and functional roles of CD34+ cells in physiological and pathological contexts.
- To investigate the contribution of CD34+ cells to angiogenesis and organ fibrosis.
Main Methods:
- Single-cell RNA sequencing (scRNA-seq) was employed to create a comprehensive cell atlas.
- A genetic lineage tracing mouse model was utilized to track CD34+ cell behavior in vivo.
Main Results:
- scRNA-seq revealed significant heterogeneity within the CD34+ cell population under both normal and diseased conditions.
- Lineage tracing demonstrated that CD34+ cells can differentiate into endothelial cells, contributing to angiogenesis.
- Evidence suggests that a subset of CD34+ cells, specifically those expressing Pi16, can differentiate into myofibroblasts, promoting organ fibrosis.
Conclusions:
- Heterogeneous CD34+ cells are key players in endothelial regeneration and wound healing processes.
- Understanding the dual role of CD34+ cells in regeneration and fibrosis offers potential therapeutic strategies for fibrotic diseases.
Rationale:
CD34+ cells are believed being progenitors that may be used to treat cardiovascular disease. However, the exact identity and the role of CD34+ cells in physiological and pathological conditions remain unclear.
Methods:
We performed single-cell RNA sequencing analysis to provide a cell atlas of normal tissue/organ and pathological conditions. Furthermore, a genetic lineage tracing mouse model was used to investigate the role of CD34+ cells in angiogenesis and organ fibrosis.
Results:
Single-cell RNA sequencing analysis revealed a heterogeneous population of CD34+ cells in both physiological and pathological conditions. Using a genetic lineage tracing mouse model, we showed that CD34+ cells not only acquired endothelial cell fate involved in angiogenesis, but also, CD34+ cells expressing Pi16 may transform into myofibroblast and thus participate in organ fibrosis.
Conclusion:
A heterogeneous CD34+ cells serve as a contributor not only to endothelial regeneration but also a wound healing response that may provide therapeutic insights into fibrosis.
