Insights from Lineage Tracing Models Shed Light on the Reassessment of Endothelial-to-Mesenchymal Transition in Mouse Bone Marrow
Endothelial-to-mesenchymal transition (EndMT) is a biological process in which endothelial cells, which line the inner surface of blood vessels, acquire mesenchymal characteristics and transform into cells with fibroblast-like properties. This process has been implicated in various physiological and pathological conditions, including embryonic development, tissue fibrosis, and cancer progression. However, recent studies using lineage tracing models have challenged the traditional understanding of EndMT in the context of mouse bone marrow.
A study published in Nature Communications by researchers from the University of XYZ provides new insights into the reassessment of EndMT in mouse bone marrow. The researchers utilized sophisticated lineage tracing techniques to track the fate of endothelial cells in the bone marrow microenvironment.
Traditionally, it was believed that EndMT contributes to the generation of mesenchymal stem cells (MSCs) in the bone marrow. MSCs are multipotent cells that can differentiate into various cell types, including osteoblasts, adipocytes, and chondrocytes. These cells play a crucial role in bone homeostasis and repair. However, the precise origin of MSCs in the bone marrow has remained elusive.
The researchers employed a genetic mouse model that allowed them to label and track endothelial cells specifically. Surprisingly, they found that endothelial cells in the bone marrow did not undergo EndMT to give rise to MSCs. Instead, they observed that a distinct population of perivascular cells, known as leptin receptor-positive (LepR+) cells, were the source of MSCs.
By comparing the fate of endothelial cells and LepR+ cells using lineage tracing techniques, the researchers demonstrated that LepR+ cells directly differentiated into MSCs without undergoing an intermediate EndMT stage. This finding challenges the long-standing notion that EndMT is a major contributor to MSC generation in the bone marrow.
Furthermore, the researchers investigated the functional role of EndMT in bone marrow homeostasis and regeneration. They selectively induced EndMT in endothelial cells and assessed the impact on bone formation and repair. Surprisingly, they found that manipulating EndMT did not significantly affect bone remodeling or fracture healing. This suggests that EndMT may not be essential for bone regeneration, contrary to previous assumptions.
The study also shed light on the potential role of EndMT in pathological conditions. The researchers examined the contribution of EndMT to fibrosis, a process characterized by excessive deposition of extracellular matrix components. They found that inhibiting EndMT in a mouse model of fibrosis reduced fibrotic tissue formation, suggesting that targeting this process could be a potential therapeutic strategy for fibrotic diseases.
In conclusion, the study provides valuable insights into the reassessment of EndMT in mouse bone marrow. By utilizing lineage tracing models, the researchers demonstrated that endothelial cells do not undergo EndMT to generate MSCs in the bone marrow microenvironment. Instead, LepR+ cells directly differentiate into MSCs, challenging the traditional understanding of MSC origin. Additionally, the study highlights the potential role of EndMT in fibrosis and suggests its therapeutic targeting as a potential treatment strategy. These findings contribute to our understanding of cellular plasticity and have implications for regenerative medicine and fibrotic diseases.
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