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Mesenchymal Stem Cells

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Mesenchymal stem cells (MSCs) are adult stem cells that can differentiate into most connective tissue cell types, except for hematopoietic cells, depending upon the source of MSCs. For example, bone-marrow-derived MSCs (BM-MSCs) can differentiate into osteocytes, hepatocytes, and pancreatic and neuronal cells. MSCs can be isolated from various sources such as bone marrow, placenta, adipose tissue, teeth, and Wharton’s jelly, a gelatinous substance in the umbilical cord. The ease of their...
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The development of lymphatic tissues and vessels in embryonic life begins around the fifth week. These structures originate from the mesoderm layer, with lymph sacs emerging from developing veins.
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Hemangioblasts are multipotent stem cells originating from the mesoderm. They give rise to hematopoietic stem cells (HSCs), which undergo hematopoiesis to produce all the formed elements of blood. This process is regulated by a complex network of hematopoietic growth factors, including transcription factors, growth factors, and cytokines. These factors stimulate the HSCs to divide and differentiate, though some HSCs remain undifferentiated to maintain a self-renewing pool.
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Bone marrow-derived mesenchymal stem cells drive lymphangiogenesis.

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Area of Science:

  • Cancer biology
  • Stem cell research
  • Vascular biology

Background:

  • Bone-Marrow Mesenchymal Stem Cells (BM-MSC) are known to aid cancer progression via angiogenesis.
  • The role of BM-MSC in lymphangiogenesis, the formation of lymphatic vessels, is not well understood.

Purpose of the Study:

  • To investigate the potential lymphangiogenic effects of BM-MSC.
  • To elucidate the mechanisms by which BM-MSC influence lymphatic vessel development.

Main Methods:

  • BM-MSC were isolated from mice.
  • In vivo studies involved co-injection of BM-MSC and tumor cells, and an ear sponge assay.
  • In vitro studies utilized lymphatic endothelial cells (LEC) and conditioned media from BM-MSC.
  • VEGF-A and VEGFR-2 pathways were analyzed using inhibitors and soluble receptors.

Main Results:

  • Co-injection of BM-MSC with tumor cells increased tumor growth and lymphatic vessel density in mice.
  • BM-MSC conditioned media promoted lymphatic vessel recruitment in vivo and enhanced LEC proliferation and migration in vitro.
  • These effects were dependent on VEGF-A secreted by BM-MSC, acting through VEGFR-2 on LEC.

Conclusions:

  • BM-MSC exert a paracrine pro-lymphangiogenic effect, promoting tumor growth.
  • VEGF-A secretion by BM-MSC is a key mechanism driving this lymphangiogenesis via the VEGFR-2 pathway on LEC.