Platelet interaction with progenitor cells: vascular regeneration or inquiry?

Konstantinos Stellos1, Stephan Gnerlich, Bjoern Kraemer

  • 1Medizinische Klinik III, Eberhard Karls-Universität Tübingen, Otfried-Müller 10, Tübingen, Germany.

Increasing evidence supports the role of stem and progenitor cells in vascular regeneration or injury. Following tissue ischemia, progenitor cells are mobilized from their bone marrow or peripheral niches into circulation, adhere at sites of vascular lesion and differentiate into a variety of mature cell types according to their origin and the local environment. Impairment in this pathophysiological process due to either low numbers of circulating progenitor cells or dysfunctional progenitor cells leads to inadequate vascular repair and upon co-existence with different cardiovascular risk factors to vascular injury and atherosclerosis. Vascular repair is a complex process which includes mobilization, chemotaxis, adhesion, proliferation and differentiation of progenitor cells. The common cardiovascular risk factors can impair this process resulting into inhibition of vascular healing and enhancement of inflammatory pathways which ultimately leads to atherosclerosis. Although homing of progenitor cells into bone marrow has been extensively studied, domiciliation of precursor cells into peripheral tissues and differentiation into mature cells are poorly understood so far. Recently, the role of platelets in domiciliation and subsequent differentiation of progenitor cells has been highlighted. Adherent platelets recruit circulating progenitor cells in vitro and in vivo and induce differentiation of the latter into endothelial cells or macrophages and foam cells. Although further studies are needed to describe the mechanisms that lie underneath these observations, it seems that platelet interaction with progenitor cells is an essential step in both vascular regeneration and injury.

Related Concept Videos

Formation of the Platelet Plug01:22

Formation of the Platelet Plug

The platelet phase, the second stage of hemostasis, commences around 15-20 seconds after an injury. It follows and overlaps with the vascular phase, during which blood vessels constrict to minimize blood loss.
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...
Structure and Function of Platelets01:18

Structure and Function of Platelets

The cell fragments known as platelets are disc-shaped, with an average diameter of about 3 μm and a thickness of roughly 1 μm. They play a crucial role in the body's vascular clotting system, which also involves plasma proteins, blood cells, and blood vessel tissues.
Platelets are continually replenished, circulating in the bloodstream for 9-12 days before being removed by phagocytes, primarily in the spleen. A microliter of circulating blood contains between 150,000 and 450,000 platelets, with...
Clot Retraction and Fibrinolysis01:16

Clot Retraction and Fibrinolysis

After a fibrin clot is formed, the next step is clot retraction, a vital process facilitated by platelet contractile proteins, such as actin and myosin. These proteins pull the fibrin strands closer together and condense the clot. This action reduces the size of the clot, creating a smaller, denser structure that effectively seals off the damaged vessel. Clot retraction consolidates the clot and helps with wound healing by bringing the edges of the damaged blood vessel closer together.
Introduction to Hemostasis01:05

Introduction to Hemostasis

Hemostasis is a complex physiological process that prevents excessive bleeding when a blood vessel is injured. It's crucial for maintaining the integrity of the circulatory system, as it ensures that our blood remains fluid while still within the vascular network and yet clots to prevent blood loss upon vessel injury.
The three phases of hemostasis involve many clotting factors present in plasma and several substances released by platelets and injured tissue cells. It is a fast, localized, and...
Extrinsic and Intrinsic Pathways of Hemostasis01:20

Extrinsic and Intrinsic Pathways of Hemostasis

Blood clotting or coagulation involves extrinsic and intrinsic pathways, which ultimately merge into the common pathway, forming a fibrin clot.
The Extrinsic Pathway
The extrinsic pathway of coagulation is typically initiated by tissue damage that exposes blood to tissue factor (TF), a protein released by the damaged tissue cells outside the blood vessels—this interaction with TF triggers biochemical reactions involving specific clotting factors. The key player here is Factor VII, which forms a...
Multipotency of Hematopoietic Stem Cells01:19

Multipotency of Hematopoietic Stem Cells

The hematopoietic stem cells or HSCs are multipotent, meaning they can differentiate and give rise to all blood and immune cells. HSCs are maintained in the quiescent stage until an external stimulus initiates their differentiation. The multipotent HSCs exist as two heterogeneous populations, long-term repopulating cells (LTRC) and short-term repopulating cells (STRC). The two HSC populations have different surface markers or receptors and are classified based on quiescence and long-term...