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Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
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Hematopoietic growth factors are molecules that regulate the differentiation rate of hematopoietic stem cells (HSCs). Erythropoietin (EPO), primarily produced by the kidneys, plays a crucial role in erythrocyte production. When oxygen levels in the blood are low, EPO is released into the bloodstream, reaching the bone marrow, where it stimulates HSCs to differentiate and mature into erythrocytes, which are vital for oxygen transport.
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The process of blood cell formation is called hematopoiesis. Hematopoiesis starts early during development, on the seventh day of embryogenesis. This phase of hematopoiesis is called the primitive wave, wherein the extraembryonic yolk sac allows the production of erythroid cells and endothelial cells from a common precursor called hemangioblast. The erythroid cells provide oxygen to support the growth of the rapidly dividing embryo. Hemangioblasts later develop into hematopoietic stem cells or...
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All blood and immune cells are produced from the multipotent hematopoietic stem cells (HSCs) by the process of hematopoiesis. However, they all have a limited life span. In addition, many are depleted in immune surveillance or combatting an injury or infection. This makes blood one of the most regenerative tissues. Hematopoiesis helps replenish these blood and immune cells, restoring the body's normal functioning. However, overproduction of blood and immune cells can make them cancerous or...
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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.
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Clonal hematopoiesis JAKs up plaque formation.

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Clonal hematopoiesis (CH) involves mutations in blood stem cells, increasing with age and linked to cardiovascular disease (CVD). A new mouse model helps study CH-associated atherosclerosis and identifies potential therapeutic targets.

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Area of Science:

  • Hematology
  • Cardiovascular Science
  • Genetics

Background:

  • Clonal hematopoiesis (CH) is the acquisition of mutations in hematopoietic stem cells (HSCs), increasing with age.
  • CH is associated with age-related diseases, particularly cardiovascular disease (CVD) and atherosclerosis.
  • JAK2 mutations in HSCs can cause CH and are linked to atherosclerosis, but modeling low-frequency mutations is challenging.

Purpose of the Study:

  • To develop a novel low-allele-burden (LAB) mouse model for studying CH-associated atherosclerosis.
  • To investigate the mechanisms linking CH, inflammation, and plaque development in a relevant disease context.
  • To identify potential therapeutic targets for CH-associated CVD.

Main Methods:

  • Development of a LAB mouse model by transplanting a small number of Jak2VF-mutant bone marrow cells into hyperlipidemic mice.
  • Assessment of atherosclerotic plaque development in the established mouse model.
  • Identification of downstream molecular targets, including phagocytic receptors and inflammatory cytokines.

Main Results:

  • The LAB mouse model successfully recapitulated key features of atherosclerosis development.
  • The study identified MERTK and TREM2 phagocytic receptors as downstream targets of the inflammatory cytokine IL-1.
  • These findings elucidate molecular pathways involved in CH-associated cardiovascular pathology.

Conclusions:

  • A novel LAB mouse model provides a valuable tool for studying CH-associated atherosclerosis.
  • The IL-1 pathway and its downstream targets MERTK and TREM2 are implicated in CH-related CVD.
  • These discoveries offer potential therapeutic strategies for preventing or treating CH-associated cardiovascular complications.