Publications by authors named "Rebekka Schneckmann"

Article Synopsis
  • Red blood cells (RBCs) possess endothelial NO synthase (eNOS) and transport nitric oxide (NO), which is important for heart health, but the role of RBC eNOS in protecting the heart from damage is not well understood.
  • Researchers used specially modified mice to differentiate between the functions of eNOS in RBCs and endothelial cells, discovering that RBC eNOS is crucial for limiting damage after heart attacks (acute myocardial infarction or AMI).
  • While endothelial cell (EC) eNOS affects blood flow and heart function, RBC eNOS was found to specifically protect against heart tissue damage during AMI, suggesting it could be a viable target for new heart attack treatments.
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Article Synopsis
  • Arginase 1 (Arg1) is an enzyme that converts l-arginine into l-ornithine and urea, and its role in endothelial cells (ECs) may limit l-arginine availability for nitric oxide (NO) production, leading to vascular issues.
  • A study was conducted using EC-specific gene-targeted knockout (KO) mice to examine how the absence of Arg1 affects eNOS, vascular tone, and endothelial function in normal conditions.
  • Results showed that EC Arg1 KO mice maintained normal levels of l-arginine and NO, displayed preserved vascular relaxation, but had increased vasoconstriction response, suggesting that while Arg1 affects NO in specific organs, it does not majorly
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Article Synopsis
  • * In a study using a colitis model, systemic inhibition of HA synthesis via 4-Methylumbelliferone (4-MU) worsened disease symptoms, while global deficiency of HA synthase 3 (Has3) significantly protected against colitis.
  • * The protective effect was particularly noted when Has3 was absent in endothelial cells, suggesting that targeting HA synthesis in specific cell types may be a promising avenue for treating IBD in humans.
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Objective: The dominant driver of arteriogenesis is elevated shear stress sensed by the endothelial glycocalyx thereby promoting arterial outward remodeling. Hyaluronan, a critical component of the endothelial glycocalyx, is synthesized by 3 HAS isoenzymes (hyaluronan synthases 1-3) at the plasma membrane. Considering further the importance of HAS3 for smooth muscle cell and immune cell functions we aimed to evaluate its role in collateral artery growth.

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Background: Current paradigms suggest that nitric oxide (NO) produced by endothelial cells (ECs) through endothelial nitric oxide synthase (eNOS) in the vessel wall is the primary regulator of blood flow and blood pressure. However, red blood cells (RBCs) also carry a catalytically active eNOS, but its role is controversial and remains undefined. This study aimed to elucidate the functional significance of RBC eNOS compared with EC eNOS for vascular hemodynamics and nitric oxide metabolism.

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Rationale: Immediate changes in the ECM (extracellular matrix) microenvironment occur after myocardial ischemia and reperfusion (I/R) injury.

Objective: Aim of this study was to unravel the role of the early hyaluronan (HA)-rich ECM after I/R.

Methods And Results: Genetic deletion of Has2 and Has1 was used in a murine model of cardiac I/R.

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