6 results match your criteria: "University of Zurich and Zurich Center for Integrative Human Physiology (ZIHP)[Affiliation]"

Unlabelled: Reduced activity of histone deacetylase 2 (HDAC2) has been described in patients with chronic obstructive pulmonary disease (COPD), but the mechanisms resulting in decreased expression of this important epigenetic modifier remain unknown. Here, we employed several in vitro experiments to address the role of microRNAs (miRNAs) on the regulation of HDAC2 in endothelial cells. Manipulation of miRNA levels in human pulmonary artery endothelial cells (HPAEC) was achieved by using electroporation with anti-miRNAs and miRNA mimics.

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Featured Article: microRNA-125a in pulmonary hypertension: Regulator of a proliferative phenotype of endothelial cells.

Exp Biol Med (Maywood)

December 2015

Division of Pulmonology, University Hospital Zurich, Zurich CH-8091, Switzerland Institute of Veterinary Physiology, University of Zurich and Zurich Center for Integrative Human Physiology (ZIHP), Zurich CH-8057, Switzerland

Article Synopsis
  • Vascular remodeling, characterized by the excessive growth of endothelial and smooth muscle cells, is a key feature of pulmonary hypertension.
  • Recent research highlights the role of microRNAs (miRNAs) in this process, specifically how miR-125a silences the bone morphogenetic protein receptor type II (BMPR2), impacting cell proliferation.
  • Functional studies show that inhibiting miR-125a boosts endothelial cell proliferation, increases BMPR2 levels, and lowers tumor suppressor expression, confirming the significance of this pathway in both animal models and human patients with pulmonary hypertension.
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Excessive proliferation of human pulmonary artery smooth muscle cells (HPASMC) is one of the major factors that trigger vascular remodeling in hypoxia-induced pulmonary hypertension. Several studies have implicated that hypoxia inhibits the tumor suppressor p21 (CDKN1A). However, the precise mechanism is unknown.

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Erythroblasts proliferate and differentiate in hematopoietic organs within erythroblastic islands (EI) composed of erythropoietic progenitor cells attached to a central macrophage. This cellular interaction crucially involves the erythroid intercellular adhesion molecule-4 (ICAM-4) and αv integrin. Because integrins are biologically active as α/β heterodimers, we asked whether β3 could be a heterodimerization partner of αv integrin in EIs.

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Transcriptome analysis revealed unique genes as targets for the anti-inflammatory action of activated protein C in human macrophages.

PLoS One

October 2010

Inflammation Research Unit, Division of Internal Medicine, University Hospital of Zurich and Zurich Center for Integrative Human Physiology ZIHP, University of Zurich, Zurich, Switzerland.

Background: Activated protein C (APC) has been introduced as a therapeutic agent for treatment of patients with severe sepsis due to its unique anticoagulant and anti-inflammatory properties in the vascular system. In this study we investigated novel targets for the anti-inflammatory action of APC in human macrophages.

Methods: Using a genome-wide approach, effects of APC on the expression profile in inflammatory activated human macrophages were analyzed.

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Autoregulation, an important feature of the cerebral circulation, is affected in many diseases. Since genetically modified mice are a fundamental tool in biomedical research, including neuro(bio)logy also in this specie measurements of cerebral autoregulation (CA) are mandatory. However, this requires anesthesia that unfortunately significantly impacts cerebral perfusion and consequently might distort CA measurements directly or by altering arterial pCO(2).

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