Linked Life Data

18444787

Source:http://linkedlifedata.com/resource/pubmed/id/18444787

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2009-3-16
pubmed:abstractText
Acute adrenergic stress is a cause of hematopoietic failure that accompanies severe injury. Although the communication between neuronal and immune system is well documented and catecholamines are known as important regulators of homeostasis, the molecular mechanisms of hematopoietic failure are not well understood. To study the influence of adrenergic stress on hematopoietic progenitor cells (HPCs), which recently have been found to express adrenergic receptors, Lin(-),Sca(+), cells were isolated and treated with alpha- and beta-adrenergic agonists in vitro. Indeed, this stimulation resulted in significantly decreased colony formation capacity using granulocyte/macrophage colony-forming unit assays. This decline was dependent on the formation of reactive oxygen species (ROS) and activation of the p38/mitogen-activated protein kinase (MAPK) pathway, since the addition of antioxidants or a p38 inhibitor restored CFU formation. DNA damage by adrenergically induced ROS, however, does not seem to account for the reduction of colonies. Thus, catecholamine/p38/MAPK is identified as a key signal transduction pathway in HPCs besides those dependent on Wnt, Notch, and sonic hedgehog. Furthermore, a well-known target of p38 signaling, p16 is transcriptionally activated after adrenergic stimulation, suggesting that cell cycle arrest might importantly contribute to hematopoietic failure and immune dysfunctions after severe injury. Since increased levels of catecholamines are also observed in other conditions, such as during aging which is linked with decline of immune functions, adrenergic stress might as well contribute to the lowered immune defence in the elderly.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1557-8534
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
18
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
215-27
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:18444787-Adrenergic alpha-Agonists, pubmed-meshheading:18444787-Adrenergic beta-Agonists, pubmed-meshheading:18444787-Animals, pubmed-meshheading:18444787-Apoptosis, pubmed-meshheading:18444787-Cell Proliferation, pubmed-meshheading:18444787-Colony-Forming Units Assay, pubmed-meshheading:18444787-DNA Damage, pubmed-meshheading:18444787-Extracellular Signal-Regulated MAP Kinases, pubmed-meshheading:18444787-Hematopoietic Stem Cells, pubmed-meshheading:18444787-Humans, pubmed-meshheading:18444787-MAP Kinase Signaling System, pubmed-meshheading:18444787-Male, pubmed-meshheading:18444787-Mice, pubmed-meshheading:18444787-Mice, Inbred C57BL, pubmed-meshheading:18444787-Models, Biological, pubmed-meshheading:18444787-Nerve Tissue Proteins, pubmed-meshheading:18444787-Nuclear Proteins, pubmed-meshheading:18444787-Phosphorylation, pubmed-meshheading:18444787-Reactive Oxygen Species, pubmed-meshheading:18444787-Stress, Physiological, pubmed-meshheading:18444787-p38 Mitogen-Activated Protein Kinases
pubmed:year
2009
pubmed:articleTitle
Acute adrenergic stress inhibits proliferation of murine hematopoietic progenitor cells via p38/MAPK signaling.
pubmed:affiliation
Institute of Pathophysiology and Immunology, Center of Molecular Medicine, Medical University of Graz, Graz, Austria. elisabeth.schraml@boku.ac.at
pubmed:publicationType
Journal Article