STOREDB:STUDY1105 The PI3K/Akt/mTOR pathway is a key player in the premature senescence of primary human endothelial cells exposed to chronic radiation [DOI:10.20348/STOREDB/1105]

Study meta-data


STUDYIDSTOREDB:STUDY1105
CREATEDON2018-02-07 13:52:19
MODIFIEDON2018-02-07 13:52:19
UPLOADEROmid Azimzadeh
DOIDOI:10.20348/STOREDB/1105

Study details


STUDY NAME
The PI3K/Akt/mTOR pathway is a key player in the premature senescence of primary human endothelial cells exposed to chronic radiation
STUDY STATUS
Published: Open access to everyone
DATA SHARING POLICY
CC-Attribution Non-Commercial Share Alike
COUNTRY
Germany
PRINCIPAL INVESTIGATOR
Dr.Soile Tapio
SPECIES
Homo sapiens
SIZE OF COHORT
0-999
OUTCOME
Cardiovascular
MELODI RESEARCH PRIORITY
Analysis of mechanisms involved in low dose radiation through use and development of suitable cellular and animal models
EXPOSURE CONTEXT
Occupational
INTERNAL OR EXTERNAL EXPOSURE
External
TYPE OF EXTERNAL EXPOSURE
gamma
RADIONUCLIDE
caesium
AGE AT EXPOSURE
Adult
EXPOSURE PATTERN
Transitory
DOSE RATE
Low
BIOLOGICAL SAMPLE AVAILABLE
No
STUDY DESCRIPTION
The etiology of radiation-induced cardiovascular disease (CVD) after chronic exposure to low doses of ionizing radiation is only marginally understood. We have previously shown that a chronic low-dose rate exposure (4.1 mGy/h) causes human umbilical vein endothelial cells (HUVECs) to prematurely senesce. We now show that a dose rate of 2.4 mGy/h is also able to trigger premature senescence in HUVECs, primarily indicated by a loss of growth potential and the appearance of the senescence-associated markers -galactosidase (SA--gal) and p21. In contrast, a lower dose rate of 1.4 mGy/h was not sufficient to inhibit cellular growth or increase SA--gal-staining despite an increased expression of p21. We used reverse phase protein arrays and triplex Isotope Coded Protein Labeling with LC-ESI-MS/MS to study the proteomic changes associated with chronic radiation-induced senescence. Both technologies identified inactivation of the PI3K/Akt/mTOR pathway accompanying premature senescence. In addition, expression of proteins involved in cytoskeletal structure and EIF2 signaling was reduced. Age-related diseases such as CVD have been previously associated with increased endothelial cell senescence. We postulate that a similar endothelial aging may contribute to the increased rate of CVD seen in populations chronically exposed to low-dose-rate radiation.
PUBMED ID
23936371
MEAN DURATION OF FOLLOW-UP (WEEKS)
6

STOREDB:DATASET1156 continuous radiation exposure using lower dose rates (1.4 mGy/h and 2.4 mGy/h) / HUVECs [DOI:10.20348/STOREDB/1105/1156]


Created on:2018-02-07 13:54:04 Modified On:2018-02-07 13:54:04
DATASET NAME
continuous radiation exposure using lower dose rates (1.4 mGy/h and 2.4 mGy/h) / HUVECs
DOIDOI:10.20348/STOREDB/1105/1156
LINK TO FILE
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0070024
DATASET DESCRIPTION
proteomics lists