STOREDB:STUDY1104 Quantitative proteomic analysis reveals induction of premature senescence in human umbilical vein endothelial cells exposed to chronic low-dose rate gamma-radiation [DOI:10.20348/STOREDB/1104]

Study meta-data


STUDYIDSTOREDB:STUDY1104
CREATEDON2018-02-07 13:44:44
MODIFIEDON2018-02-07 13:44:44
UPLOADEROmid Azimzadeh
DOIDOI:10.20348/STOREDB/1104

Study details


STUDY NAME
Quantitative proteomic analysis reveals induction of premature senescence in human umbilical vein endothelial cells exposed to chronic low-dose rate gamma-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
Chronic low-dose ionizing radiation induces cardiovascular disease in human populations but the mechanism is largely unknown. We suggested that chronic radiation exposure may induce endothelial cell senescence that is associated with vascular damage in vivo. We investigated whether chronic radiation exposure is causing a change in the onset of senescence in endothelial cells in vitro. Indeed, when exposed to continuous low-dose rate gamma radiation (4.1 mGy/h) primary human umbilical vein endothelial cells (HUVECs) initiated senescence much earlier than the non-irradiated control cells. We investigated the changes in the protein expression of HUVECs before and during the onset of radiation-induced senescence. Cellular proteins were quantified using isotope-coded protein label technology after 1, 3, and 6 weeks of radiation exposure. Several senescence-related biological pathways were influenced by radiation, including cytoskeletal organisation, cell-cell communication and adhesion, and inflammation. Immunoblot analysis showed an activation of the p53/p21 pathway corresponding to the progressing senescence. Our data suggest that chronic radiation-induced DNA damage and oxidative stress result in induction of p53/p21 pathway that inhibits the replicative potential of HUVECs and leads to premature senescence. This study contributes to the understanding of the increased risk of cardiovascular diseases seen in populations exposed to chronic low-dose irradiation.
PUBMED ID
23349028
MEAN DURATION OF FOLLOW-UP (WEEKS)
12

STOREDB:DATASET1155 continuous low-dose rate gamma irradiation (4.1 mGy/h) of primary human umbilical vein endothelial cells (HUVECs) [DOI:10.20348/STOREDB/1104/1155]


Created on:2018-02-07 13:47:15 Modified On:2018-02-07 13:47:15
DATASET NAME
continuous low-dose rate gamma irradiation (4.1 mGy/h) of primary human umbilical vein endothelial cells (HUVECs)
DOIDOI:10.20348/STOREDB/1104/1155
LINK TO FILE
http://onlinelibrary.wiley.com/doi/10.1002/pmic.201200463/abstract;jsessionid=A0EF1A8F9C5AB51A583E4E0B2CDA1AAA.f03t03
DATASET DESCRIPTION
Proteomics lists