| STUDYID | STOREDB:STUDY1105 |
|---|---|
| CREATEDON | 2018-02-07 13:52:19 |
| MODIFIEDON | 2018-02-07 13:52:19 |
| UPLOADER | Omid Azimzadeh |
| DOI | DOI:10.20348/STOREDB/1105 |
| 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 | ||
| RADONORM 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 ß-galactosidase (SA-ß-gal) and p21. In contrast, a lower dose rate of 1.4 mGy/h was not sufficient to inhibit cellular growth or increase SA-ß-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 | ||
| DATASET NAME | ||
|---|---|---|
| continuous radiation exposure using lower dose rates (1.4 mGy/h and 2.4 mGy/h) / HUVECs | ||
| DOI | DOI:10.20348/STOREDB/1105/1156 | |
| LINK TO FILE | ||
| http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0070024 | ||
| DATASET DESCRIPTION | ||
| proteomics lists | ||
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Uploaded on: 2018-02-07 13:55:09
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