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| Status |
Public on Nov 06, 2019 |
| Title |
Transcriptome profiling of liver derived from calcium channel ITPR2 KO mice |
| Organism |
Mus musculus |
| Experiment type |
Expression profiling by array
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| Summary |
Cellular senescence is induced by multiple stresses and results in a stable proliferation arrest accompanied by a pro-inflammatory secretome. Senescent cells accumulate during aging, promoting various age-related pathologies and thus limiting lifespan. The endoplasmic reticulum ITPR2 release channel and calcium fluxes from the ER to the mitochondria have been identified as drivers of cellular senescence in human cells. Here we show that Itpr2 knockout mice display improved aging such as increased lifespan, a better response to metabolic stress, less immunosenescence, as well as less liver steatosis and fibrosis. Cellular senescence, which is known to promote these alterations, is decreased in both Itpr2 KO mice and Itpr2 KO embryo-derived cells. Interestingly, ablation of ITPR2 in vivo and in vitro decreases the number of contacts between the mitochondria and the ER and forced contacts between these two organelles induce premature senescence in normal cells. These new findings shed light on the role of contacts and facilitated exchanges between the ER and the mitochondria through ITPR2 in regulating senescence and physiological aging.
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| Overall design |
Transcriptome analysis has been performed on liver tissue derived from 3 independent WT or Itpr2 KO mice
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| Contributor(s) |
Ziegler DV, Vindrieux D, Bernard D, Flaman J |
| Citation missing |
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| |
| Submission date |
Nov 05, 2019 |
| Last update date |
Nov 08, 2019 |
| Contact name |
jean-michel flaman |
| E-mail(s) |
[email protected]
|
| Phone |
+33687477812
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| Organization name |
Inserm 1052
|
| Department |
CRCL
|
| Street address |
28 rue Laennec
|
| City |
Lyon |
| ZIP/Postal code |
69373 |
| Country |
France |
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| Platforms (1) |
| GPL11202 |
Agilent-026655 Whole Mouse Genome Microarray 4x44K v2 (Probe Name version) |
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| Samples (6)
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| Relations |
| BioProject |
PRJNA587751 |
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