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| Status |
Public on Jul 25, 2024 |
| Title |
Vascular endothelial S1PR2 aggravates cardiac ischemia/reperfusion injury through triggering mitochondrial dysfunctions and endothelial pyroptosis via RHO/ROCK1/DRP1/NLRP3 pathway [endothelial cells] |
| Organism |
Mus musculus |
| Experiment type |
Expression profiling by high throughput sequencing
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| Summary |
Endothelial cell dysfunction plays an essential role in the process of cardiac ischemia-reperfusion (I/R) injury. Mitochondria damage, which can trigger inflammasome activation and subsequent pyroptosis, perturbs endothelial homeostasis, leading to aggravated cardiac I/R injury. Sphingosine 1-phosphate (S1P), a bioactive lipid molecule, exerts multifaceted effect on I/R injury via its different S1P receptors. However, the effect of EC-expressing S1P receptors on endothelial dysfunction, mitochondrial damage-induced inflammasome activation and consequent pyroptosis during cardiac I/R injury remain unclear. Our findings suggest a pivotal role of EC-expressing S1PR2 to control EC mitochondrial homeostasis and demonstrate that S1PR2-meidated mitochondrial dysfunction can trigger inflammasome activation and pyroptosis in ECs, which significantly influences inflammatory responses and heart injuries following I/R.
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| Overall design |
We provided an RNA-seq analysis on heart endothelial cells of WT and VECre-S1pr2-/- mouse after cardiac ischemia-reperfusion.
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| Contributor(s) |
Duan Y, Zhang L |
| Citation(s) |
38909407 |
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| Submission date |
Oct 22, 2023 |
| Last update date |
Jul 25, 2024 |
| Contact name |
yunhao duan |
| E-mail(s) |
dyhdyh281@hotmail.com
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| Organization name |
Shanghai East Hospital
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| Street address |
150 Jimo Rd, Pudong New District
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| City |
Shanghai |
| ZIP/Postal code |
200120 |
| Country |
China |
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| Platforms (1) |
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| Samples (6)
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| Relations |
| BioProject |
PRJNA1030931 |
| Supplementary file |
Size |
Download |
File type/resource |
| GSE245988_GEO_submission-2EC.txt.gz |
236.9 Kb |
(ftp)(http) |
TXT |
SRA Run Selector |
| Raw data are available in SRA |
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