Asset Details
Do you wish to reserve the book?
MiRNA-130a promotes inflammation to accelerate atherosclerosis via the regulation of proliferator-activated receptor γ (PPARγ) expression
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
MiRNA-130a promotes inflammation to accelerate atherosclerosis via the regulation of proliferator-activated receptor γ (PPARγ) expression
Do you wish to request the book?
MiRNA-130a promotes inflammation to accelerate atherosclerosis via the regulation of proliferator-activated receptor γ (PPARγ) expression
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
MiRNA-130a promotes inflammation to accelerate atherosclerosis via the regulation of proliferator-activated receptor γ (PPARγ) expression
2021
Overview
In this study, we aimed to evaluate the possible function of miR-130a in atherosclerosis (AS), protection against AS, and its molecular biological mechanism.
Apoe-/- mice were fed a high-fat diet as the AS mice model. Human umbilical vein endothelial cells (HUVECs) were used as in vitro model. Serum samples or cells were used to measure the expression of inflammation. Serum samples or cells were used to determine MiRNA expression profiles using the edgeR tool from Bioconductor. Western Blot analysis was used to assess protein expressions of proliferator-activated receptor γ (PPARγ) and nuclear factor (NF)-κB.
MiRNA-130a expression was up-regulated in atherosclerotic mice. In addition, over-expression of miRNA-130a promoted inflammation factors [tumor necrosis factor (TNF)-α and interleukin (IL)-1β, IL-6, and IL-8] in the in vitro model of AS. However, down-regulation of miRNA-130a reduced inflammation (suppressed TNF-α, IL-1β, IL-6 and IL-8) in the in vitro model. Furthermore, over-expression of miRNA-130a could also suppress the protein expression of PPARγ and induce NF-κB protein expression in the in vitro model. However, suppression of miRNA-130a induced the protein expression of PPARγ and suppressed NF-κB protein expression in the in vitro model of AS. Activation of PPARγ reduced the pro-inflammatory effects of miRNA-130a on the AS-induced in vitro model.
These results strongly support that miRNA-130a suppression can protect against atherosclerosis through inhibiting inflammation by regulating the PPARγ/ NF-κB expression.
Publisher
Turkish Society of Cardiology,KARE Publishing
