ArticleMolecular medicine reports2016
Rspo2 suppresses CD36-mediated apoptosis in oxidized low density lipoprotein-induced macrophages.
Article in Molecular medicine reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 10 citations in OpenAlex.
- The biological functions and related signaling pathways of SPON2.Frontiers in oncology · 2023Review
- Identification of Monocyte-Associated Genes Related to the Instability of Atherosclerosis Plaque.Oxidative medicine and cellular longevity · 2022Article
- Article
- Metformin protects against oxidized low density lipoprotein-induced macrophage apoptosis and inhibits lipid uptake.Experimental and therapeutic medicine · 2018Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oxidized low density lipoprotein (oxLDL)-induced apoptosis of macrophages contributes to the formation of atherosclerotic plaques. R‑spondin 2 (Rspo2), a member of the cysteine‑rich secreted proteins, has been shown to be involved in the oncogenesis of several types of cancer. It has also been found to be abundantly expressed among the four R‑spondin members in macrophages. The present study was performed to determine whether Rspo2 is involved in the ox‑LDL‑induced apoptosis of macrophages. It was identified that Rspo2 inhibited oxLDL‑induced apoptosis in the presence of endoplasmic reticulum (ER) stress activator using flow cytometry. In addition, Rspo2 was observed to suppress oxLDL‑induced ER stress and reactive oxygen species production as demonstrated by western blotting. Furthermore, analysis of the role of Rspo2 in macrophage lipid uptake identified that Rspo2 negatively regulated the Dil‑oxLDL uptake by inhibiting the expression of cluster of differentiation (CD)36, through the transcription factor, peroxisome proliferator‑activated receptor (PPAR)‑γ. The manipulation of Rspo2 had a direct effect on PPAR‑γ nuclear translocation. In addition, chromatin immunoprecipitation analysis revealed that Rspo2 manipulation led to regulation of the direct binding between PPAR‑γ and CD36. In conclusion, Rspo2 was found to have a negative regulatory effect during oxLDL‑induced macrophage apoptosis by regulating lipid uptake.
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