ArticleThe Journal of biological chemistry2016
Activation of Peroxisome Proliferator-activated Receptor γ (PPARγ) and CD36 Protein Expression: THE DUAL PATHOPHYSIOLOGICAL ROLES OF PROGESTERONE.
Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 34 citations in OpenAlex.
- High progesterone levels are associated with family history of premature coronary artery disease in young healthy adult men.PloS one · 2019Trial
- Review
- Article
- Preventing ovarian aging: from redox-targeted strategies to extracellular vesicle-based therapies.Frontiers in aging · 2026Review
- Macrophage clock of pregnancy: circadian and metabolic control of decidual macrophage.Seminars in immunopathology · 2025Review
- Phenotypic and Functional Outcomes in Macrophages Exposed to an Environmentally Relevant Mixture of Organophosphate EstersEnvironmental health perspectives · 2024Article
- Liver ChREBP deficiency inhibits fructose-induced insulin resistance in pregnant mice and female offspring.EMBO reports · 2024Article
- CD36 inhibition reduces non-small-cell lung cancer development through AKT-mTOR pathway.Cell biology and toxicology · 2024Article
- ACSL1 is a key regulator of inflammatory and macrophage foaming induced by short-term palmitate exposure or acute high-fat feeding.iScience · 2023Article
- ATF4-mediated CD36 upregulation contributes to palmitate-induced lipotoxicity in hepatocytes.American journal of physiology. Gastrointestinal and liver physiology · 2023Article
- Diabetic cardiomyopathy: a brief summary on lipid toxicity.ESC heart failure · 2023Review
- The Farnesoid X Receptor as a Master Regulator of Hepatotoxicity.International journal of molecular sciences · 2022Review
- The activation of PPARγ enhances Treg responses through up-regulating CD36/CPT1-mediated fatty acid oxidation and subsequent N-glycan branching of TβRII/IL-2Rα.Cell communication and signaling : CCS · 2022Article
- Expression of the Adipocyte Progenitor Markers MSCA1 and CD36 is Associated With Adipose Tissue Function in Children.The Journal of clinical endocrinology and metabolism · 2022Observational
- MPA alters metabolic phenotype of endometrial cancer-associated fibroblasts from obese women via IRS2 signaling.PloS one · 2022Article
- Tuberculosis alters immune-metabolic pathways resulting in perturbed IL-1 responses.Frontiers in immunology · 2022Article
- S100A4 enhances protumor macrophage polarization by control of PPAR-γ-dependent induction of fatty acid oxidation.Journal for immunotherapy of cancer · 2021Article
- Glucose and fatty acid metabolism involved in the protective effect of metformin against ulipristal-induced endometrial changes in rats.Scientific reports · 2021Article
- TL1A inhibits atherosclerosis in apoE-deficient mice by regulating the phenotype of vascular smooth muscle cells.The Journal of biological chemistry · 2020Article
- IDH2 Deficiency Is Critical in Myogenesis and Fatty Acid Metabolism in Mice Skeletal Muscle.International journal of molecular sciences · 2020Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Progesterone or its analog, one of components of hormone replacement therapy, may attenuate the cardioprotective effects of estrogen. However, the underlying mechanisms have not been fully elucidated. Expression of CD36, a receptor for oxidized LDL (oxLDL) that enhances macrophage/foam cell formation, is activated by the transcription factor peroxisome proliferator-activated receptor γ (PPARγ). CD36 also functions as a fatty acid transporter to influence fatty acid metabolism and the pathophysiological status of several diseases. In this study, we determined that progesterone induced macrophage CD36 expression, which is related to progesterone receptor (PR) activity. Progesterone enhanced cellular oxLDL uptake in a CD36-dependent manner. Mechanistically, progesterone increased PPARγ expression and PPARγ promoter activity in a PR-dependent manner and the binding of PR with the progesterone response element in the PPARγ promoter. Specific deletion of macrophage PPARγ (MφPPARγ KO) expression in mice abolished progesterone-induced macrophage CD36 expression and cellular oxLDL accumulation. We also determined that, associated with gestation and increased serum progesterone levels, CD36 and PPARγ expression in mouse adipose tissue, skeletal muscle, and peritoneal macrophages were substantially activated. Taken together, our study demonstrates that progesterone can play dual pathophysiological roles by activating PPARγ expression, in which progesterone increases macrophage CD36 expression and oxLDL accumulation, a negative effect on atherosclerosis, and enhances the PPARγ-CD36 pathway in adipose tissue and skeletal muscle, a protective effect on pregnancy.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.