Peroxisome Proliferator-Activated Receptors Alpha, Beta, and Gamma mRNA and Protein Expression in Human Fetal Tissues
Barbara D. Abbott,
Carmen R. Wood,
Andrew M. Watkins,
Kaberi P. Das,
Christopher S. Lau
Affiliations
Barbara D. Abbott
Toxicity Assessment Division, Developmental Toxicology Branch, National Health and Environmental Effects Research Laboratory, (MD-67), Office of Research and Development, US Environmental Protection Agency, Research Triangle Park, NC 27711, USA
Carmen R. Wood
Toxicity Assessment Division, Developmental Toxicology Branch, National Health and Environmental Effects Research Laboratory, (MD-67), Office of Research and Development, US Environmental Protection Agency, Research Triangle Park, NC 27711, USA
Andrew M. Watkins
Toxicity Assessment Division, Developmental Toxicology Branch, National Health and Environmental Effects Research Laboratory, (MD-67), Office of Research and Development, US Environmental Protection Agency, Research Triangle Park, NC 27711, USA
Kaberi P. Das
Toxicity Assessment Division, Developmental Toxicology Branch, National Health and Environmental Effects Research Laboratory, (MD-67), Office of Research and Development, US Environmental Protection Agency, Research Triangle Park, NC 27711, USA
Christopher S. Lau
Toxicity Assessment Division, Developmental Toxicology Branch, National Health and Environmental Effects Research Laboratory, (MD-67), Office of Research and Development, US Environmental Protection Agency, Research Triangle Park, NC 27711, USA
Peroxisome proliferator-activated receptors (PPARs) regulate lipid and glucose homeostasis, are targets of pharmaceuticals, and are also activated by environmental contaminants. Almost nothing is known about expression of PPARs during human fetal development. This study examines expression of PPAR𝛼, 𝛽, and 𝛾 mRNA and protein in human fetal tissues. With increasing fetal age, mRNA expression of PPAR𝛼 and 𝛽 increased in liver, but PPAR𝛽 decreased in heart and intestine, and PPAR𝛾 decreased in adrenal. Adult and fetal mean expression of PPAR𝛼, 𝛽, and 𝛾 mRNA did not differ in intestine, but expression was lower in fetal stomach and heart. PPAR𝛼 and 𝛽 mRNA in kidney and spleen, and PPAR𝛾 mRNA in lung and adrenal were lower in fetal versus adult. PPAR𝛾 in liver and PPAR𝛽 mRNA in thymus were higher in fetal versus adult. PPAR𝛼 protein increased with fetal age in intestine and decreased in lung, kidney, and adrenal. PPAR𝛽 protein in adrenal and PPAR𝛾 in kidney decreased with fetal age. This study provides new information on expression of PPAR subtypes during human development and will be important in evaluating the potential for the developing human to respond to PPAR environmental or pharmaceutical agonists.
