Prolactin receptor antagonism uncouples lipids from atherosclerosis susceptibility
| Autor: | Menno Hoekstra, Anne Q Reuwer, Miranda Van Eck, Vincent Goffin, Ronald J. van der Sluis, Tim van den Aardweg, Florence Boutillon, Marcel Th B Twickler |
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| Jazyk: | angličtina |
| Rok vydání: | 2014 |
| Předmět: |
Male
medicine.medical_specialty Very low-density lipoprotein Receptors Prolactin Endocrinology Diabetes and Metabolism Gene Expression Mice Transgenic Inflammation Biology Mice chemistry.chemical_compound Endocrinology Internal medicine Leukocytes medicine Animals Aorta Bone Marrow Transplantation Mice Knockout Cholesterol Prolactin receptor Atherosclerosis Lipid Metabolism Recombinant Proteins Prolactin Mice Inbred C57BL Receptors LDL chemistry LDL receptor Disease Susceptibility Human medicine medicine.symptom Signal Transduction Lipoprotein Hormone |
| Zdroj: | The journal of endocrinology |
| ISSN: | 0022-0795 |
| Popis: | The pituitary-derived hormone prolactin has been suggested to stimulate the development of atherosclerosis and cardiovascular disease through its effects on metabolism and inflammation. In this study, we aimed to challenge the hypothesis that inhibition of prolactin function may beneficially affect atherosclerosis burden. Hereto, atherosclerosis-susceptible LDL receptor (Ldlr) knockout mice were transplanted with bone marrow from transgenic mice expressing the pure prolactin receptor antagonist Del1-9-G129R-hPRL or their non-transgenic littermates as control. Recipient mice expressing Del1-9-G129R-hPRL exhibited a decrease in plasma cholesterol levels (−29%; PP3 μm2 for Del1-9-G129R-hPRL vs 259±32×103 μm2 for controls) and the lesional macrophage and collagen contents were not different between the two groups of bone marrow recipients. Importantly, Del1-9-G129R-hPRL exposure increased levels of circulating neutrophils (+91%; PPPPLdlr knockout mice. Despite an associated decrease in VLDL/LDL cholesterol levels, application of the prolactin receptor antagonist Del1-9-G129R-hPRL does not alter the susceptibility for initial development of atherosclerotic lesions probably due to the parallel increase in circulating leukocyte concentrations. |
| Databáze: | OpenAIRE |
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