Prolactin regulates liver growth during postnatal development in mice
| Autor: | Xarubet Ruiz-Herrera, Ericka A. de los Ríos, Yazmín Macotela, Carmen Clapp, Marco Bravo-Manríquez, Pamela Reyes-Ortega, Maria G. Ledesma-Colunga, Bibiana Moreno-Carranza, Gonzalo Martínez de la Escalera, Arelí Baez |
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| Rok vydání: | 2018 |
| Předmět: |
Male
0301 basic medicine endocrine system medicine.medical_specialty Receptors Prolactin Physiology Period (gene) Neovascularization Physiologic Suppressor of Cytokine Signaling Proteins Growth Biology Growth hormone Mice 03 medical and health sciences 0302 clinical medicine Pregnancy Physiology (medical) Internal medicine medicine Animals Insulin-Like Growth Factor I Cell Proliferation Mice Knockout Prolactin Mice Inbred C57BL 030104 developmental biology Endocrinology Liver Suppressor of Cytokine Signaling 3 Protein Female hormones hormone substitutes and hormone antagonists 030217 neurology & neurosurgery |
| Zdroj: | American Journal of Physiology-Regulatory, Integrative and Comparative Physiology. 314:R902-R908 |
| ISSN: | 1522-1490 0363-6119 |
| Popis: | The liver grows during the early postnatal period first at slower and then at faster rates than the body to achieve the adult liver-to-body weight ratio (LBW), a constant reflecting liver health. The hormone prolactin (PRL) stimulates adult liver growth and regeneration, and its levels are high in the circulation of newborn infants, but whether PRL plays a role in neonatal liver growth is unknown. Here, we show that the liver produces PRL and upregulates the PRL receptor in mice during the first 2 wk after birth, when liver growth lags behind body growth. At postnatal week 4, the production of PRL by the liver ceases coinciding with the elevation of circulating PRL and the faster liver growth that catches up with body growth. PRL receptor null mice ( Prlr−/−) show a significant decrease in the LBW at 1, 4, 6, and 10 postnatal weeks and reduced liver expression of proliferation [cyclin D1 ( Ccnd1)] and angiogenesis [platelet/endothelial cell adhesion molecule 1 ( Pecam1)] markers relative to Prlr+/+ mice. However, the LBW increases in Prlr−/− mice at postnatal week 2 concurring with the enhanced liver expression of Igf-1 and the liver upregulation and downregulation of suppressor of cytokine signaling 2 ( Socs2) and Socs3, respectively. These findings indicate that PRL acts locally and systemically to restrict and stimulate postnatal liver growth. PRL inhibits liver and body growth by attenuating growth hormone-induced Igf-1 liver expression via Socs2 and Socs3-related mechanisms. |
| Databáze: | OpenAIRE |
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