| First Author | Yuan R | Year | 2005 |
| Journal | Mol Cell Endocrinol | Volume | 229 |
| Issue | 1-2 | Pages | 193-203 |
| PubMed ID | 15607543 | Mgi Jnum | J:95948 |
| Mgi Id | MGI:3528127 | Doi | 10.1016/j.mce.2004.06.013 |
| Citation | Yuan R, et al. (2005) Targeted overexpression of calcitonin in gonadotrophs of transgenic mice leads to chronic hypoprolactinemia. Mol Cell Endocrinol 229(1-2):193-203 |
| abstractText | It was previously shown that calcitonin-like pituitary peptide (pit-CT) is synthesized and secreted by gonadotrophs, and pit-CT inhibits PRL gene transcription and lactotroph cell proliferation. Present studies examined long-term consequences of pit-CT overexpression on the functioning of mouse anterior pituitary (AP) gland. Targeted overexpression of pit-CT in gonadotrophs of mouse pituitaries was achieved by generating mice overexpressing bovine luteinizing hormone (LH)-alpha subunit promoter-pit-CT cDNA transgene. Transgenic (pit-CT+) mice displayed chronic but selective overexpression of pit-CT in gonadotrophs. The mice also displayed a dramatic decline in PRL gene expression as assessed by PRL mRNA abundance, PRL immunohistochemistry (IHC) and serum PRL levels. LH secretion in pit-CT+ mice was also reduced, without any change in FSH secretion. Reproductive abnormalities such as prolonged estrous cycles, reduced pregnancy rate, delivery of smaller litters, increased neonatal mortality and deficient lactation were also observed. Administration of PRL during early pregnancy significantly increased the pregnancy rate and neonatal survival of newborns. These results demonstrate that overexpression of pit-CT leads to chronic hypoprolactinemia and reproductive dysfunction in female mice, and reinforces the possibility that gonadotroph-derived pit-CT is an important paracrine regulator of lactotroph function. |
