Effects of calcitonin and parathyroid hormone on the regulation of cabindin-D(9k) in the uterus, placenta, and fetal membrane of rats related to blood calcium level during late gestation.
Calbindin-D(9k) (CaBP-9k) gene is expressed in the uterus of pregnant rats, which is regulated by steroid hormones during estrous cycle or gestation. We hypothesized that there is a positive correlation between altered CaBP-9k expression and change in one or more of the hormones to provide a clue to the mechanism responsible for the altered calcium levels in the uterus, placenta, and fetal membrane during late gestation. Thus, in the present study, we investigated the effects of the hormones including estradiol (E2), calcitonin (CT), and parathyroid hormone (PTH) on the regulation of CaBP-9k in these tissues. There was an increase in the level of CaBP-9k in the uterus, placenta, and extra-embryonic membrane at late gestation, as blood calcium level increased. The protein level of CaBP-9k remained lower in the uterus at two-thirds of pregnancy, and then it rebounded abruptly during late pregnancy. During late gestation, E2 is postulated to be a dominant factor in the regulation of uterine CaBP-9k gene expression. Furthermore, we assumed that there is a positive correlation between altered expression of CaBP-9k and blood calcium level during pregnancy. The present study demonstrated the regulation of CaBP-9k mRNA in the uterus, placenta, and fetal membrane of rats, implying a role for CaBP-9k gene in the control of blood calcium in placenta and the calcium passing from maternal blood to fetal circulation. Taken together, these results suggest that major alterations in calcium metabolism caused by maternal thyroparathyroidectomy (TPTX), are sufficient to affect the changes in reproductive tissues during late pregnancy. In addition, an increase of blood calcium level is one of the most significant factors in the regulation of CaBP-9k at the transcriptional and/or translational levels in the reproductive tissues during late pregnancy.
Hong
Eui-Ju
EJ
Laboratory of Veterinary Biochemistry and Molecular Biotechnology, College of Veterinary Medicine, Chungbuk National University, Cheongju, Chungbuk, Republic of Korea.
Choi
Kyung-Chul
KC
Hyun
Sang-Hwan
SH
Jeung
Eui-Bae
EB
D000818:Animals; D064026:Calbindins; D002116:Calcitonin / Q000494:pharmacology*; D002118:Calcium / Q000097:blood; D004958:Estradiol / Q000494:pharmacology; D005321:Extraembryonic Membranes / Q000187:drug effects* / Q000378:metabolism; D005260:Female; D015870:Gene Expression / Q000187:drug effects; D005786:Gene Expression Regulation; D012739:Gonadal Steroid Hormones / Q000037:antagonists & inhibitors; D006727:Hormone Antagonists / Q000494:pharmacology; D010281:Parathyroid Hormone / Q000494:pharmacology*; D010920:Placenta / Q000187:drug effects* / Q000378:metabolism; D011247:Pregnancy; D011270:Pregnancy, Animal / Q000235:genetics / Q000378:metabolism*; D014176:Protein Biosynthesis / Q000187:drug effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D064030:S100 Calcium Binding Protein G / Q000235:genetics / Q000378:metabolism*; D014599:Uterus / Q000187:drug effects* / Q000378:metabolism
D064026:Calbindins; D012739:Gonadal Steroid Hormones; D006727:Hormone Antagonists; D010281:Parathyroid Hormone; D064030:S100 Calcium Binding Protein G; D004958:Estradiol; D002116:Calcitonin; D002118:Calcium