Effects of sex steroids on expression of adenylyl cyclase messenger RNA in rat uterus

Abstract

The aim of our study was to investigate the effects of estradiol (E2) and/or progesterone (P4) bilateral ovariectomized rats on gene expressions of adenylyl cyclases (AC2, AC4, AC6, AC9). Non-pregnant (NP) Wister rats (between post-natal 10 and 12 weeks) and normal pregnant rats (between postnatal 10 and 14 weeks) were used. NP rats were divided into five groups: 1) control NP rats, 2) ovariectomy rats (OVX), 3) OVX injected with E2 (6 microg) for 4 days (E2), 4) OVX injected with P4 (5 mg) for 4 days (P4), 5) ovariectomy rats injected with E2 (6 microg) and P4 (5 mg) for 4 days (E2/P4). The ovariectomized rats were sacrificed by anesthesia of diethyl ether after 24 h from the last injection. The pregnant group was sacrificed in the same way on 14 (P14), 17 (P17) and 21 (P21) of pregnancy, because the days between P14 and P17 were the second trimester of pregnancy and P21 was the third trimester. Total RNA were prepared from the uteri of each subject, and expression of ACs was analyzed by reverse transcription-polymerase chain reaction (RT-PCR). Expression of mRNAs for AC2, AC4, AC6 and AC9 were maximally increased on P17 and then decreased on P21. In OVX rats, expression of mRNAs for AC2, AC4, and AC9 were decreased as compared to NP. AC2 mRNA was significantly increased by E2 treatment. AC4 and AC9 mRNA was significantly increased by injection of E2 or P4. AC6 mRNA level was not affected by E2 and/or P4. In conclusion, AC2, AC4 and AC9 gene expression is affected by estrogen and/or P4. On the contrary, AC6 gene expression was not changed by OVX or hormone treatment. Since, all ACs mRNA examined here are increased during pregnancy, AC6 may be affected by other factor(s) other than estrogen and P4.

17β‐Estradiol reduces mitochondrial cAMP content and cytochrome oxidase activity in a phosphodiesterase 2‐dependent manner

“…Estradiol positively regulated cAMP signalling in a variety of cell types, for example, in rat cardiomyocytes (Buitrago et al ., ) or coronary artery smooth muscle cells (Yu et al ., ), through non‐genomic action of plasmalemmal ER on the tmAC activity. Similarly, the limited data demonstrating a genomic action of estradiol on cAMP signalling support its positive regulatory effect (Asano et al ., ; Ismail et al ., ).…”

Network Pharmacology Integrated with Molecular Docking Explores the Mechanisms of Naringin against Osteoporotic Fracture by Regulating Oxidative Stress

“…CDKN1A (p21), as a G 1 phase regulatory protein, inactivates the CDK4-cyclin complex by binding to it, leading to cell cycle stagnation in the G 1 phase [ 45 ]. An animal experiment [ 46 ] has proved that the expression of p21 in osteoblasts was significantly increased in rats after ovariectomy ( P < 0.01). It is also reported that the downregulation of p21 protein expression can promote the proliferation of osteoblasts [ 45 ].…”