A5009439470- Reproductive Biology and Fertility
- Phosphodiesterase function and regulation
- Fibroblast Growth Factor Research
- Connective tissue disorders research
- Peptidase Inhibition and Analysis
- Reproductive System and Pregnancy
- Ovarian function and disorders
- Neuroendocrine regulation and behavior
- Endometriosis Research and Treatment
- PI3K/AKT/mTOR signaling in cancer
- Proteoglycans and glycosaminoglycans research
- Sperm and Testicular Function
- Renal and related cancers
- Preterm Birth and Chorioamnionitis
- Cancer-related gene regulation
- Reproductive Physiology in Livestock
- Reproductive biology and impacts on aquatic species
UConn Health
2012-2021
Significance By imaging cyclic GMP (cGMP) in live ovarian follicles from mice, we show how luteinizing hormone signaling the follicle periphery results a rapid decrease cGMP oocyte, thus reinitiating meiosis. Luteinizing lowers outer cells of follicle, then oocyte decreases as consequence diffusion through gap junctions. These findings demonstrate directly that physiological signal initiated by stimulus one region an intact tissue can travel across many layers via nucleotide
In mammals, the meiotic cell cycle of oocytes starts during embryogenesis and then pauses. Much later, in preparation for fertilization, within preovulatory follicles resume meiosis response to luteinizing hormone (LH). Before LH stimulation, arrest is maintained by diffusion cyclic (c)GMP into oocyte from surrounding granulosa cells, where it produced guanylyl cyclase natriuretic peptide receptor 2 (NPR2). rapidly reduces production cGMP, but how this occurs unknown. Here, using rat...
The meiotic cell cycle of mammalian oocytes in preovulatory follicles is held prophase arrest by diffusion cGMP from the surrounding granulosa cells into oocyte. Luteinizing hormone (LH) then releases lowering cells. LH-induced reduction caused part a decrease guanylyl cyclase activity, but observation that phosphodiesterase PDE5 phosphorylated during LH signaling suggests an increase activity could also contribute. To investigate this idea, we measured cGMP-hydrolytic rat ovarian follicles....
Activating mutations in fibroblast growth factor (FGF) receptor 3 and inactivating the NPR2 guanylyl cyclase both cause severe short stature, but how these two signaling systems interact to regulate bone is poorly understood. Here, we show that elongation increased when cannot be dephosphorylated thus produces more cyclic GMP. By developing an vivo imaging system measure GMP production intact tibia, FGF-induced dephosphorylation of decreases its activity plate chondrocytes living bone. The...
Luteinizing hormone (LH) acts on the granulosa cells that surround oocyte in mammalian preovulatory follicles to cause meiotic resumption and ovulation. Both of these responses are mediated primarily by an increase cyclic adenosine monophosphate (cAMP) cells, activity cAMP phosphodiesterases (PDEs), including PDE4, contributes preventing premature responses. However, two other cAMP-specific PDEs, PDE7 PDE8, also expressed at high levels raising question whether PDEs contribute uncontrolled...
Activating mutations in fibroblast growth factor receptor 3 (FGFR3) and inactivating the natriuretic peptide 2 (NPR2) guanylyl cyclase both result decreased production of cyclic GMP chondrocytes severe short stature, causing achondroplasia (ACH) acromesomelic dysplasia, type Maroteaux, respectively. Previously, we showed that an NPR2 agonist BMN-111 (vosoritide) increases bone mice mimicking ACH (Fgfr3Y367C/+). Here, because FGFR3 signaling decreases activity by dephosphorylating protein,...
Abstract Activating mutations in fibroblast growth factor (FGF) receptor 3 and inactivating the NPR2 guanylyl cyclase cause similar forms of dwarfism, but how these two signaling systems interact to regulate bone is poorly understood. Here, by use a mouse model which cannot be dephosphorylated, we show that elongation opposed when dephosphorylated thus produces less cyclic GMP. By developing an vivo imaging system measure GMP levels intact tibia, FGF-induced dephosphorylation decreases its...
ABSTRACT Activating mutations in fibroblast growth factor receptor 3 (FGFR3) and inactivating the natriuretic peptide 2 (NPR2) guanylyl cyclase both result decreased production of cyclic GMP (cGMP) chondrocytes severe short stature, causing achondroplasia (ACH) acrosomelic dysplasia type Maroteaux, respectively. Previously we showed that an NPR2 agonist BMN-111 (vosoritide) increases bone mice mimicking ACH ( Fgfr3 Y367C/+ ), control plate chondrocytes, FGFR3 signaling decreases activity by...
Background The meiotic cell cycle of mammalian oocytes starts during embryogenesis and then pauses until luteinizing hormone (LH) restarts the cycle. This arrest is maintained by cGMP, which produced in granulosa cells C-type natriuretic peptide (CNP) activation NPR2 [1]. LH decreases cGMP cells, via equilibration through gap junctions, cyclic GMP also oocyte, thus releasing [2]. causes dephosphorylation inactivation [3,4], but whether required for resumption not known. Seven regulatory...
Background In mammalian ovarian follicles, granulosa cells keep fully grown oocytes arrested in meiotic prophase. A key inhibitory signal is cGMP, which diffuses into the oocyte from cells, where it synthesized by guanylyl cyclase B/ natriuretic peptide receptor 2 (NPR2) response to agonist C-type (CNP) [1]. Then luteinizing hormone (LH), cGMP and decreases, promoting resumption of meiosis [2]. The primary mechanism LH signaling reduces reducing activity NPR2; this occurs a rapid...