scholarly journals Regulation of bovine oviductal NO synthesis by follicular steroids and prostaglandins

Reproduction ◽  
2016 ◽  
Vol 151 (6) ◽  
pp. 577-587 ◽  
Author(s):  
Yoshihiko Kobayashi ◽  
Yuki Yamamoto ◽  
Soichi Kageyama ◽  
Hiroki Hirayama ◽  
Koji Kimura ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Mrna Expression ◽  
No Synthase ◽  
Specific Difference ◽  
Embryo Survival ◽  
Pge2 Receptor ◽  
Estradiol 17Β ◽  
Esr1 Expression ◽  
Estrogen Receptorα

Abstract Nitric oxide (NO) is a regulator of sperm motility, oocyte/embryo survival, and waves of contraction/relaxation in mammalian oviducts. As follicles control oviductal functions by two routes at least, (1) a systemic way via blood vessels before ovulation, (2) a direct way by entering of follicular fluid through fimbria at ovulation, we hypothesized that NO synthesis in the bovine oviduct is regulated by follicular steroids and prostaglandins (PGs). Quantification of mRNA expressions in the ampullary tissues showed that inducible NO synthase (NOS2) mRNA expression was highest on the day of ovulation (day 0). By contrast, NOS2 mRNA expression in the isthmus was highest on days 5–6 and lowest on days 19–21. Endothelial NOS (NOS3) mRNA expressions in either the ampulla or the isthmus did not change during the estrous cycle. PGE2 and PGF2α increased NOS2 mRNA expressions in cultured ampullary oviductal epithelial cells after 1-h incubation. These increases were suppressed by an antagonist of E-prostanoid receptor type 2, one of the PGE2 receptor. Estradiol-17β decreased the expression of NOS2 mRNA expression in cultured isthmic epithelial cells 24h after treatment. This effect was suppressed by an antagonist of estrogen receptorα(ESR1). Expression of ESR1 was highest on days 19–21 in the isthmic tissues. The overall findings indicate region-specific difference of NO synthesis in the oviduct. PGs flowed from ruptured follicle may up-regulate NO synthesis in the oviductal epithelium, whereas circulating E2 seems to inhibit NO synthesis via ESR1 in the isthmus at the follicular stage.

Peripheral mononuclear TNF-α, visfatin, and resistin mRNA expression in overweight women with type 2 diabetes

2007 ◽  
Vol 2 (04) ◽  
Author(s):  
P Tsiotra ◽  
C Tsigos ◽  
E Yfanti ◽  
E Anastasiou ◽  
SA Raptis
Keyword(s):  
Type 2 Diabetes ◽  
Mrna Expression ◽  
Overweight Women ◽  
Tnf Α ◽  
Resistin Mrna

scholarly journals The type 2 vascular endothelial growth factor receptor recruits insulin receptor substrate-1 in its signalling pathway

2002 ◽  
Vol 368 (1) ◽  
pp. 49-56 ◽  
Author(s):  
Duraisamy SENTHIL ◽  
Goutam GHOSH CHOUDHURY ◽  
Basant K. BHANDARI ◽  
Balakuntalam S. KASINATH
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Protein Synthesis ◽  
Growth Factor ◽  
Epithelial Cells ◽  
Tyrosine Phosphorylation ◽  
Kinase Activity ◽  
Insulin Receptor Substrate ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor

Vascular endothelial growth factor (VEGF) isoforms exert their biological effects through receptors that possess intrinsic tyrosine kinase activity. Whether VEGF binding to its receptors recruits insulin receptor substrate (IRS) family of docking proteins to the receptor is not known. Following incubation of mouse kidney proximal tubular epithelial cells with VEGF, we observed an increase in tyrosine phosphorylation of several proteins, including one of 200kDa, suggesting possible regulation of phosphorylation of IRS proteins. VEGF augmented tyrosine phosphorylation of IRS-1 in kidney epithelial cells and rat heart endothelial cells in a time-dependent manner. In the epithelial cells, association of IRS-1 with type 2 VEGF receptor was promoted by VEGF. VEGF also increased association of IRS-1 with the p85 regulatory subunit of phosphoinositide 3-kinase (PI 3-kinase), and PI 3-kinase activity in IRS-1 immunoprecipitates was increased in VEGF-treated cells. Incubation of epithelial cells with antisense IRS-1 oligonucleotide, but not sense oligonucleotide, reduced expression of the protein and VEGF-induced PI 3-kinase activity in IRS-1 immunoprecipitates. Additionally, VEGF-induced protein synthesis was also impaired by antisense but not sense IRS-1 oligonucleotide. These data provide the first evidence that binding of VEGF to its type 2 receptor promotes association of IRS-1 with the receptor complex. This association may account for some of the increase in VEGF-induced PI 3-kinase activity, and the increase in de novo protein synthesis seen in renal epithelial cells.

mRNA Expression of IGF-1 and IGF-1R in Patients with Colorectal Adenocarcinoma and Type 2 Diabetes

2014 ◽  
Vol 45 (4) ◽  
pp. 318-324 ◽  
Author(s):  
Rui Liu ◽  
Li-Ling Hu ◽  
Ao Sun ◽  
Ya-Jing Cao ◽  
Tao Tang ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Mrna Expression ◽  
Colorectal Adenocarcinoma

scholarly journals Kinetics of human-T cell leukemia virus type 2 (HTLV-2) mRNA expression in PBMCs isolated from infected subjects

Retrovirology ◽  
2009 ◽  
Vol 6 (Suppl 2) ◽  
pp. P86
Author(s):  
Cecilia Bender ◽  
Paola Ronzi ◽  
Francesca Rende ◽  
Alessia Cotena ◽  
Marco Turci ◽  
...  
Keyword(s):  
T Cell ◽  
Mrna Expression ◽  
Virus Type ◽  
Leukemia Virus ◽  
Cell Leukemia ◽  
Cell Leukemia Virus Type ◽  
Human T Cell ◽  
T Cell Leukemia Virus ◽  
Kinetics Of

scholarly journals Herpes simplex virus type 2 virion host shutoff protein suppresses innate dsRNA antiviral pathways in human vaginal epithelial cells

2011 ◽  
Vol 92 (9) ◽  
pp. 1981-1993 ◽  
Author(s):  
Xiao-Dan Yao ◽  
Kenneth Lee Rosenthal
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Epithelial Cells ◽  
Herpes Simplex Virus Type ◽  
Innate Immune ◽  
Antiviral Responses ◽  
Virion Host Shutoff ◽  
Vaginal Epithelial Cells ◽  
Simplex Virus

Viruses that establish persistent infections have evolved numerous strategies to evade host innate antiviral responses. We functionally assessed the role of herpes simplex virus type 2 (HSV-2) virion host shutoff (vhs) protein on innate immune sensing pathways in human vaginal epithelial cells (VK2 ECs). Infection of cells with wild-type (WT) HSV-2 significantly decreased expression of innate immune sensors of viral infection, Toll-like receptor (TLR)2, TLR3, retinoic acid inducible gene I (RIG-I) and melanoma differentiation-associated gene 5 (Mda-5), relative to cells infected with a mutant that lacks vhs (vhsB) or mock-infected cells. Transfection with HSV-2 vhs similarly decreased expression of TLR2, TLR3, RIG-I and Mda-5, which was also confirmed in human embryonic kidney (HEK) 293 cells. vhsB infection of VK2 cells caused robust increases in the active form of interferon regulatory factor (IRF)3 and its translocation to the nucleus compared with the WT. Additionally, IRF3 activation by Sendai virus and polyinosinic : polycytidylic acid-induced stimulation of beta interferon (IFN-β) was significantly inhibited in vhs-transfected cells. Overall, our findings provide the first evidence that HSV-2 vhs plays roles in selectively inhibiting TLR3 and RIG-I/Mda-5, as well as TLR2-mediated antiviral pathways for sensing dsRNA and effectively suppresses IFN-β antiviral responses in human vaginal ECs.

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