Differential regulation of betacellulin and heparin-binding EGF-like growth factor in cultured zebrafish ovarian follicle cells by EGF family ligands

2009 ◽  
Vol 153 (1) ◽  
pp. 13-17 ◽  
Author(s):  
Anna Chung-Kwan Tse ◽  
Wei Ge
Keyword(s):  
Growth Factor ◽  
Ovarian Follicle ◽  
Differential Regulation ◽  
Follicle Cells ◽  
Heparin Binding ◽  
Egf Family

scholarly journals Baboon placental heparin-binding epidermal growth factor-like growth factor

Reproduction ◽  
2020 ◽  
Vol 160 (1) ◽  
pp. 31-37
Author(s):  
D Randall Armant ◽  
Graham W Aberdeen ◽  
Brian A Kilburn ◽  
Gerald J Pepe ◽  
Eugene D Albrecht
Keyword(s):  
Growth Factor ◽  
First Trimester ◽  
Extravillous Trophoblast ◽  
Immunocytochemical Staining ◽  
Heparin Binding ◽  
Spiral Artery ◽  
Primate Model ◽  
Artery Remodeling ◽  
Egf Family

Placental extravillous trophoblast remodeling of the uterine spiral arteries is important for promoting blood flow to the placenta and fetal development. Heparin-binding EGF-like growth factor (HB-EGF), an EGF family member, stimulates differentiation and invasive capacity of extravillous trophoblasts in vitro. Trophoblast expression and maternal levels of HB-EGF are reduced at term in women with preeclampsia, but it is uncertain whether HB-EGF is downregulated earlier when it may contribute to placental insufficiency. A nonhuman primate model has been established in which trophoblast remodeling of the uterine spiral arteries is suppressed by shifting the rise in estrogen from the second to the first trimester of baboon pregnancy. In the present study, we used this model to determine if placental HB-EGF is altered by prematurely elevating estrogen early in baboon gestation. Uterine spiral artery remodeling and placental expression of HB-EGF and other EGF family members were assessed on day 60 of gestation in baboons treated with estradiol (E2) daily between days 25 and 59 of gestation (term = 184 days). The percentages of spiral artery remodeling were 90, 84 and 70% lower (P < 0.01), respectively, for vessels of 26–50, 51–100 and >100 µm diameter in E2-treated compared with untreated baboons. HB-EGF protein quantified by immunocytochemical staining/image analysis was decreased three-fold (P < 0.01) in the placenta of E2-treated versus untreated baboons, while amphiregulin (AREG) and EGF expression was unaltered. Therefore, we propose that HB-EGF modulates the estrogen-sensitive remodeling of the uterine spiral arteries by the extravillous trophoblast in early baboon pregnancy.

scholarly journals The Gene for Heparin-Binding Epidermal Growth Factor-Like Growth Factor is Stress-Inducible: Its Role in Cerebral Ischemia

1999 ◽  
Vol 19 (3) ◽  
pp. 307-320 ◽  
Author(s):  
Nobutaka Kawahara ◽  
Kazuhiko Mishima ◽  
Shigeki Higashiyama ◽  
Naoyuki Taniguchi ◽  
Akira Tamura ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Dentate Gyrus ◽  
Transforming Growth Factor ◽  
Adult Brain ◽  
Normal Brain ◽  
Heparin Binding ◽  
Epidermal Growth ◽  
Egf Family

The functions of the epidermal growth factor (EGF) family members in the adult brain are not known. This study investigated the changes in the expression of members of the EGF family following global ischemia employing in situ hybridization and immunohistochemical techniques to elucidate their roles in pathological conditions. EGF mRNA was not detected in either the control or the postischemic rat brain. Although transforming growth factor-α (TGF-α) mRNA was widely expressed in the normal brain, its expression did not change appreciably following ischemia. By contrast, heparin-binding EGF-like growth factor (HB-EGF) mRNA expression was rapidly increased in the CA3 sector and the dentate gyrus of the hippocampus, cortex, thalamus, and cerebellar granule and Purkinje cell layers. EGF receptor mRNA, which was widely expressed, also showed an increase in the CA3 sector and dentate gyrus. Conversely, HB-EGF mRNA did not show any increase prior to ischemic neuronal injury in the CA1 sector, the region most vulnerable to ischemia. Immunohistochemical detection of HB-EGF in the postischemic brain suggested a slight increase of immunostaining in the dentate gyrus of the hippocampus and the cortex. These findings showed that the gene encoding HB-EGF is stress-inducible, indicating the like-lihood that HB-EGF is a neuroprotective factor in cerebral ischemia.

scholarly journals Role of membrane-anchored heparin-binding epidermal growth factor-like growth factor and CD9 on macrophages

1997 ◽  
Vol 328 (3) ◽  
pp. 923-928 ◽  
Author(s):  
Noriyuki OUCHI ◽  
Shinji KIHARA ◽  
Shizuya YAMASHITA ◽  
Shigeki HIGASHIYAMA ◽  
Tsutomu NAKAGAWA ◽  
...  
Keyword(s):  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Surface Marker ◽  
Heparin Binding ◽  
Atherosclerotic Lesions ◽  
Growth Activity ◽  
Epidermal Growth ◽  
Egf Family ◽  
Formalin Fixed

Heparin-binding epidermal-growth-factor-like growth factor (HB-EGF) is a potent mitogen for smooth-muscle cells (SMCs) belonging to the EGF family. We have previously determined that HB-EGF is expressed in macrophages and SMCs of human atherosclerotic lesions and that its membrane-anchored precursor, proHB-EGF, also has a juxtacrine mitogenic activity which is markedly enhanced by CD9, a surface marker of lymphohaemopoietic cells. Therefore, when both proHB-EGF and CD9 are expressed on macrophages, they may strongly promote the development of atherosclerosis. In the present study we have investigated the changes in proHB-EGF and CD9 in THP-1 cells during differentiation into macrophages and by the addition of oxidized low-density lipoproteins (OxLDL) and assessed juxtacrine growth activity of THP-1 macrophages for human aortic SMCs. HB-EGF and CD9 at both the mRNA and the protein level were up-regulated after differentiation into macrophages, and further expression of HB-EGF was induced by the addition of OxLDL or lysophosphatidylcholine. Juxtacrine induction by formalin-fixed growth was suppressed to control levels by an inhibitor of HB-EGF and was partially decreased by anti-CD9 antibodies. These results suggest that co-expression of proHB-EGF and CD9 on macrophages plays an important role in the development of atherosclerosis by a juxtacrine mechanism.

scholarly journals Involvement of Cyclic Adenosine 3′,5′-Monophosphate in the Differential Regulation of Activin βA and βB Expression by Gonadotropin in the Zebrafish Ovarian Follicle Cells

Endocrinology ◽  
2003 ◽  
Vol 144 (2) ◽  
pp. 491-499 ◽  
Author(s):  
Yajun Wang ◽  
Wei Ge
Keyword(s):  
Oocyte Maturation ◽  
Ovarian Follicle ◽  
Mrna Level ◽  
Specific Inhibitor ◽  
Inhibitory Effect ◽  
Differential Regulation ◽  
Follicle Cells ◽  
Intracellular Camp ◽  
Dependent Manner

Activin is a dimeric protein consisting of two similar but distinct β-subunits, βA and βB. In our previous studies, both activin A (βAβA) and activin B (βBβB) have been demonstrated to stimulate oocyte maturation and promote oocyte maturational competence in the zebrafish. Follistatin, a specific activin-binding protein, can block both activin- and gonadotropin-induced final oocyte maturation in vitro, suggesting that activin is likely a downstream mediator of gonadotropin actions in the zebrafish ovary. In the present study, a full-length cDNA encoding zebrafish ovarian activin βA was cloned and sequenced. The precursor of zebrafish activin βA consists of 395 amino acids and its mature region exhibits about 78% homology with that of mammals. Using an in vitro primary culture of the ovarian follicle cells and semiquantitative RT-PCR assays, we examined the regulation of activin βA and βB expression by human chorionic gonadotropin (hCG) and its intracellular signal transduction mechanisms. hCG (15 IU/ml) increased the mRNA level of activin βA-subunit; however, it significantly down-regulated the steady-state expression level of activin βB in a time- and dose-dependent manner. The differential regulation of the two β-subunits by hCG could be mimicked by 3-isobutyl-1-methylxanthine, forskolin, and dibutyryl-cAMP, suggesting involvement of the intracellular cAMP pathway. Interestingly, H89 (a specific inhibitor of protein kinase A, PKA) could effectively block hCG- and forskolin-stimulated activin βA expression at 10 μm, but it was unable to reverse the inhibitory effects of hCG and forskolin on βB expression. This suggests that the hCG-stimulated activin βA expression is dependent on the activation of the cAMP-PKA pathway, whereas the inhibitory effect of hCG on activin βB expression is likely mediated by PKA-independent pathway(s).

Gastrin regulates the heparin-binding epidermal-like growth factor promoter via a PKC/EGFR-dependent mechanism

2004 ◽  
Vol 286 (6) ◽  
pp. G992-G999 ◽  
Author(s):  
Natalie F. Sinclair ◽  
Wandong Ai ◽  
Raktima Raychowdhury ◽  
Meixia Bi ◽  
Timothy C. Wang ◽  
...  
Keyword(s):  
Growth Factor ◽  
Egf Receptor ◽  
Gastric Cancer Cell Line ◽  
Cancer Cell Line ◽  
Luciferase Reporter ◽  
Human Gastric Cancer ◽  
Heparin Binding ◽  
Cis Acting ◽  
Signal Transduction Inhibitors ◽  
Egf Family

Gastrin is a known growth/differentiation factor for the gastric mucosa. Its effects are likely mediated by the induction of heparin-binding epidermal-like growth factor (HB-EGF), a member of the EGF family of growth factors that is expressed by gastric parietal cells. In this study, we investigated the regulation of the HB-EGF promoter by gastrin in a human gastric cancer cell line. Serial human HB-EGF promoter-luciferase reporter deletion constructs and heterologous promoter constructs were transfected into AGS-E cells and stimulated with gastrin (10−7M) with or without various signal transduction inhibitors. EMSA were also performed. Gastrin stimulation resulted in a fivefold increase in HB-EGF-luciferase activity. The cis-acting element mediating gastrin responsiveness was mapped to the −69 to −58 region of the HB-EGF promoter. Gastrin stimulation was PKC dependent and at least partially mediated by activation of the EGF receptor.

scholarly journals Expression of fringe is down regulated by Gurken/Epidermal Growth Factor Receptor signalling and is required for the morphogenesis of ovarian follicle cells

2000 ◽  
Vol 113 (21) ◽  
pp. 3781-3794 ◽  
Author(s):  
D. Zhao ◽  
D. Clyde ◽  
M. Bownes
Keyword(s):  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Cell Fate ◽  
Ovarian Follicle ◽  
Growth Factor Receptor ◽  
Signal Transduction Pathway ◽  
Follicle Cells ◽  
Egg Chambers ◽  
Epidermal Growth

Signalling by the Gurken/Epidermal Growth Factor Receptor (Grk/EGFR) pathway is involved in epithelial cell fate decision, morphogenesis and axis establishment in Drosophila oogenesis. In the search for genes downstream of the Grk/EGFR signal transduction pathway (STP), we isolated a number of genes that are components of other STPs. One of them is a known gene, called fringe (fng). Drosophila fng encodes a putative secreted protein that is required at other development stages for mediating interactions between dorsal and ventral cells via Notch signalling. Here we show that fng has a dynamic expression pattern in oogenesis and that its expression in specific groups of follicle cells along the anterior-posterior and dorsal-ventral axes is defined by the repression of fng by Grk. Interfering with fng expression using antisense RNA experiments resulted in a typical fng mutant phenotype in the wing, and malformed egg chambers and abnormal organisation of the follicle cells in the ovaries, revealing that fng is essential in oogenesis for the proper formation of the egg chamber and for epithelial morphogenesis. This has been confirmed by re-examination of fng mutants and analysis of fng mutant clones in oogenesis.

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