174 EPIDERMAL GROWTH FACTORS AND CALBINDIN-D9k GENE EXPRESSIONS DURING PREGANCY IN THE PORCINE UTERUS

2008 ◽  
Vol 20 (1) ◽  
pp. 167
Author(s):  
Y.-J. Kim ◽  
E.-M. Jung ◽  
G.-S. Lee ◽  
S.-H. Hyun ◽  
E.-B. Jeung
Keyword(s):  
Growth Factors ◽  
Growth Factor ◽  
Transforming Growth Factor ◽  
Expression Patterns ◽  
Negative Control ◽  
Heparin Binding ◽  
Gene Expressions ◽  
Calbindin D9k ◽  
Genes Encoding ◽  
Epidermal Growth

To stably maintain pregnancy, several genes are expressed in the uterus. In particular, the endometrial expression of genes encoding growth factors appears to play a key role in maternal–fetal communication. Previous studies have characterized the endometrial expression kinetics of the genes encoding epidermal growth factor (EGF), its receptor (EGFR), transforming growth factor-alpha (TGF-α), amphiregulin (Areg), heparin-binding (Hb) EGF, and calbindin-D9k (CaBP-9k) in the pig during implantation. Here, we further characterized the expression patterns of these molecules during the entire porcine pregnancy. Porcine (n = 3 per PD) were collected at pregnancy days (PD) 12, 15, 30, 60, 90, and 110 and subjected to semi-quantitative RT-PCR. The data were analyzed with a nonparametric one-way analysis of variance using the Kruskal-Wallis test, followed by Dunnett's test for multiple comparisons to the negative control. EGF and EGFR showed similar expression patterns, being highly expressed around implantation time and then disappearing. TGF-α and Areg expression levels rose steadily until they peaked at PD30, after which they gradually decreased to PD12 levels. The Areg mRNA expression pattern was confirmed by real-time PCR, and similar Areg protein expression patterns were observed. Immunohistochemical analysis of PD60 uteri revealed Areg in the glandular and luminal epithelial cells. Hb-EGF was steadily expressed throughout the entire pregnancy while CaBP-9k was expressed strongly on PD12, and then declined sharply in PD15 before recovering slightly for the remainder of the pregnancy. Thus, the EGF family may play a key role during implantation in pigs. In addition, CaBP-9k may help maintain uterine quiescence during pregnancy by sequestering cytoplasmic Ca2+.

scholarly journals Contemporary concepts of uterine fibroids’ pathogenesis

2019 ◽  
Vol 10 (1) ◽  
pp. 91-99
Author(s):  
Anna N. Taits ◽  
Nikolai N. Ruhljada ◽  
Valeriy I. Matukhin ◽  
Aleksandra D. Somova ◽  
Kristina A. Dudova
Keyword(s):  
Growth Factors ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Transforming Growth Factor ◽  
Uterine Fibroids ◽  
Transforming Growth Factor Β ◽  
Reproductive Age ◽  
Heparin Binding ◽  
Common Benign Tumor ◽  
Epidermal Growth

Uterine myoma is the most common benign tumor among women which affects mainly those of reproductive age. Moreover, the frequency of emergence of this pathology in population is growing while the age of patients is steadily decreasing. Despite the enormous prevalence of this disease, its pathogenesis has not been studied properly. This article is concerned with an analysis of publications devoted to the study of the mechanisms of growth and development of uterine fibroids, it provides some data on the role of various factors in its extension. The article concerns the most popular concepts of the pathogenesis of this disease according to which the illness may be caused by increased levels of sex hormones (estrogens and progestins), enhanced expression of their receptors, impaired apoptosis, the effect of growth factors (e. g. epidermal growth factor, heparin-binding epidermal growth factor, acid and basic fibroblast growth factors, vascular endothelial growth factor, insulin-like growth factor, platelet-derived growth factor, transforming growth factor-β, activin, myostatin), abnormal deposition extracellular matrix, genetic (chromosomal aberration and various MED12 gene defect) and epigenetic mechanisms (such as action microRNA), circulatory disorders and impairment of cell differentiation from a population of accessory stem cells. However, it is noted that the pathogenesis of this pathology requires further detailed study, as the understanding of the processes leading to its development could greatly contribute to the improvement of the tactics of treatment and possibly allow to elaborate some preventive measures to avert the development of fibroids.

115 RAT EPIDERMAL GROWTH FACTOR GENE EXPRESSION CONTROLLED BY PROGESTERONE DURING PREGNANCY

2008 ◽  
Vol 20 (1) ◽  
pp. 138
Author(s):  
H.-S. Byun ◽  
S.-H. Ko ◽  
G.-S. Lee ◽  
S.-H. Hyun ◽  
E.-B. Jeung
Keyword(s):  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Egf Receptor ◽  
Transforming Growth Factor ◽  
Expression Patterns ◽  
Uterine Wall ◽  
Mrna Levels ◽  
Heparin Binding ◽  
Pregnant Rats ◽  
Epidermal Growth

The implantation of the developing blastocyst into the uterine wall is regulated by a precisely timed interplay of the ovarian hormones estrogen and progesterone, which control a set of regulatory factors that make the uterus receptive to implantation. These factors include EGF receptor (Egfr) and members of the epidermal growth factor (Egf) family, namely, EGF, heparin-binding EGF (Hbegf), transforming growth factor-alpha (Tgfa), and amphiregulin (Areg). However, the exact role(s) these factors play in pregnancy remain unclear. To address this, a group of three rats was euthanized every day from gestation day (GD) 0 through to GD21. The uterus, attached uterus (these tissues are mostly composed of stromal cells), and placenta were rapidly excised and used directly for total RNA. We used real-time PCR with the TaqMan system (Applied Biosystems, Foster City, CA, ISA) to examine the uterine expression patterns of these factors in rats during the entire pregnancy. Data were analyzed by nonparametric one-way analysis of variance using the Kruskal-Wallis test, followed by Dunnett's test for multiple comparisons. Egf and Egfr mRNA levels increased significantly at implantation, especially on GD3 and GD6, after which their expression gradually decreased. Hbegf and Tgfa showed a modest spike of transcription around the implantation period (GD4 and GD3, respectively) but were much more strongly expressed at mid-pregnancy, which is when progesterone is secreted at high levels. Areg expression peaked strongly around implantation (GD4) and at mid-pregnancy (GD12). Treatment of pregnant rats on GD5 or GD8 with the progesterone receptor antagonist RU486 (2.5 mg per rat) blocked the expression of all of the genes on the days of treatment. Moreover, injection of immature rats with progesterone induced the uterine expression of all of the genes except Hbegf, while injection with estrogen or estrogen plus progesterone had no effect. Taken together, all genes tested may be assumed to regulate the implantation process. Moreover, Hbegf, Tgfa, and Areg may participate during mid-pregnancy. In addition, all of these activities are likely to be controlled by progesterone in the uterus of rats during pregnancy.

Growth factors and metanephrogenesis

1992 ◽  
Vol 262 (4) ◽  
pp. F523-F532 ◽  
Author(s):  
M. R. Hammerman ◽  
S. A. Rogers ◽  
G. Ryan
Keyword(s):  
Growth Factors ◽  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Kidney Development ◽  
Transforming Growth Factor ◽  
Polypeptide Growth Factors ◽  
Metanephric Kidney ◽  
Epidermal Growth ◽  
Factor Alpha ◽  
Editorial Review

The formation of all organs during embryogenesis, including kidney, is dependent on the timed and sequential expression of a number of polypeptide growth factors. Synthesis and actions of one or more members of the insulin-like growth factor, epidermal growth factor/transforming growth factor-alpha, transforming growth factor-beta, platelet-derived growth factor, fibroblast growth factor, and nerve growth factor families have been characterized in the developing metanephric kidney. Studies originating from a number of laboratories have defined the localization of growth factor mRNAs, receptors and peptides, have delineated patterns of growth factor synthesis, and have established the growth factor dependency of embryonic kidney development. The results of these investigations will be summarized in this editorial review and integrated within the broader context of growth factor cellular physiology and growth factor expression in nonrenal systems.

Transforming Growth Factor α and Epidermal Growth Factor Receptor in Reactive and Malignant Mesothelial Proliferations

2004 ◽  
Vol 128 (1) ◽  
pp. 68-70
Author(s):  
Yun-Cai Cai ◽  
Victor Roggli ◽  
Eugene Mark ◽  
Philip T. Cagle ◽  
Armando E. Fraire
Keyword(s):  
Epidermal Growth Factor Receptor ◽  
Growth Factors ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Transforming Growth Factor ◽  
Malignant Tumors ◽  
Growth Factor Receptor ◽  
Transforming Growth Factor Α ◽  
Epidermal Growth ◽  
Factor Α

Abstract Background.—Growth factors such as transforming growth factor α (TGF-α) and epidermal growth factor receptor (EGFR) play an important role in cell proliferation. The immunohistochemical expression of these factors has been extensively studied in malignant tumors including mesothelioma. However, the comparative expression of these growth factors in mesothelioma and reactive mesothelial proliferations has been less well studied. Objective.—To evaluate the possible role of TGF-α and EGFR in the clinically important distinction between reactive mesothelial proliferations and malignant mesothelioma. Methods.—The expression of TGF-α and EGFR was studied in 39 cases of mesothelioma and 30 cases of reactive mesothelial proliferations by means of immunohistochemistry. Results.—Fourteen (70%) of 20 reactive mesothelial proliferations tested and 29 (76%) of 38 mesotheliomas tested expressed TGF-α. One (3%) of 30 reactive mesothelial proliferations and 17 (45%) of 39 mesotheliomas expressed EGFR. Conclusions.—These results suggest an up-regulation of EGFR in mesothelioma as compared with reactive mesothelial proliferations. This up-regulation further suggests a possible use of EGFR as an adjunct immunohistochemical test in the differential diagnosis of mesothelioma and reactive mesothelial proliferations.

scholarly journals Neuroblastoma cells express c-sis and produce a transforming growth factor antigenically related to the platelet-derived growth factor.

1985 ◽  
Vol 5 (9) ◽  
pp. 2289-2297 ◽  
Author(s):  
E J van Zoelen ◽  
W J van de Ven ◽  
H J Franssen ◽  
T M van Oostwaard ◽  
P T van der Saag ◽  
...  
Keyword(s):  
Growth Factors ◽  
Growth Factor ◽  
Transforming Growth Factor ◽  
Rat Kidney ◽  
Molecular Size ◽  
Platelet Derived Growth Factor ◽  
Kidney Cells ◽  
Transforming Growth Factors ◽  
Normal Rat ◽  
Epidermal Growth

Mouse neuroblastoma Neuro-2A cells produce transforming growth factors during exponential growth in a defined hormone-free medium, which, on Bio-Gel columns in 1 M HAc, elute at a molecular size of 15 to 20 kilodaltons (kDa). These neuroblastoma-derived transforming growth factors have strong mitogenic activity, but they do not compete with epidermal growth factor for receptor binding (E. J. J. van Zoelen, D. R. Twardzik, T. M. J. van Oostwaard, P. T. van der Saag, S. W. de Laat, and G. J. Todaro, Proc. Natl. Acad. Sci. U.S.A. 81:4085-4089, 1984). In this study approximately 80% of the mitogenic activity was immunoprecipitated by antibodies raised against platelet-derived growth factor (PDGF). Immunoblotting indicated a true molecular size of 32 kDa for this PDGF-like growth factor. Analysis of poly(A)+ RNA from Neuro-2A cells demonstrated the expression of the c-sis oncogene in this cell line, whereas in vitro translation of the RNA yielded a 20-kDa protein recognized by anti-PDGF antibodies. Separation by reverse-phase high-pressure liquid chromatography demonstrated the presence of two distinct mitogenic activities in neuroblastoma-derived transforming growth factor preparations, one of which is antigenically related to PDGF. Both activities had the ability to induce anchorage-independent growth in normal rat kidney cells, both in the presence and in the absence of epidermal growth factor. It is concluded that Neuro-2A cells express c-sis with concomitant production and secretion of a PDGF-like growth factor, which plays a role in the induction of phenotypic transformation on normal rat kidney cells.

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.

Growth factor and somatic cell regulation of mouse gonocyte-derived colony formation in vitro

Reproduction ◽  
2000 ◽  
pp. 85-91 ◽  
Author(s):  
S Hasthorpe ◽  
S Barbic ◽  
PJ Farmer ◽  
JM Hutson
Keyword(s):  
Growth Factors ◽  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Colony Formation ◽  
Inhibitory Action ◽  
Transforming Growth Factor ◽  
Epidermal Growth ◽  
Growth Factor Beta

At birth, the mouse gonocyte does not resume mitotic activity for several days in vivo but, in an in vitro clonogenic system, cell division commences soon after culture. Somatic testis cell underlays had potent inhibitory activity on gonocyte-derived colony formation (23 +/- 15% compared with 84 +/- 1% in controls; P = 0.0001) when added to cultures of gonocytes in vitro. A Sertoli cell line, TM4B, had an even more pronounced effect on gonocyte clonogenic capacity, with 1 +/- 1% compared with 72 +/- 17% colony formation in controls (P = 0.0003). Testis cells appeared to have a direct inhibitory effect since testis-conditioned medium did not show a significant reduction in the number of colonies. The observed reduction in colony formation with the testis cell underlay was not accounted for by decreased attachment of gonocytes as simultaneous addition of a single cell suspension of testis cells was still effective in significantly reducing colony number when compared with controls (P = 0.01). Therefore, the observed inhibition exerted by testis cells appears to be a consequence of decreased proliferation of gonocytes. Growth factors belonging to the transforming growth factor beta superfamily which are known to be expressed in testis, such as transforming growth factor beta and epidermal growth factor, did not exert any inhibitory action on gonocyte-derived colony formation when added together or alone. However, a shift to a smaller colony size occurred in the presence of transforming growth factor beta and transforming growth factor beta plus epidermal growth factor, indicating a reduction in colony cell proliferation. Evidence for the expression of the Mullerian inhibiting substance receptor on newborn gonocytes using in situ hybridization was inconclusive. This finding was in agreement with the lack of a direct action of Mullerian inhibiting substance on the formation of gonocyte-derived colonies in vitro. Leukaemia inhibitory factor, alone or in combination with forskolin, had neither an inhibitory nor an enhancing effect on gonocyte-derived colony formation. An in vitro clonogenic method to assay for the proliferation of gonocytes in the presence of specific growth factors, cell lines, testis cell underlays and cell suspensions was used to identify a somatic cell-mediated inhibitor which may be responsible for the inhibitory action on gonocyte proliferation in vivo shortly after birth.

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