Localisation of stem cell factor, stanniocalcin-1, connective tissue growth factor and heparin-binding epidermal growth factor in the bovine uterus at the time of blastocyst formation

2017 ◽  
Vol 29 (11) ◽  
pp. 2127 ◽  
Author(s):  
M. Muñoz ◽  
D. Martin ◽  
S. Carrocera ◽  
M. Alonso-Guervos ◽  
M. I. Mora ◽  
...  
Keyword(s):  
Stem Cell ◽  
Growth Factors ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Connective Tissue ◽  
Stem Cell Factor ◽  
Tissue Growth ◽  
Heparin Binding ◽  
Epidermal Growth

Early embryonic losses before implantation account for the highest rates of reproductive failure in mammals, in particular when in vitro-produced embryos are transferred. In the present study, we used molecular biology techniques (real-time quantitative polymerase chain reaction), classical immunohistochemical staining coupled with confocal microscopy and proteomic analysis (multiple reaction monitoring and western blot analysis) to investigate the role of four growth factors in embryo–uterine interactions during blastocyst development. Supported by a validated embryo transfer model, the study investigated: (1) the expression of stem cell factor (SCF), stanniocalcin-1 (STC1), connective tissue growth factor (CTGF) and heparin-binding epidermal growth factor-like growth factor (HB-EGF) in bovine uterine fluid; (2) the presence of SCF, STC1, CTGF and HB-EGF mRNA and protein in the bovine endometrium and embryos; and (3) the existence of reciprocal regulation between endometrial and embryonic expression of SCF, STC1, CTGF and HB-EGF. The results suggest that these growth factors most likely play an important role during preimplantation embryo development in cattle. The information obtained from the present study can contribute to improving the performance of in vitro culture technology in cattle and other species.

scholarly journals Connective tissue growth factor is a new ligand of epidermal growth factor receptor

2013 ◽  
Vol 5 (5) ◽  
pp. 323-335 ◽  
Author(s):  
Sandra Rayego-Mateos ◽  
Raquel Rodrigues-Díez ◽  
Jose Luis Morgado-Pascual ◽  
Raul R. Rodrigues Díez ◽  
Sebastian Mas ◽  
...  
Keyword(s):  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Connective Tissue ◽  
Connective Tissue Growth Factor ◽  
Growth Factor Receptor ◽  
Tissue Growth ◽  
Epidermal Growth

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.

scholarly journals Epidermal growth factor receptor regulates pancreatic fibrosis

2009 ◽  
Vol 297 (3) ◽  
pp. G434-G441 ◽  
Author(s):  
Stacy A. Blaine ◽  
Kevin C. Ray ◽  
Kevin M. Branch ◽  
Pamela S. Robinson ◽  
Robert H. Whitehead ◽  
...  
Keyword(s):  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Growth Factor Receptor ◽  
Pancreatic Fibrosis ◽  
Pancreatic Stellate Cells ◽  
Heparin Binding ◽  
Epidermal Growth

The development of pancreatic fibrosis has been shown to be a major component in several diseases of the pancreas including pancreatic cancer, chronic pancreatitis, and type 2 diabetes mellitus, but its actual role in the progression of these disorders is still unknown. This fibrosis is characterized by stromal expansion and the excessive deposition of extracellular matrix (ECM) that replaces pancreatic tissue. This eventually leads to dysregulation of ECM turnover, production of cytokines, restriction of blood flow, and often exocrine and endocrine insufficiencies. Activated pancreatic stellate cells (PSCs) have been identified as key mediators in the progression of pancreatic fibrosis, serving as the predominant source of excess ECM proteins. Previously, we found that overexpression of the growth factor heparin-binding epidermal growth factor-like growth factor (HB-EGF) in pancreatic islets led to intraislet fibrosis. HB-EGF binds to and activates two receptors, epidermal growth factor receptor (EGFR) and ErbB4, as well as heparin moieties and CD9/DRAP27. To understand the mechanism underlying the induction of fibrogenesis by HB-EGF, we utilized a hypomorphic allele of Egfr, the Waved-2 allele, to demonstrate that EGFR signaling regulates fibrogenesis in vivo. Using an in vitro cell migration assay, we show that HB-EGF regulates both chemoattraction and stimulation of proliferation of PSCs via EGFR activation.

scholarly journals The metalloendopeptidase nardilysin (NRDc) is potently inhibited by heparin-binding epidermal growth factor-like growth factor (HB-EGF)

2002 ◽  
Vol 367 (1) ◽  
pp. 229-238 ◽  
Author(s):  
Véronique HOSPITAL ◽  
Eiichiro NISHI ◽  
Michael KLAGSBRUN ◽  
Paul COHEN ◽  
Nabil G. SEIDAH ◽  
...  
Keyword(s):  
Amino Acid ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Cell Surface ◽  
Active Site ◽  
Regulatory Element ◽  
Enzymic Activity ◽  
Heparin Binding ◽  
Epidermal Growth

Nardilysin (N-arginine dibasic convertase, or NRDc) is a cytosolic and cell-surface metalloendopeptidase that, in vitro, cleaves substrates upstream of Arg or Lys in basic pairs. NRDc differs from most of the other members of the M16 family of metalloendopeptidases by a 90 amino acid acidic domain (DAC) inserted close to its active site. At the cell surface, NRDc binds heparin-binding epidermal growth factor-like growth factor (HB-EGF) and enhances HB-EGF-induced cell migration. An active-site mutant of NRDc fulfills this function as well as wild-type NRDc, indicating that the enzyme activity is not required for this process. We now demonstrate that NRDc starts at Met49. Furthermore, we show that HB-EGF not only binds to NRDc but also potently inhibits its enzymic activity. NRDc—HB-EGF interaction involves the 21 amino acid heparin-binding domain (P21) of the growth factor, the DAC of NRDc and most probably its active site. Only disulphide-bonded P21 dimers are inhibitory. We also show that Ca2+, via the DAC, regulates both NRDc activity and HB-EGF binding. We conclude that the DAC is thus a key regulatory element for the two distinct functions that NRDc fulfills, i.e. as an HB-EGF modulator and a peptidase.

Insulin-Induced Ectodomain Shedding of Heparin-Binding Epidermal Growth Factor-Like Growth Factor in Adipocytes In Vitro

Obesity ◽  
2010 ◽  
Vol 18 (10) ◽  
pp. 1888-1894 ◽  
Author(s):  
Takanobu Yamamoto ◽  
Takayoshi Suganami ◽  
Minako Kiso-Narita ◽  
Peggy A. Scherle ◽  
Yasutomi Kamei ◽  
...  
Keyword(s):  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Ectodomain Shedding ◽  
Heparin Binding ◽  
Epidermal Growth

Heparin-binding EGF-like growth factor regulates elastin and FGF-2 expression in pulmonary fibroblasts

2003 ◽  
Vol 285 (5) ◽  
pp. L1106-L1115 ◽  
Author(s):  
Jianghuai Liu ◽  
Celeste B. Rich ◽  
Jo Ann Buczek-Thomas ◽  
Matthew A. Nugent ◽  
Mikhail P. Panchenko ◽  
...  
Keyword(s):  
Growth Factors ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Growth Factor Receptor ◽  
Inhibitory Effect ◽  
Nuclear Accumulation ◽  
Mrna Levels ◽  
Heparin Binding ◽  
Pulmonary Fibroblasts ◽  
Epidermal Growth

Elastase degradation of elastin within alveolar walls is an important event in the development of pulmonary emphysema. In addition to elastolytic activities, elastases release growth factors from extracellular matrices and interstitial cell surfaces that can regulate elastogenesis and other cellular responses. In the present study, we demonstrate that brief treatment of matrix-laden rat pulmonary fibroblast cultures with pancreatic elastase results in the release of soluble heparin-binding epidermal growth factor-like growth factor (HB-EGF) concomitant with a decrease in HB-EGF binding to both heparan sulfate proteoglycan and receptor sites on the cells. In undigested, matrix-laden fibroblasts, HB-EGF significantly downregulates elastin mRNA via activation of epidermal growth factor receptor. Results from nuclear run-on analyses show that HB-EGF downregulates elastin mRNA via transcriptional suppression. HBEGF treatment stimulates MAP or ERK kinase (MEK)-dependent ERK1/2 phosphorylation and leads to nuclear accumulation of Fra-1. Blocking ERK1/2 activation by MEK1/2 inhibitors (PD-98059 or U-0126) diminishes HB-EGF-induced Fra-1 accumulation and subsequent downregulation of elastin mRNA. Coaddition of two elastase-released growth factors, HB-EGF and FGF-2, results in an additive inhibitory effect on elastin mRNA levels. Furthermore, HB-EGF addition to pulmonary fibroblasts increases FGF-2 mRNA and protein levels. These data suggest that HB-EGF and FGF-2 act in concert to regulate the synthesis of elastin in injury/repair situations.

scholarly journals Heparin-Binding Epidermal Growth Factor-Like Growth Factor Stimulates Androgen-Independent Prostate Tumor Growth and Antagonizes Androgen Receptor Function

Endocrinology ◽  
2002 ◽  
Vol 143 (12) ◽  
pp. 4599-4608 ◽  
Author(s):  
Rosalyn M. Adam ◽  
Jayoung Kim ◽  
Jianqing Lin ◽  
Anna Orsola ◽  
Liyan Zhuang ◽  
...  
Keyword(s):  
Androgen Receptor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Neuron Specific Enolase ◽  
Continuous Exposure ◽  
Heparin Binding ◽  
Independent State ◽  
Epidermal Growth ◽  
Androgen Independent

Abstract Peptide growth factors have been implicated in progression of prostate cancer (PCa) to the androgen-independent state; however, much of the evidence linking diffusible mitogens and survival factors to this process remains circumstantial. Heparin-binding epidermal growth factor-like growth factor (HB-EGF), a prostate stroma-derived factor, promotes survival, proliferation, and neuroendocrine differentiation of androgen-dependent LNCaP PCa cells in vitro. To test whether sustained exposure to HB-EGF can confer an androgen-independent phenotype, we generated stable populations of LNCaP cells that express constitutively a secreted form of HB-EGF (LNCaP/sHB). LNCaP/sHB cells proliferated more rapidly under androgen-depleted conditions in vitro and formed larger tumors with higher frequency in intact and castrated severe combined immunodeficient mice, in comparison to control cells. LNCaP/sHB tumors also expressed higher levels of the neuroendocrine marker, neuron-specific enolase, compared with control tumors. In castrates, increased neuron-specific enolase expression in LNCaP/sHB tumors was associated with reduced androgen receptor (AR) levels. In vitro, AR protein levels were reduced in LNCaP/sHB cells, and in transient transfection assays using an androgen-responsive promoter (mouse mammary tumor virus-long terminal repeat), LNCaP/sHB cells showed reduced sensitivity to dihydrotestosterone compared with controls. This is the first demonstration that continuous exposure of AR-positive PCa cells to a single growth factor can promote an androgen-independent phenotype in vivo. These findings also emphasize the potential role of pathways other than the AR axis in acquisition of androgen independence.

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