共查询到20条相似文献,搜索用时 15 毫秒
1.
Hong HJ Liu JC Chan P Juan SH Loh SH Lin JG Cheng TH 《Journal of biomedical science》2004,11(1):27-36
It is well documented that 17-estradiol (E2) exerts a cardiovascular protective effect. A possible role of E2 in the regulation of endothelin-1 (ET-1) production has been reported. However, the complex mechanisms by which E2 inhibits ET-1 expression are not completely understood. The aims of this study were to examine whether E2 may alter angiotensin II (Ang II)-induced cell proliferation and ET-1 gene expression and to identify the putative underlying signaling pathways in rat aortic smooth muscle cells. Cultured rat aortic smooth muscle cells were preincubated with E2, then stimulated with Ang II, and [3H]thymidine incorporation and ET-1 gene expression were examined. The effect of E2 on Ang-II-induced extracellular signal-regulated kinase (ERK) phosphorylation was tested to elucidate the intracellular mechanism of E2 in proliferation and ET-1 gene expression. Ang II increased DNA synthesis which was inhibited with E2 (1–100 nM). E2, but not 17-estradiol, inhibited the Ang-II-induced ET-1 gene expression as revealed by Northern blotting and promoter activity assay. This effect was prevented by coincubation with the estrogen receptor antagonist ICl 182,780 (1 µM). E2 also inhibited Ang-II-increased intracellular reactive oxygen species (ROS) as measured by a redox-sensitive fluorescent dye, 2,7-dichlorofluorescin diacetate, and ERK phosphorylation. Furthermore, E2 and antioxidants, such as N-acetyl cysteine and diphenylene iodonium, decreased Ang-II-induced cell proliferation, ET-1 promoter activity, ET-1 mRNA, ERK phosphorylation, and activator protein-1-mediated reporter activity. In summary, our results suggest that E2 inhibits Ang-II-induced cell proliferation and ET-1 gene expression, partially by interfering with the ERK pathway via attenuation of ROS generation. Thus, this study provides important new insight regarding the molecular pathways that may contribute to the proposed beneficial effects of estrogen on the cardiovascular system. 相似文献
2.
Summary The effect of long-term treatment (52 weeks) with high doses of 17-estradiol (1.28 mg/kg/week intramuscularly) on gonadotrophs was studied in the pituitary gland of the beagle bitch. For immunochemical staining the immunoperoxidase technique and antisera to the specific beta () subunits of FSH and LH were employed. For control purposes antisera to the following hormones were also used: bovine TSH, canine GH, canine PRL and porcine ACTH1. In the pars distalis and pars tuberalis of control bitches, in addition to the cells which react solely with antisera to either LH or FSH, most cells were reactive to both antisera. The cells stained for FSH were less numerous than those shown to contain LH. TSH, PRL, GH and ACTH/MSH were localized in distinctly different cell types in the pars distalis of all control animals. In the treated bitches, almost complete regression of cells classically identified as gonadotrophs and stained for LH was observed. On the other hand, using the antiserum to FSH, selective immunochemical staining was localized in cells fitting the morphological characteristics of TSH cells. All these cells were also stained for TSH. However, a few cells were also shown to react solely with the antiserum to TSH. These cells, which seem to contain both TSH and FSH, were further clearly differentiated from PRL, GH and ACTH/MSH cells on the basis of their cytological features, intraglandular distribution and by immunochemical double staining. These observations support the concept that the one cell-one hormone theory may not necessarily apply to the glycoprotein hormones of the dog pituitary gland.Abbreviations of Hormones cited in this Paper ACTH
Adrenocorticotropin
- FSH
Follicle Stimulating Hormone
- GH
Growth Hormone
- LH
Luteinizing Hormone
- MSH
Melanocyte Stimulating Hormone
- PRL
Prolactin
- TSH
Thyrotropin
The authors are grateful to Mrs. K. Oertel for carrying out the experimental work on animals, to Mrs. B. Schilk and Miss U. Tüshaus for their excellent technical assistance, and to Dr. P. Günzel for his advice and encouragement 相似文献
3.
Elham Hasanzadeh Somayeh Ebrahimi-Barough Narges Mahmoodi Amir Mellati Houra Nekounam Arefeh Basiri Shiva Asadpour Diba Ghasemi Jafar Ai 《Cell biology international》2021,45(1):140-153
Human endometrial stem cells (hEnSCs) that can be differentiated into various neural cell types have been regarded as a suitable cell population for neural tissue engineering and regenerative medicine. Considering different interactions between hormones, growth factors, and other factors in the neural system, several differentiation protocols have been proposed to direct hEnSCs towards specific neural cells. The 17β-estradiol plays important roles in the processes of development, maturation, and function of nervous system. In the present research, the impact of 17β-estradiol (estrogen, E2) on the neural differentiation of hEnSCs was examined for the first time, based on the expression levels of neural genes and proteins. In this regard, hEnSCs were differentiated into neuron-like cells after exposure to retinoic acid (RA), epidermal growth factor (EGF), and also fibroblast growth factor-2 (FGF2) in the absence or presence of 17β-estradiol. The majority of cells showed a multipolar morphology. In all groups, the expression levels of nestin, Tuj-1 and NF-H (neurofilament heavy polypeptide) (as neural-specific markers) increased during 14 days. According to the outcomes of immunofluorescence (IF) and real-time PCR analyses, the neuron-specific markers were more expressed in the estrogen-treated groups, in comparison with the estrogen-free ones. These findings suggest that 17β-estradiol along with other growth factors can stimulate and upregulate the expression of neural markers during the neuronal differentiation of hEnSCs. Moreover, our findings confirm that hEnSCs can be an appropriate cell source for cell therapy of neurodegenerative diseases and neural tissue engineering. 相似文献
4.
Puerarin suppresses invasion and vascularization of endometriosis tissue stimulated by 17β-estradiol
Background
Puerarin, a phytoestrogen with a weak estrogenic effect, binds to estrogen receptors, thereby competing with 17β-estradiol (E2) and producing an anti-estrogenic effect. This study was to investigate whether puerarin could suppress the invasion and vascularization of E2-stimulated endometriotic tissue.Methodology/Principal Findings
The endometriotic stromal cells (ESCs) were successfully established and their invasive ability under different treatments was assessed through a Transwell Assay. Simultaneously, matrix metallopeptidase 9 (MMP-9) and tissue inhibitor of metalloproteinase 1 (TIMP-1) were detected by western blotting. Vascularization of endometriotic tissues was observed by chicken chorioallantoic membrane (CAM) assay. The staining of MMP-9, intercellular adhesion molecule 1 (ICAM-1), TIMP-1, and vascular endothelial growth factor (VEGF) in grafted endometriotic tissues was examined using immunohistochemistry analysis. The purity of ESCs in isolated cells was >95%, as determined by the fluoroimmunoassay of vimentin. E2 (10−8 mol/L) promoted the invasiveness of ESCs by increasing MMP-9 accumulation and decreasing TIMP-1 accumulation. Interestingly, puerarin (10−9 mol/L) significantly reversed these effects (P<0.01). The CAM assay indicated that puerarin (10−9 mol/L) also inhibited the angiopoiesis of endometriotic tissue stimulated by the E2 (10−8 mol/L) treatment (P<0.05). Accordingly, immunohistochemistry showed that the accumulation of MMP-9, ICAM-1, and VEGF was reduced whereas that of TIMP-1 increased in the combination treatment group compared with the E2 treatment group.Conclusions/Significance
This study demonstrated that puerarin could suppress the tissue invasion by ESCs and the vascularization of ectopic endometrial tissues stimulated by E2, suggesting that puerarin may be a potential drug for the treatment of endometriosis. 相似文献5.
6.
MacNeil LG Baker SK Stevic I Tarnopolsky MA 《American journal of physiology. Regulatory, integrative and comparative physiology》2011,300(6):R1443-R1451
17β-estradiol (E2) attenuates exercise-induced muscle damage and inflammation in some models. Eighteen men completed 150 eccentric contractions after random assignment to placebo (Control group) or E2 supplementation (Experimental group). Muscle biopsies and blood samples were collected at baseline, following 8-day supplementation and 3 h and 48 h after exercise. Blood samples were analyzed for sex hormone concentration, creatine kinase (CK) activity and total antioxidant capacity. The mRNA content of genes involved in lipid and cholesterol homeostasis [forkhead box O1 (FOXO1), caveolin 1, and sterol regulatory element binding protein-2 (SREBP2)] and antioxidant defense (SOD1 and -2) were measured by RT-PCR. Immunohistochemistry was used to quantify muscle neutrophil (myeloperoxidase) and macrophage (CD68) content. Serum E2 concentration increased 2.5-fold with supplementation (P < 0.001), attenuating neutrophil infiltration at 3 h (P < 0.05) and 48 h (P < 0.001), and the induction of SOD1 at 48 h (P = 0.02). Macrophage density at 48 h (P < 0.05) and SOD2 mRNA at 3 h (P = 0.01) increased but were not affected by E2. Serum CK activity was higher at 48 h for both groups (P < 0.05). FOXO1, caveolin 1 and SREBP2 expression were 2.8-fold (P < 0.05), 1.4-fold (P < 0.05), and 1.5-fold (P < 0.001) and higher at 3 h after exercise with no effect of E2. This suggests that E2 attenuates neutrophil infiltration; however, the mechanism does not appear to be lesser oxidative stress or membrane damage and may indicate lesser neutrophil/endothelial interaction. 相似文献
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9.
The renal distal tubules and collecting ducts play a key role in the control of electrolyte and fluid homeostasis. The discovery of highly calcium selective channels, Transient Receptor Potential Vanilloid 5 (TRPV5) of the TRP superfamily, has clarified the nature of the calcium entry channels. It has been proposed that this channel mediates the critical Ca2+ entry step in transcellular Ca2+ re-absorption in the kidney. The regulation of transmembrane Ca2+ flux through TRPV5 is of particular importance for whole body calcium homeostasis.In this study, we provide evidence that the TRPV5 channel is present in rat cortical collecting duct (RCCD2) cells at mRNA and protein levels. We demonstrate that 17β-estradiol (E2) is involved in the regulation of Ca2+ influx in these cells via the epithelial Ca2+ channels TRPV5. By combining whole-cell patch-clamp and Ca2+-imaging techniques, we have characterized the electrophysiological properties of the TRPV5 channel and showed that treatment with 20-50 nM E2 rapidly (<5 min) induced a transient increase in inward whole-cell currents and intracellular Ca2+ via TRPV5 channels. This rise was significantly prevented when cells were pre-treated with ruthenium red and completely abolished in cells treated with siRNA specifically targeting TRPV5.These data demonstrate for the first time, a novel rapid modulation of endogenously expressed TRPV5 channels by E2 in kidney cells. Furthermore, the results suggest calcitropic effects of E2. The results are discussed in relation to present concepts of non-genomic actions of E2 in Ca2+ homeostasis. 相似文献
10.
Nardinocchi L Pantisano V Puca R Porru M Aiello A Grasselli A Leonetti C Safran M Rechavi G Givol D Farsetti A D'Orazi G 《PloS one》2010,5(12):e15048
Background
Hypoxia inducible factor-1α (HIF-1α) is responsible for the majority of HIF-1-induced gene expression changes under hypoxia and for the “angiogenic switch” during tumor progression. HIF-1α is often upregulated in tumors leading to more aggressive tumor growth and chemoresistance, therefore representing an important target for antitumor intervention. We previously reported that zinc downregulated HIF-1α levels. Here, we evaluated the molecular mechanisms of zinc-induced HIF-1α downregulation and whether zinc affected HIF-1α also in vivo.Methodology/Principal Findings
Here we report that zinc downregulated HIF-1α protein levels in human prostate cancer and glioblastoma cells under hypoxia, whether induced or constitutive. Investigations into the molecular mechanisms showed that zinc induced HIF-1α proteasomal degradation that was prevented by treatment with proteasomal inhibitor MG132. HIF-1α downregulation induced by zinc was ineffective in human RCC4 VHL-null renal carcinoma cell line; likewise, the HIF-1αP402/P564A mutant was resistant to zinc treatment. Similarly to HIF-1α, zinc downregulated also hypoxia-induced HIF-2α whereas the HIF-1β subunit remained unchanged. Zinc inhibited HIF-1α recruitment onto VEGF promoter and the zinc-induced suppression of HIF-1-dependent activation of VEGF correlated with reduction of glioblastoma and prostate cancer cell invasiveness in vitro. Finally, zinc administration downregulated HIF-1α levels in vivo, by bioluminescence imaging, and suppressed intratumoral VEGF expression.Conclusions/Significance
These findings, by demonstrating that zinc induces HIF-1α proteasomal degradation, indicate that zinc could be useful as an inhibitor of HIF-1α in human tumors to repress important pathways involved in tumor progression, such as those induced by VEGF, MDR1, and Bcl2 target genes, and hopefully potentiate the anticancer therapies. 相似文献11.
17β-hydroxysteroid dehydrogenase activity in cultured myometrial cells: Effect of serial subcultures
《Journal of steroid biochemistry》1982,16(1):95-100
17β-Hydroxysteroid dehydrogenase (17β-SDH) activity was studied in culture ovine rayometrial cells. After primary culture, cells were routinely subcultured (every 7th day), seeded at 5–105 cells per dish and grown in a medium with 2% of serum. 17β-SDH activity was measured by incubating intact cell monolayers with [3H]-estradiol (5·10−6) in serum-free medium. Metabolites were extracted from both cells and medium, and separated by thin-layer chromatography. 17β-SDH was expressed as total E i formed (cells + medium) in fmol/mg of protein as a function of time. 17β-SDH has an approximate Km of 5–10−6 M. After 3 min of incubation, all measurable E1 is within the cells; it is progressively released but after l h only 40% of E1 is found in the medium. 17β-SDH decreases from day 2 to day 8 of each subculture, whereas total proteins increase. Subculture partially restores 17β-SDH activity so that it is always higher on day 2 of any subculture than on day 8 of the previous one. however a progressive decline occurs with successive subcultures. This decline parallels the slowing of cell growth and overall protein synthesis and probably reflects cell ageing. 相似文献
12.
J.N. Laverriere D. Gourdji R. Picart A. Tixier-Vidal 《Biochemical and biophysical research communications》1981,103(3):833-840
The time-course of thyroliberin transfer to the nucleus of GH3/B6 rat pituitary prolactin cells was studied by both autoradiography and cell fractionation of intact cells exposed to [3H]thyroliberin at 4°C or 37°C. It was previously shown that thyroliberin is not degraded in these conditions. It is found by autoradiography that [3H]-thyroliberin is transferred to the nucleus of GH3/B6 cells within 5 min at least at both 37° C and 4°C. Consistent results are obtained by fractionation of cells exposed to [3H]thyroliberin at 37°C. However after binding at 4°C 50% of the cell radioactivity is extractible by glutaraldehyde and after fractionation the isolated nuclei retain only 1–1.5% of the cell radioactivity. This suggests the existence of both tightly bound and loosely bound internalized thyroliberin molecules. 相似文献
13.
Julius Brtko Peter Filipčík Soňa Hudecová Vladimír Štrbák Anastázia Brtková 《Biological trace element research》1995,48(2):173-183
The present study was undertaken in order to investigate the effects of sodium selenite on:
- The growth of rat pituitary GH4C1 cells;
- The nuclear T3 receptor gene expression;
- The cytoplasmic protein phosphorylation; and
- The prolactin secretion in rat pituitary GH4C1 cell line.
14.
15.
June Hyun Han Min Su Kim Moo Yeol Lee Tae Hyoung Kim Mi-Kyung Lee Hye Ryoun Kim Soon Chul Myung 《Cytokine》2010,49(2):209-214
We investigated the expression of HBD-1 and -2 in vaginal epithelial cells treated with lipopolysaccharide (LPS) and the effects on HBD-2 expressions by 17β-estradiol and progesterone. Primary vaginal epithelial cells were isolated from a segment of normal anterior vaginal wall obtained during vaginoplasty and were cultured in keratinocyte growth medium and were allowed to undergo their 3rd passage. Expression of HBD-1 and -2 by different stimuli using LPS 0.5 μg/ml, 17β-estradiol 2 nM and progesterone 1 μM was measured by RT-PCR, ELISA and real-time RT-PCR, respectively. HBD-1 was produced constitutively in vaginal epithelial cells and the production of HBD-1 was not influenced by LPS, 17β-estradiol and progesterone, but the production of HBD-2 was increased inducibly by LPS. 17β-Estradiol and progesterone did not change the production of HBD-2 in normal state, but 17β-estradiol increased the production of HBD-2 and progesterone suppressed the production of HBD-2 under the circumstances with infection. The HBD-2 plays an important role at innate host defense on genitourinary tract. The lacks of estrogen during menopause or uses of a progesterone-based oral contraceptive in sexually active women may influence production of HBD-2 in vaginal epithelium and may increase susceptibility to bacterial vaginitis or recurrent UTI. 相似文献
16.
Primary cell cultures of rat mammary carcinoma R3230AC exhibited a rapid, reversible and dose-related inhibition of carrier-mediated 3-0-methyl-D-glucose transport when estrone, 17β-estradiol, estriol, diethylstilbestrol or phloretin was present during the transport assay. With 17β-estradiol, maximal transport inhibition (66%) was observed at 40μM, a concentration also effective in preventing cell growth when present in the media. Cultures preincubated in growth media containing 5mM glucose plus 40μM 17β-estradiol for one day displayed enhanced rates of carrier mediated 3-0-methyl-D-glucose transport. This increase was prevented by 50mM glucose and can be explained as an adaptive response to a condition simulating glucose starvation. 相似文献
17.
《Steroids》1999,64(1-2):5-13
The focus of our work on rapid actions of estrogens has been on the immuno-identification of a membrane version of the estrogen receptor-α (mERα) and the correlation of the presence of this receptor to the rapid secretion of prolactin in pituitary tumor cells. We demonstrated the mERα by both fluorescence and immuno-enzyme-cytochemistry and with both conventional and confocal microscopy in the cell line GH3/B6 and its sublines. Its presence on cells (including recently subcloned ones) is very heterogenous, unlike the nuclear ERα, which is present in every cell. An impeded ligand (estradiol covalently linked to BSA) binds to mERα and elicits the same response. A total of eight antibodies to ERα recognize mERα, making it likely that the membrane and nuclear proteins are highly related. Immuno-identification techniques have also been used to identify mERα on the MCF-7 human breast cancer cell line. Estradiol at very low concentrations elicits prolactin release from GH3/B6 cells within a few minutes of application. This response is bimodal, with effective concentrations in both the picomolar and nanomolar ranges. Prolactin release is also elicited or inhibited by ERα-specific antibodies. The characteristics of mERα and the membrane receptor for glucocorticoids have many similarities, suggesting that this mode of subcellular location/function alternative might be used by other members of the gene family. 相似文献
18.
Th17 cells: positive or negative role in tumor? 总被引:1,自引:0,他引:1
Th17 cells have been recently identified as a distinct Th cell lineage and found in an experimental animal model of cancer
and in human cancers, but whether these cells promote tumor growth or regulate antitumor responses remains controversial.
This review provides a summary of the current literature regarding interleukin (IL)-17/IL-23 and Th17 cells in cancer and
discusses their potential roles in cancer development. Finally, we note several issues in this research area that must be
resolved before the design of novel therapeutic approaches specifically targeting Th17 cells in cancer become feasible. 相似文献
19.
Airway disease distribution and/or severity exhibit sex differences suggesting that sex hormones are involved in the respiratory system physiology and pathophysiology. The implication of airway smooth muscle cells (ASMCs) in the physiology of the airways and the pathogenetic mechanism of airway remodeling is of great interest. Therefore, we studied the effect of testosterone and 17β-estradiol on ASMC proliferation and the mechanisms involved.Cell proliferation was estimated using the methyl-[3H]thymidine incorporation and Cell Titer 96® AQueous One Solution Assay methods. ASMC isolated from adult male or female rabbit trachea were incubated with testosterone (1 pM-1 μM) or 17β-estradiol (1 pM-1 μM), in the presence or absence of the androgen receptor antagonist flutamide (10 nM) or estrogen receptor antagonist ICI182780 (10 nM), as well as of the PI3K inhibitors LY294002 (20 μM) or wortmannin (1 μM), or the MAPK inhibitors PD98059 (100 μM) or U0126 (1 μM).After 24 h of incubation, testosterone and 17β-estradiol increased methyl-[3H]thymidine incorporation and cell number, in ASMC isolated from male or female animals. The induction of ASMC proliferation by testosterone or 17β-estradiol was inhibited by flutamide or ICI182780 respectively, as well as by LY294002, wortmannin, PD98059 or U0126.In conclusion, testosterone and 17β-estradiol have a mitogenic effect on ASMC, which is receptor-mediated and involves the MAPK and PI3K signaling pathways. Moreover, their effect is the same for ASMC from male and female animals. It is possible that gender-related differences in ASMC remodeling, may be influenced by the different patterns of sex steroid hormone secretion in males and females. 相似文献
20.
A significant number of adult male patients with acquired immunodeficiency syndrome develop cerebral atrophy and progressive brain disorders such as dementia complex and neuropsychiatric problems. Upon entering the brain via activated macrophages or microglias, the human immunodeficiency type 1 virus (HIV-1) may produce cytotoxic factors such as HIV-1 envelope protein (gp 120) and protease. Owing to significant proteolysis of nonviral proteins, the protease derived from HIV-1 may be detrimental to brain cells and neurons. Our results revealed that HIV-1 protease, at nanomolar concentrations, was as potent as gp 120 in causing neurotoxicity in human neuroblastoma neurotypic SH-SY5Y cells. As shown by the Oncor ApopTag staining procedure, HIV-1 protease significantly increased the number of apoptotic cells over the serum-free controls. Moreover, HIV-1 protease-induced neurotoxicity was blocked by a selective protease inhibitor, kynostatin (KNI-272). Antioxidants such as 17-estradiol, melatonin, andS-nitrosoglutathione also prevented protease-induced neurotoxicity. These findings indicate that oxidative proteolysis may mediate HIV-1 protease-induced apoptosis and the degeneration of neurons and other brain cells. Centrally active protease inhibitors and antioxidants may play an important role in preventing cerebral atrophy and associated dementia complex caused by HIV-1. 相似文献