scholarly journals TOXOPLASMA GONDII AS A FACTOR OF PROGRESSION OF CARCINOGENIC PROCESSES AT THE MOLECULAR-GENETIC LEVEL IN AN INTERMEDIATE HOST

2021 ◽  
Vol 20 (4) ◽  
pp. 46-52
Author(s):  
E.S. Pashinskaya ◽  
◽  
V.M. Semenov ◽  
Keyword(s):  
Body Weight ◽  
Growth Factor ◽  
Toxoplasma Gondii ◽  
Intermediate Host ◽  
Molecular Genetic ◽  
Female Rats ◽  
Parasite Development ◽  
Pcr Analysis ◽  
Genetic Level ◽  
Endothelial Growth Factor

Objectives. To study Toxoplasma gondii as a factor of carcinogenic processes progression at the molecular-genetic level in an intermediate host. Material and methods. In the experiment, the expression of the proto-oncogenes survivin (BIRC5), epidermal growth factor (ErbB-2/HER2-Neu), GLI, vascular endothelial growth factor (VEGF) and anti-oncogene TP53 was determined in comparison with the reference genes - β-actin (ACTB) and GAPDH by means of PCR analysis in the tissues of animals with C6 tumor in situ infected with toxoplasma in different doses. A statistical comparison was made between the data of the experimental groups, depending on the dose of infection and the stage of the parasite development. Results. It has been revealed that toxoplasma can cause an increase in the expression of survivin (BIRC5), VEGF, ErbB-2/HER2-Neu, GLI in the tumors, lungs, liver, spleen, brain, both when invaded at a dose of 25 toxoplasma tachyzoites per 1 g of body weight (5000 tachyzoites per female) and when infected at a dose of 50 toxoplasma tachyzoites per 1 g of body weight (10000 tachyzoites per female). The degree of an increased expression of proto-oncogenes is directly dependent on the dose and stage of the parasite development. Infection of female rats having glioma with toxoplasma tachyzoites leads to a decrease in the expression of the anti-oncogene TP53 in the tissues of glioma, the lungs, liver, spleen, and brain of female rats. The decrease in the expression of TP53 depends on the dose of infection and the stage of toxoplasma development. Conclusions. Experimental toxoplasmosis causes an increase in the expression of BIRC5, ErbB-2/HER2-Neu, GLI, VEGF and a decrease in the expression of the anti-oncogene TP53, which can lead to the development of aggressive blastomogenic processes in mammalian tissues.

scholarly journals THE EFFECT OF TOXOPLASMAS ON THE CHANGES IN THE EXPRESSION OF BIRC5, ERBB-2/HER2-NEU, GLI, VEGF PROTOONCOGENES AND THE ANTI-ONCOGENE TP53 IN RATS IN THE EXPERIMENT

2021 ◽  
Vol 20 (3) ◽  
pp. 25-33
Author(s):  
E.S. Pashinskaya ◽  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Body Weight ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Parasite Development ◽  
Vascular Endothelial ◽  
Infection Dose ◽  
Animal Body ◽  
Epidermal Growth ◽  
Endothelial Growth Factor

Objectives. To study the effect of toxoplasmas on the changes in the expression of protooncogenes BIRC5, ERBB-2/HER2-NEU, GLI, VEGF and the anti-oncogene TP53 in rats in an experiment depending on the infection dose and the period of parasite development. Material and methods.The experiment was conducted on female Wistar rats to determine changes in the expression of the protooncogenes survivin (BIRC5), epidermal growth factor (ErbB-2/HER2-Neu), GLI 1, vascular endothelial growth factor (VEGF) and the anti-oncogene TP53 in comparison with the reference genes β-actin (ACTB) and GAPDH by means of PCR analysis in the tissues of 10 healthy and 120 animals invaded at different doses. Statistical comparison of the results of all groups was drawn with the data of the «control» series (healthy animals, biopsies of the lungs, liver, spleen, brain). The results obtained in the experimental groups were as follows: the infection dose of 25 toxoplasma tachyzoites per 1 g of the animal body weight (5000 tachyzoites per female) and the infection dose of 50 toxoplasma tachyzoites per 1 g of the animal body weight (10000 tachyzoites per female), then they were also compared with each other. Statistical processing of the obtained data was carried out using the program Statistica 10.0. The differences were considered to be reliable at a significance level of less than 0.05 (p<0.05). Results. Toxoplasma was found to cause an infection dose-dependent increase in the expression of the protooncogenes survivin (BIRC5), epidermal growth factor (ErbB-2/HER2-Neu), GLI, vascular endothelial growth factor (VEGF) and a change in the strength expression of the anti-oncogene TP53 at all stages of the parasite development. Conclusions. Experimental toxoplasmosis alters the expression of the protooncogenes survivin (BIRC5), epidermal growth factor (ErbB-2/HER2-Neu), GLI, vascular endothelial growth factor (VEGF), and the anti-oncogene TP53 in the tissues of the intermediate host.

scholarly journals Vascular endothelial growth factor regulates germ cell survival during establishment of spermatogenesis in the bovine testis

Reproduction ◽  
2009 ◽  
Vol 138 (4) ◽  
pp. 667-677 ◽  
Author(s):  
Kyle C Caires ◽  
Jeanene de Avila ◽  
Derek J McLean
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Germ Cell ◽  
Cell Survival ◽  
Germ Cells ◽  
Pcr Analysis ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor ◽  
Testis Tissue

Vascular endothelial growth factor-A (VEGFA) is a hypoxia-inducible peptide essential for angiogenesis and targets nonvascular cells in a variety of tissues and cell types. The objective of the current study was to determine the function of VEGF during testis development in bulls. We used an explant tissue culture and treatment approach to test the hypothesis that VEGFA-164 could regulate the biological activity of bovine germ cells. We demonstrate that VEGFA, KDR, and FLT1 proteins are expressed in germ and somatic cells in the bovine testis. Treatment of bovine testis tissue with VEGFA in vitro resulted in significantly more germ cells following 5 days of culture when compared with controls. Quantitative real-time RT-PCR analysis determined that VEGF treatment stimulated an intracellular response that prevents germ cell death in bovine testis tissue explants, as indicated by increased expression of BCL2 relative to BAX and decreased expression of BNIP3 at 3, 6, and 24 h during culture. Blocking VEGF activity in vitro using antisera against KDR and VEGF significantly reduced the number of germ cells in VEGF-treated testis tissue to control levels at 120 h. Testis grafting provided in vivo evidence that bovine testis tissue treated with VEGFA for 5 days in culture contained significantly more differentiating germ cells compared with controls. These findings support the conclusion that VEGF supports germ cell survival and sperm production in bulls.

Overexpression of vascular endothelial growth factor and its receptors in bronchial dypslasia demonstrated by quantitative RT-PCR analysis

Lung Cancer ◽  
2005 ◽  
Vol 48 (1) ◽  
pp. 31-45 ◽  
Author(s):  
Daniel T. Merrick ◽  
Jerry Haney ◽  
Sheila Petrunich ◽  
Michio Sugita ◽  
York E. Miller ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Pcr Analysis ◽  
Vascular Endothelial ◽  
Rt Pcr ◽  
Endothelial Growth Factor

scholarly journals Estrogen Receptor-α Overexpression Suppresses 17β-Estradiol-Mediated Vascular Endothelial Growth Factor Expression and Activation of Survival Kinases

Endocrinology ◽  
2008 ◽  
Vol 149 (8) ◽  
pp. 3881-3889 ◽  
Author(s):  
Shameena Bake ◽  
Lijiang Ma ◽  
Farida Sohrabji
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Estrogen Receptor ◽  
Growth Factors ◽  
Growth Factor ◽  
Cell Line ◽  
Female Rats ◽  
High Dose ◽  
Vascular Endothelial ◽  
17Β Estradiol ◽  
Endothelial Growth Factor

Estrogen and its receptors influence growth and differentiation by stimulating the production and secretion of growth factors. Our previous studies indicate an increased expression of estrogen receptor (ER)-α and decreased growth factor synthesis in the olfactory bulb of reproductive senescent female rats as compared with young animals. The present study tests the hypothesis that abnormal overexpression of ERα contributes to decreased growth factor synthesis. We developed the HeLa-Tet-On cell line stably transfected with ERα (HTERα) that expresses increasing amounts of ERα with increasing doses of doxycycline (Dox). Increasing doses of Dox had no effect on vascular endothelial growth factor (VEGF) secretion in HTERα cells. However, in the presence of 40 nm 17β-estradiol, VEGF secretion increased in low-dose Dox-exposed HTERα cultures, which was attenuated by the ERα antagonist, 1,3-Bis(4-hydroxyphenyl)-4-methyl-5-[4-(2-piperidinylethoxy)phenol]1H-pyrazole dihydrochloride. However, at high-dose Dox and, consequently, high ERα levels, estradiol failed to increase VEGF. In the HeLa X6 cell line in which the Tet-On construct is upstream of an unrelated gene (Pitx2A), estradiol failed to induce VEGF at any Dox dose. Furthermore, in the HTERα cell line, estradiol selectively down-regulates phospho-ERK2 and phospho-Akt at high ERα expression. This study clearly demonstrates that the dose of receptor critically mediates estradiol’s ability to regulate growth factors and survival kinases. The present data also support the hypothesis that 17β-estradiol treatment to an ERα overexpressing system, such as the senescent brain, could reverse the normally observed beneficial effect of estrogen.

scholarly journals Estrogen Deprivation and Replacement Modulate Cerebral Capillary Density with Vascular Expression of Angiogenic Molecules in Middle-Aged Female Rats

2003 ◽  
Vol 23 (2) ◽  
pp. 181-189 ◽  
Author(s):  
Subrina Jesmin ◽  
Yuichi Hattori ◽  
Ichiro Sakuma ◽  
Ming-Yue Liu ◽  
Chishimba N. Mowa ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Capillary Density ◽  
Cerebral Vessels ◽  
Female Rats ◽  
Sham Operation ◽  
Vascular Endothelial ◽  
Middle Aged ◽  
Cerebral Capillary ◽  
Endothelial Growth Factor

The effect of postmenopausal estrogen replacement therapy (ERT) on the risk or severity of cerebrovascular disorders is as yet unclear, and the evidence for flow preservation being a mechanism of estrogen neuroprotection remains elusive. The authors examined whether estrogen-mediated flow-preserving neuroprotective mechanisms, if any, may involve its angiogenic action. This study was conducted using middle-aged (44 weeks) female rats because of the importance of aging in cerebrovascular disease in women. Middle-aged female rats were subjected to sham operation, ovariectomy, or ovariectomy with ERT. The anatomic cerebral capillary morphology showed a significant reduction in the total capillary density in the frontal cortex after ovariectomy. This was associated with marked decreases in protein and gene expression of vascular endothelial growth factor and its angiogenic receptors in cerebral vessels, as demonstrated by immunohistochemistry and in situ hybridization. The expression levels of both estrogen receptor (ER) subtypes, ERα and ERβ, in cerebral vessels were significantly reduced after ovariectomy, but ERβ was more dramatically downregulated as assessed by the ERβ/ERα ratio. These ovariectomy-induced changes were completely prevented by ERT. Vascular endothelial growth factor appears to be a critical regulatory molecule for physiologic cerebral angiogenesis in middle-aged female rats and may play an important role in the flow-preserving neuroprotective action of estrogen through its angiogenic and antiapoptotic properties.

scholarly journals Evaluation of the Reproductive Ability of Male Rats in Acute Toxoplasmosis

2021 ◽  
Vol 6 (4) ◽  
pp. 44-49
Author(s):  
M. S. Kosova ◽  
◽  
E. S. Pashinskaya ◽  
Keyword(s):  
Body Weight ◽  
Toxoplasma Gondii ◽  
Female Rats ◽  
Reproductive Capacity ◽  
Male Rats ◽  
Reproductive Ability ◽  
Male Wistar Rats ◽  
Implantation Sites ◽  
Acute Toxoplasmosis ◽  
Post Implantation

Toxoplasmosis is a parasitic disease of humans and animals caused by Toxoplasma gondii. Toxoplasma is an intracellular parasite that belongs to the simplest and has a complex development cycle. Infection with Toxoplasma is possible orally, transplacentally, percutaneously (if the integrity of the skin is damaged). This invasion is often the cause of problems with bearing pregnancy, as well as the development of congenital anomalies in children. The purpose of the study was to study the reproductive ability of male rats in acute toxoplasmosis. Materials and methods. The experiment was performed on 90 female and 45 male Wistar rats with a body weight of 180-200 g. The intact control males were orally injected with 2 ml of 0.2% starch gel. Experimental groups of males were infected with an invasive Toxoplasma gondii culture at a dose of 25 tachyzoites per 1 g of body weight (5000 tachyzoites per rat) and 50 tachyzoites per 1 g of body weight (10000 tachyzoites per rat). Then the males of all groups were coupled with the females for 3 days. The effect of toxoplasmas on the reproductive ability of male rats was assessed by the development of pregnancy and changes in the levels of pre- and post-implantation embryo death in female rats on the 7th, 14th, and 21st days after pregnancy. To account for changes in the pre- and post-implantation death of embryos in female rats after removal from the experiment, the uterus and ovaries were isolated, the uterine horns were opened, the number of implantation sites, the total number of embryos, the number of living and dead embryos, the number of resorption, and the number of yellow bodies in the ovaries were determined. Results and discussion. In the females of the 4th, 5th and 6th groups (coupling with males infected at the dose of 25 tachyzoites per 1 g of body weight), a decrease in the number of implantation sites in the uterus, the total number of embryos and the number of live embryos was recorded by 1.8-1.9 times compared to the control parameters. In female rats of the 7th, 8th and 9th groups (coupling with males infected at the dose of 50 tachyzoites per 1 g of body weight), there was a decrease in the number of implantation sites in the uterus, the total number of embryos and the number of live embryos by 5.6-6.8 times compared to the control. When compared to the results obtained from the females of the 4th, 5th and 6th groups, a decrease in these indicators was recorded by 3.1-3.5 times. Conclusion. Toxoplasma gondii has an effect on reproductive capacity in male rats expressed in changes of the levels of preimplantation mortality in female rats. The obtained effect depends on the dose of infection and the period of parasitosis development in males

Long-term reductions in GH, insulin-like growth factor-I and body weight gain in rats treated neonatally with antibodies to rat GH

1990 ◽  
Vol 124 (3) ◽  
pp. 381-386 ◽  
Author(s):  
M. J. Gardner ◽  
D. J. Flint
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Growth Factor ◽  
Body Weight Gain ◽  
Female Rats ◽  
Serum Prolactin ◽  
Insulin Like Growth Factor ◽  
Factor I ◽  
Growth Factor I

ABSTRACT Treatment of neonatal rats on days 2–5 with antibodies against rat GH (rGH) markedly reduced body weight gain and serum concentrations of insulin-like growth factor-I for 6–8 weeks in both females and males, after which weight gain normalized without evidence of catch-up growth. There were no significant effects on serum prolactin, tri-iodothyronine or corticosterone. Testis and ovarian weights were reduced, although only in proportion to body size. In females, but not males, the treated rats, though lighter, had increased fat deposition in the parametrial depot. Pituitary weight was considerably reduced over 100 days later, as was the pituitary content of GH, but not prolactin. The response to GH-releasing factor of both male and female rats was also greatly reduced at this time. Taken together with the fact that these rGH antibodies can bind directly to somatotrophs, we propose that the long-term effects of the antibodies are induced by specific somatotroph destruction. Journal of Endocrinology (1990) 124, 381–386

scholarly journals 17β-Estradiol Increases Astrocytic Vascular Endothelial Growth Factor (VEGF) in Adult Female Rat Hippocampus

Endocrinology ◽  
2011 ◽  
Vol 152 (5) ◽  
pp. 1745-1751 ◽  
Author(s):  
Sharon Barouk ◽  
Tana Hintz ◽  
Ping Li ◽  
Aine M. Duffy ◽  
Neil J. MacLusky ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Adult Female ◽  
Serum Levels ◽  
Female Rats ◽  
Female Rat ◽  
Vascular Endothelial ◽  
17Β Estradiol ◽  
Endothelial Growth Factor ◽  
Vegf Protein

Vascular endothelial growth factor (VEGF) is critical to angiogenesis and vascular permeability. It is also important in the endocrine system, in which VEGF mediates the vascular effects of estrogens in target tissues such as the uterus, a response attributed to an estrogen response element on the VEGF gene. Here we asked whether 17β-estradiol increases VEGF levels in the brain. We focused on the hippocampus, in which 17β-estradiol and VEGF both have important actions, and used immunocytochemistry to evaluate VEGF protein. VEGF immunoreactivity was compared in adult female rats sampled during the estrous cycle when serum levels of 17β-estradiol peak (proestrous morning) as well as when they are low (metestrous morning). In addition, adult rats were ovariectomized and compared after treatment with 17β-estradiol or vehicle. The results demonstrated that VEGF immunoreactivity was increased when serum levels of 17β-estradiol were elevated. Confocal microscopy showed that VEGF immunofluorescence was predominantly nonneuronal, often associated with astrocytes. Glial VEGF labeling was primarily punctate rather than diffuse and labile because glial VEGF immunoreactivity was greatly reduced if tissue sections were left in an aqueous medium overnight. We conclude that VEGF protein in normal female hippocampus is primarily nonneuronal rather than neuronal and suggest that glial VEGF immunoreactivity has been underestimated by past studies with other methods because there is a labile extracellular pool. We suggest that estrogens may exert actions on female hippocampal structure and function by increasing hippocampal VEGF.

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