scholarly journals Gene Expression of Calcium Channel Components in Dahl Salt‐Resistant Rat Mesenteric Arteries by RT‐PCR

2011 ◽  
Vol 25 (S1) ◽  
Author(s):  
Ana Pena ◽  
Mahesh Joshi ◽  
Nikolaos Tsoukias
Keyword(s):  
Gene Expression ◽  
Calcium Channel ◽  
Mesenteric Arteries ◽  
Rt Pcr

Quantitative Fluorescent RT-PCR Measurements of Postnatal Calcium Channel Gene Expression in Rat Hippocampal Subfields

1999 ◽  
Vol 868 (1 MOLECULAR AND) ◽  
pp. 228-232
Author(s):  
SHAN M. PRADHAN ◽  
SHUNDI GE ◽  
CHIEKO KURODA ◽  
JULIUS PETERS ◽  
CHARLES E. NIESEN
Keyword(s):  
Gene Expression ◽  
Calcium Channel ◽  
Rt Pcr ◽  
Hippocampal Subfields ◽  
Channel Gene

Estrogen decreases biglycan mRNA expression in resistance blood vessels

2003 ◽  
Vol 285 (4) ◽  
pp. R754-R761 ◽  
Author(s):  
Manoj C. Rodrigo ◽  
Douglas S. Martin ◽  
Kathleen M. Eyster
Keyword(s):  
Gene Expression ◽  
Microarray Data ◽  
Dna Microarrays ◽  
Mesenteric Arteries ◽  
Ovariectomized Rats ◽  
Rt Pcr ◽  
New Gene ◽  
The Media ◽  
Estrogen Effects ◽  
Estrogenic Regulation

This study was designed to identify new gene targets of estrogen in the mesenteric arteries and to determine whether the soy phytoestrogens could mimic estrogen effects. Ovariectomized rats were treated with estradiol, genistein, or daidzein for 4 days. The mesenteric arteries were harvested, total RNA was extracted, mRNA was reverse transcribed in the presence of [33P]dCTP, and the labeled probes were hybridized with DNA microarrays. Analysis of the microarray data identified biglycan as a target of estrogenic regulation. Semiquantitative RT-PCR was used to confirm and quantitate the decrease in biglycan gene expression in response to estrogen (-37%), genistein (-15%), and daidzein (-10%). Treatment with the pure estrogen receptor antagonist ICI-182,780 reversed the inhibition of biglycan gene expression. The decrease in biglycan gene expression in response to estrogens was paralleled with a decrease in biglycan protein expression. Biglycan protein was localized to the media of the mesenteric arteries by immunohistochemistry. Collectively, these data suggest that biglycan is a vascular protein regulated at the genomic level by estrogens.

scholarly journals Differential expression of VEGFA, TIE2, and ANG2 but not ADAMTS1 in rat mesenteric microvascular arteries and veins

2009 ◽  
pp. 193-202
Author(s):  
N Mecha Disassa ◽  
B Styp-Rekowska ◽  
B Hinz ◽  
L Da Silva-Azevedo ◽  
AR Pries ◽  
...  
Keyword(s):  
Gene Expression ◽  
Endothelial Cells ◽  
Shear Stress ◽  
Wall Stress ◽  
Mesenteric Arteries ◽  
Rt Pcr ◽  
Hemodynamic Forces ◽  
Differential Gene ◽  
Structural Adaptations ◽  
Arteries And Veins

Microvessels respond to metabolic stimuli (e.g. pO2) and hemodynamic forces (e.g. shear stress and wall stress) with structural adaptations including angiogenesis, remodeling and pruning. These responses could be mediated by differential gene expression in endothelial and smooth muscle cells. Therefore, rat mesenteric arteries and veins were excised by microsurgery, and mRNA expression of four angioadaptation-related genes was quantified by real time duplex RT-PCR in equal amounts of total RNA, correlated to two different house keeping genes (ß-actin, GAPDH). The results show higher expression of VEGFA, TIE2, and ANG2 in arteries than in veins, but equal expression of ADAMTS1. Higher availability of VEGFA mRNA in endothelial cells of arteries shown here could contribute to the maintenance of mechanically stressed blood vessels and counteract pressureinduced vasoconstriction.

1650: Novel Gene Expression Markers in Renal Tumors Using Rt-PCR on Fixed Tissues Useful in Differentiating Histologic Subtypes

2004 ◽  
Vol 171 (4S) ◽  
pp. 436-436
Author(s):  
John A. Petros ◽  
Audry N. Schuetz ◽  
Andrew N. Young ◽  
Q. Yin Goen ◽  
So Dug Lim ◽  
...  
Keyword(s):  
Gene Expression ◽  
Renal Tumors ◽  
Rt Pcr ◽  
Novel Gene ◽  
Histologic Subtypes

Gene expression of collagen, fibronectin and elastin on a collagen and a collagen-fabric matrix measured by realtime RT-PCR

2004 ◽  
Vol 52 (S 1) ◽  
Author(s):  
LO Schilling ◽  
N Davies ◽  
R Autschbach ◽  
P Zilla
Keyword(s):  
Gene Expression ◽  
Rt Pcr

The Protective Effect of Metformin against Oxandrolone-Induced Infertility in Male Rats

2020 ◽  
Vol 26 ◽  
Author(s):  
Abdulqader Fadhil Abed ◽  
Yazun Bashir Jarrar ◽  
Hamzeh J Al-Ameer ◽  
Wajdy Al-Awaida ◽  
Su-Jun Lee
Keyword(s):  
Gene Expression ◽  
Male Infertility ◽  
Protective Effect ◽  
Histological Examination ◽  
Sperm Count ◽  
Serum Testosterone ◽  
Male Rats ◽  
P Value ◽  
Protective Effects ◽  
Rt Pcr

Background: Oxandrolone is a synthetic testosterone analogue that is widely used among bodybuilders and athletes. However, oxandrolone causes male infertility. Recently, it was found that metformin reduces the risk of infertility associated with diabetes mellitus. Aim: This study aimed to investigate the protective effects of metformin against oxandrolone-induced infertility in male rats. Methods: Rats continuously received one of four treatments (n=7) over 14 days: control DMSO administration, oxandrolone administration, metformin administration, or co-administration of oxandrolone and metformin. Doses were equivalent to those used for human treatment. Subsequently, testicular and blood samples were collected for morphological, biochemical, and histological examination. In addition, gene expression of the testosterone synthesizing enzyme CYP11A1 was analyzed in the testes using RT-PCR. Results: Oxandrolone administration induced male infertility by significantly reducing relative weights of testes by 48%, sperm count by 82%, and serum testosterone levels by 96% (ANOVA, P value < 0.05). In addition, histological examination determined that oxandrolone caused spermatogenic arrest which was associated with 2-fold downregulation of testicular CYP11A1 gene expression. However, co-administration of metformin with oxandrolone significantly ameliorated toxicological alterations induced by oxandrolone exposure (ANOVA, P value < 0.05). Conclusion: Metformin administration protected against oxandrolone-induced infertility in male rats. Further clinical studies are needed to confirm the protective effect of metformin against oxandrolone-induced infertility among athletes.

Global expression analysis of ECL cells in Mastomys natalensis gastric mucosa identifies alterations in the AP-1 pathway induced by gastrin-mediated transformation

2004 ◽  
Vol 20 (1) ◽  
pp. 131-142 ◽  
Author(s):  
M. Kidd ◽  
T. Hinoue ◽  
G. Eick ◽  
K. D. Lye ◽  
S. M. Mane ◽  
...  
Keyword(s):  
Gene Expression ◽  
Gastric Mucosa ◽  
Western Blot ◽  
Cell Transformation ◽  
Mastomys Natalensis ◽  
Rt Pcr ◽  
Cell Hyperplasia ◽  
Ecl Cells ◽  
Ecl Cell ◽  
Gene Expression Alterations

Enterochromaffin-like (ECL) cell hyperplasia and then irreversible neoplasia can be generated in the African rodent Mastomys natalensis using the H2 receptor blocker, loxtidine, for 8–16 wk. We used a GeneChip approach complemented by standard technologies to identify gene expression alterations in the gastric mucosa during gastrin-mediated ECL cell transformation. Gastric mucosa (mucosal scrapping) and ECL cell-enriched fractions were obtained from untreated Mastomys (controls) and from animals treated with loxtidine for 8 wk (hyperplasia). Tumor ECL cells were obtained by hand-dissection of gastric ECL cell nodules from animals treated with loxtidine for >16 wk and from a spontaneously developed ECL cell tumor. RNA was isolated, examined on rat U34A GeneChips, and comparison analysis was performed to identify altered gene expression. Alterations in gene expressions were examined further by immunohistochemistry, quantitative RT-PCR (Q-RT-PCR), sequencing and Western blot. GeneSpring analysis demonstrated alterations in few genes (<20) in hyperplastic and tumor mucosa. The histamine H1 receptor was consistently increased in proliferating mucosa. This gene change was confirmed by Q-RT-PCR. Other genes showing alterations included neural-(chromogranin A and somatostatin), cell-cycle-, and AP-1-associated genes. Immunostaining confirmed alterations in neural markers. Cluster analysis of ECL cell-enriched samples demonstrated that c- fos and junD were differently regulated. Q-RT-PCR and Western blot in prospectively collected gastric mucosal samples confirmed the differential expression of Fos and Jun. The negative regulators of AP-1, JunD, and Menin were decreased in tumor mucosa. A missense of unknown function was noted in the menin gene. Hypergastrinemia in an animal model of gastric carcinoids differentially altered the histamine type 1 receptor and gene expression and protein composition of AP-1. These results suggest that expression of this receptor and an altered composition of AP-1 with a loss of inhibition play a role in ECL cell transformation.

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