scholarly journals Expression patterns of GHRL, GHSR, LEP, LEPR, SST and CCK genes in the gastrointestinal tissues of Tibetan and Yorkshire pigs

2019 ◽  
Vol 64 (No. 6) ◽  
pp. 239-247
Author(s):  
Wen-Kui Sun ◽  
Chi Cheng ◽  
Rui Liu ◽  
Yi-Hui Chen ◽  
Kai Zeng ◽  
...  
Keyword(s):  
Feed Intake ◽  
Plasma Levels ◽  
Target Genes ◽  
Leptin Receptor ◽  
Expression Patterns ◽  
The Body ◽  
Enzyme Linked Immunosorbent Assay ◽  
Mrna Levels ◽  
Growth Difference ◽  
Yorkshire Pigs

The aim was to characterize the expression patterns of several genes in the gastrointestinal tracts of Tibetan pigs (TP) and Yorkshire pigs (YP) and to explore their correlation with digestion and growth difference of the two breeds. The body weights and growth of YP and TP were studied at 6, 12 and 24 weeks of age, and their plasma levels of ghrelin (GHRL), leptin (LEP), somatostatin (SST) and cholecystokinin (CCK) were determined by enzyme linked immunosorbent assay (ELISA). Blood and gastrointestinal sections (stomach, duodenum, jejunum, ileum, caecum and colon) were collected and assayed for mRNA expression of the six genes (GHRL, ghrelin receptor (GHSR), LEP, leptin receptor (LEPR), SST and CCK) by reverse transcription-qPCR (RT-qPCR). TP generally had higher mRNA expressions of GHSR, LEP, LEPR, SST and CCK genes compared to YP, and expressed lower levels of the GHRL gene in most tissues of the digestive tract. In both breeds, plasma levels of the expressed proteins were more closely correlated with the feed intake and growth than with mRNA levels of the target genes. Our data indicate that TP possess special gene expression patterns in the gastrointestinal tract compared to YP, which is consistent with its unique feed intake and adaptation to harsh environment.

scholarly journals Birdsong Decreases Protein Levels of FoxP2, a Molecule Required for Human Speech

2008 ◽  
Vol 100 (4) ◽  
pp. 2015-2025 ◽  
Author(s):  
Julie E. Miller ◽  
Elizabeth Spiteri ◽  
Michael C. Condro ◽  
Ryan T. Dosumu-Johnson ◽  
Daniel H. Geschwind ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Target Genes ◽  
Expression Patterns ◽  
Vocal Learning ◽  
Brain Regions ◽  
Motor Deficits ◽  
Mrna Levels ◽  
Adult Males ◽  
Protein Levels ◽  
Area X

Cognitive and motor deficits associated with language and speech are seen in humans harboring FOXP2 mutations. The neural bases for FOXP2 mutation-related deficits are thought to reside in structural abnormalities distributed across systems important for language and motor learning including the cerebral cortex, basal ganglia, and cerebellum. In these brain regions, our prior research showed that FoxP2 mRNA expression patterns are strikingly similar between developing humans and songbirds. Within the songbird brain, this pattern persists throughout life and includes the striatal subregion, Area X, that is dedicated to song development and maintenance. The persistent mRNA expression suggests a role for FoxP2 that extends beyond the formation of vocal learning circuits to their ongoing use. Because FoxP2 is a transcription factor, a role in shaping circuits likely depends on FoxP2 protein levels which might not always parallel mRNA levels. Indeed our current study shows that FoxP2 protein, like its mRNA, is acutely downregulated in mature Area X when adult males sing with some differences. Total corticosterone levels associated with the different behavioral contexts did not vary, indicating that differences in FoxP2 levels are not likely attributable to stress. Our data, together with recent reports on FoxP2's target genes, suggest that lowered FoxP2 levels may allow for expression of genes important for circuit modification and thus vocal variability.

scholarly journals Leptin Concentrations in Maternal and Umbilical Cord Blood in Relation to Maternal Weight, Birth Weight and Weight of the Placenta

1970 ◽  
Vol 23 (1) ◽  
pp. 3-7 ◽  
Author(s):  
S Ishrat ◽  
MW Rahman ◽  
MR Rahman ◽  
MZ Hussain ◽  
S Jahan
Keyword(s):  
Birth Weight ◽  
Cord Blood ◽  
Fetal Growth ◽  
Leptin Receptor ◽  
Venous Blood ◽  
The Body ◽  
Placental Weight ◽  
Enzyme Linked Immunosorbent Assay ◽  
Maternal Weight ◽  
Serum Leptin

Objective: Leptin is a hormone which regulates adipose tissue mass of the body. Substantial increase of leptin during pregnancy and detection of leptin and leptin receptor in placenta have led to the speculation that leptin is a gestational hormone with a possible role in regulation of fetal growth. The study was done to find out whether maternal and cord blood leptin correlate with birthweight and weight of the placenta. Materials and methods: A prospective cross sectional study was undertaken in the Department of Obsterics and Gynecology, Bangabandhu Sheikh Mujib Medical University from January 2005 to June 2005. The study was carried out on 39 pairs of mothers and newborns. Maternal venous blood was sampled just before delivery. Cord blood was obtained, birth weight and placental weight measurements were taken just after delivery of the baby. Serum leptin levels were measured by enzyme linked immunosorbent assay. Results: Maternal serum leptin was 24.50 ng/ml (range- 13.15-45.60 ng/ml) and cord serum leptin was 6.50 ng/ml (range- 2.02-12.30 ng/ml). There was no correlation between maternal leptin and birth weight or between maternal leptin and placental weight. Cord leptin was significantly correlated with birth weight but not with placental weight. There was no correlation between maternal and cord blood leptin. There was no significant gender differences in cord blood leptin concentrations. Conclusions: There may be an important role of leptin in regulation of fetal growth and development. Placenta may not be a major source of leptin in maternal and feto-placental circulation. Maternal leptin cannot be a reliable marker of fetal growth. Keywords: Serum leptin, birth weight, placental weight   doi: 10.3329/bjog.v23i1.3049 Bangladesh J Obstet Gynaecol, 2008; Vol. 23(1) : 3-7

scholarly journals Gene Expression Analysis of the Streptococcus pneumoniae Competence Regulons by Use of DNA Microarrays

2000 ◽  
Vol 182 (21) ◽  
pp. 6192-6202 ◽  
Author(s):  
Scott Peterson ◽  
Robin T. Cline ◽  
Hervé Tettelin ◽  
Vasily Sharov ◽  
Donald A. Morrison
Keyword(s):  
Streptococcus Pneumoniae ◽  
Dna Microarrays ◽  
Target Genes ◽  
Expression Patterns ◽  
In Vitro Models ◽  
Regulatory Genes ◽  
Mrna Levels ◽  
Similar Expression Pattern ◽  
Genes Encoding

ABSTRACT Competence for genetic transformation in Streptococcus pneumoniae is coordinated by the competence-stimulating peptide (CSP), which induces a sudden and transient appearance of competence during exponential growth in vitro. Models of this quorum-sensing mechanism have proposed sequential expression of several regulatory genes followed by induction of target genes encoding DNA-processing-pathway proteins. Although many genes required for transformation are known to be expressed only in response to CSP, the relative timing of their expression has not been established. Overlapping expression patterns for the genes cinA andcomD (G. Alloing, B. Martin, C. Granadel, and J. P. Claverys, Mol. Microbiol. 29:75–83, 1998) suggest that at least two distinct regulatory mechanisms may underlie the competence cycle. DNA microarrays were used to estimate mRNA levels for all known competence operons during induction of competence by CSP. The known competence regulatory operons, comAB, comCDE, andcomX, exhibited a low or zero initial (uninduced) signal, strongly increased expression during the period between 5 and 12 min after CSP addition, and a decrease nearly to original values by 15 min after initiation of exposure to CSP. The remaining competence genes displayed a similar expression pattern, but with an additional delay of approximately 5 min. In a mutant defective in ComX, which may act as an alternate sigma factor to allow expression of the target competence genes, the same regulatory genes were induced, but the other competence genes were not. Finally, examination of the expression of 60 candidate sites not previously associated with competence identified eight additional loci that could be induced by CSP.

Leptin is a coactivator of TGF-β in unilateral ureteral obstructive kidney disease

2007 ◽  
Vol 293 (4) ◽  
pp. F1355-F1362 ◽  
Author(s):  
Philipp Kümpers ◽  
Faikah Gueler ◽  
Song Rong ◽  
Michael Mengel ◽  
Irini Tossidou ◽  
...  
Keyword(s):  
Kidney Disease ◽  
Target Genes ◽  
Leptin Receptor ◽  
Transforming Growth Factor ◽  
Rat Kidney ◽  
Peptide Hormone ◽  
Tubulointerstitial Fibrosis ◽  
Mrna Levels ◽  
Renal Tubulointerstitial Fibrosis

Progressive tubulointerstitial fibrosis is the common end point leading to end-stage renal disease in experimental and clinical settings. Since the peptide hormone leptin is involved not only in the regulation of obesity but also in the regulation of inflammation and fibrosis, we tested the hypothesis whether leptin deficiency has an impact on tubulointerstitial fibrosis in mice. Leptin-deficient ( ob/ ob) and leptin receptor-deficient mice ( db/ db) were exposed to 14 days of unilateral ureteral obstruction (UUO). The degree of fibrosis and inflammation was compared with that in sham-operated mice by performing immunohistochemistry, quantitative PCR, and Western blotting. We found that tubulointerstitial fibrosis was significantly reduced in the obstructed kidneys of ob/ ob compared with db/ db mice or control mice. Detailed analysis of infiltrating inflammatory cells by immunohistochemistry revealed a significant reduction of CD4+ cells at 14 days after UUO in both ob/ ob and db/ db mice. In contrast, we could not detect significant differences in CD8+ cells and macrophage content. Transforming growth factor (TGF)-β mRNA levels, TGF-β-induced Smad-2/3 activation, and the upregulation of downstream target genes were significantly reduced in ob/ ob mice. In addition, we demonstrated that leptin could enhance TGF-β signaling in normal rat kidney fibroblasts in vitro. We conclude that leptin can serve as a cofactor of TGF-β activation and thus plays an important role in renal tubulointerstitial fibrosis. Therefore, selective blockade of the leptin axis might provide a therapeutic possibility to prevent or delay fibrotic kidney disease.

scholarly journals Gene networks under circadian control exhibit diurnal organization in primate organs

2021 ◽  
Author(s):  
Jie Li ◽  
Pengxing Nie ◽  
Christoph Turck ◽  
Guang-Zhong Wang
Keyword(s):  
Gene Networks ◽  
Target Genes ◽  
Expression Patterns ◽  
The Body ◽  
Gene Interactions ◽  
Molecular Clocks ◽  
Circadian Control ◽  
Genes Encoding ◽  
Basic Network ◽  
Significant Disease

Mammalian organs are individually controlled by autonomous circadian clocks. At the molecular level, this process is defined by the cyclical co-expression of both core transcription factors and off-target genes across time. While interactions between these molecular clocks are likely necessary for proper homeostasis, these features remain undefined. Here, we utilize integrative analysis of a baboon diurnal transcriptome atlas to characterize the properties of gene networks under circadian control. We found that 53.4% (8,120) of baboon genes are rhythmically expressed body-wide. In addition, >30% of gene-gene interactions exhibit periodic co-expression patterns, with core circadian genes more cyclically co-expressed than others. Moreover, two basic network modes were observed at the systems level: daytime and nighttime mode. Daytime networks were enriched for genes involved in metabolism, while nighttime networks were enriched for genes associated with growth and cellular signaling. A substantial number of diseases only form significant disease modules at either daytime or nighttime. In addition, we found that 216 of 313 genes encoding products that interact with SARS-CoV-2 are rhythmically expressed throughout the body. Importantly, more than 80% of SARS-CoV-2 related genes enriched modules are rhythmically expressed, and have significant network proximities with circadian regulators. Our data suggest that synchronization amongst circadian gene networks is necessary for proper homeostatic functions and circadian regulators have close interactions with SARS-CoV-2 infection.

scholarly journals Differential Expression of Three Hypoxia-inducible Factor-α Subunits in Pulmonary Arteries of Rat with Hypoxia-induced Hypertension

2005 ◽  
Vol 37 (10) ◽  
pp. 665-672 ◽  
Author(s):  
Qi-Fang Li ◽  
Ai-Guo Dai
Keyword(s):  
Pulmonary Hypertension ◽  
Western Blot ◽  
Right Ventricular ◽  
Ventricular Hypertrophy ◽  
Target Genes ◽  
Expression Patterns ◽  
Pulmonary Arteries ◽  
Right Ventricular Hypertrophy ◽  
Mrna Levels ◽  
Α Subunits

AbstractHypoxia inducible transcription factor (HIF)-1α plays an important role in the development of hypoxic pulmonary hypertension, but little is known about HIF-2α and HIF-3α with respect to transcriptional regulation by hypoxia. To examine the expression patterns of all HIF-α subunits (HIF-1α, HIF-2α and HIF-3α) in pulmonary arteries of rats undergoing systemic hypoxia, five groups of healthy male Wistar rats were exposed to normoxia (N) and hypoxia for 3 (H3), 7 (H7), 14 (H14) and 21 (H21) d respectively. Mean pulmonary arterial pressure (mPAP), vessel morphometry and right ventricular hypertrophy index were measured. Lungs were inflation fixed for immunohistochemistry and in situ hybridization, and homogenized for Western blot. mPAP increased significantly after 7 d of hypoxia [(18.4±0.4) vs. (14.4±0.4) mmHg, H7 vs. N], reached its peak after 14 d of hypoxia, then remained stable. Pulmonary artery remodeling and right ventricular hypertrophy developed significantly after 14 d of hypoxia. During normoxia, HIF-1α and HIF-3α staining were slightly positive regarding mRNA levels. A substantial alteration of HIF-1α and HIF-3α staining occurred in pulmonary arteries after 14 d and 7 d of hypoxia, respectively, but HIF-2α staining showed an inversed trend after 14 d of hypoxia. Protein levels of all HIF-α subunits except HIF-3α showed a marked increase corresponding to the duration of hypoxia, which was obtained by Western blot. Our study found that HIF-1α, HIF-2α and HIF-3α may not only confer different target genes, but also play key pathogenetic roles in hypoxic-induced pulmonary hypertension.

scholarly journals Maternal obesity and fetal programming: effects of a high-carbohydrate nutritional modification in the immediate postnatal life of female rats

2008 ◽  
Vol 295 (4) ◽  
pp. E895-E903 ◽  
Author(s):  
Malathi Srinivasan ◽  
Catherine Dodds ◽  
Husam Ghanim ◽  
Tao Gao ◽  
Peter J. Ross ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Plasma Levels ◽  
Body Weight Gain ◽  
The Body ◽  
Female Rats ◽  
Milk Formula ◽  
Postnatal Life ◽  
Mrna Levels ◽  
High Carbohydrate

Our earlier studies have shown that the artificial rearing of newborn rat pups [first generation high carbohydrate (1-HC)] on an HC milk formula resulted in chronic hyperinsulinemia and adult-onset obesity (HC phenotype). Offspring [second-generation HC (2-HC)] of 1-HC female rats spontaneously acquired the HC phenotype in the postweaning period. In this study, we have characterized the development of the abnormal intrauterine environment in the 1-HC female rats and the effects on fetal development under such pregnancy conditions for the offspring. 1-HC female rats demonstrated hyperphagia on laboratory chow and increased body weight gain beginning from the immediate postweaning period along with hyperinsulinemia and hyperleptinemia. During pregnancy, 1-HC female rats showed several metabolic alterations including increased body weight gain and increased plasma levels of insulin, leptin, proinflammatory markers, and lipid peroxidation products. Although there were no significant changes in the body weights or litter size of term 2-HC fetuses, the plasma levels of insulin and leptin were significantly higher compared with those of control term fetuses. Quantitation of mRNA levels by real-time RT-PCR indicated significant increases in the mRNA levels of orexigenic neuropeptides in the hypothalamus of 2-HC term fetuses. Collectively, these results indicate that the HC diet in infancy results in an adverse pregnancy condition in female rats with deleterious consequences for the offspring.

The Effects of Vitamin K1 and Warfarin on Prothrombin Expression in Human Hepatoblastoma (HepG2) Cells

1992 ◽  
Vol 68 (01) ◽  
pp. 040-047 ◽  
Author(s):  
C Scott Jamison ◽  
Bryan F Burkey ◽  
Sandra J Friezner Degen
Keyword(s):  
Total Protein ◽  
Hepg2 Cells ◽  
Enzyme Linked Immunosorbent Assay ◽  
Response Analysis ◽  
Secreted Protein ◽  
Mrna Levels ◽  
Vitamin K1 ◽  
Maximal Increase ◽  
Protein Levels ◽  
Warfarin Treatment

SummaryCultures of human hepatoblastoma (HepG2) cells were treated with vitamin K1 or warfarin and prothrombin antigen and mRNA levels were determined. With 3 and 6 h of 10 µg vitamin K1 treatment secreted prothrombin antigen levels, relative to total secreted protein levels, were increased 1.5-fold and 2.1-fold, respectively, over ethanol-treated control levels as determined by an enzyme-linked immunosorbent assay. Dose-response analysis with 3 h of 25 µg/ml vitamin K1 treatment demonstrated a maximal increase of 2.0-fold in secreted prothrombin antigen levels, relative to total secreted protein levels, over ethanol-treated control levels. Pulse-chase analysis with 35S-methionine and immunoprecipitation of 35S-labelled prothrombin demonstrated that, with vitamin K1 treatment (25 µg/ml, 3 h), the rate of prothrombin secretion increased approximately 2-fold and the total amount (intra- and extracellular) of prothrombin synthesized increased approximately 50% over ethanol-treated control levels. Warfarin treatment (1, 5, or 10 µg/ml, 24 h) resulted in decreases in secreted prothrombin antigen levels, relative to total protein levels to approximately 85%, 87% or 81% of ethanol-treated control levels. Analysis of total RNA isolated from these cultures by Northern and solution hybridization techniques demonstrated that prothrombin mRNA was approximately 2.1 kb and that neither vitamin K1 nor warfarin treatment affected the quantity of prothrombin mRNA (ranging from 240–350 prothrombin mRNA molecules per cell). These results demonstrate that vitamin K1 and warfarin, in addition to effects on γ-carboxylation, affect prothrombin synthesis post-transcriptionally, perhaps influencing translation, post-translational processing and/or secretion mechanisms.

Nanocurcumin: A Double-Edged Sword for Microcancers

2020 ◽  
Vol 26 (45) ◽  
pp. 5783-5792
Author(s):  
Kholood Abid Janjua ◽  
Adeeb Shehzad ◽  
Raheem Shahzad ◽  
Salman Ul Islam ◽  
Mazhar Ul Islam
Keyword(s):  
Intracellular Signaling ◽  
Dosage Forms ◽  
The Body ◽  
In Vivo Studies ◽  
Mrna Levels ◽  
Anticancer Activities ◽  
Road Map ◽  
Anticancer Effects

There is compelling evidence that drug molecules isolated from natural sources are hindered by low systemic bioavailability, poor absorption, and rapid elimination from the human body. Novel approaches are urgently needed that could enhance the retention time as well as the efficacy of natural products in the body. Among the various adopted approaches to meet this ever-increasing demand, nanoformulations show the most fascinating way of improving the bioavailability of dietary phytochemicals through modifying their pharmacokinetics and pharmacodynamics. Curcumin, a yellowish pigment isolated from dried ground rhizomes of turmeric, exhibits tremendous pharmacological effects, including anticancer activities. Several in vitro and in vivo studies have shown that curcumin mediates anticancer effects through the modulation (upregulation and/or downregulations) of several intracellular signaling pathways both at protein and mRNA levels. Scientists have introduced multiple modern techniques and novel dosage forms for enhancing the delivery, bioavailability, and efficacy of curcumin in the treatment of various malignancies. These novel dosage forms include nanoparticles, liposomes, micelles, phospholipids, and curcumin-encapsulated polymer nanoparticles. Nanocurcumin has shown improved anticancer effects compared to conventional curcumin formulations. This review discusses the underlying molecular mechanism of various nanoformulations of curcumin for the treatment of different cancers. We hope that this study will make a road map for preclinical and clinical investigations of cancer and recommend nano curcumin as a drug of choice for cancer therapy.

Tanshinone IIA Promotes Macrophage Cholesterol Efflux and Attenuates Atherosclerosis of apoE-/- Mice by Omentin-1/ABCA1 Pathway

2019 ◽  
Vol 20 (5) ◽  
pp. 422-432 ◽  
Author(s):  
Yu-lin Tan ◽  
Han-xiao Ou ◽  
Min Zhang ◽  
Duo Gong ◽  
Zhen-wang Zhao ◽  
...  
Keyword(s):  
Atherosclerotic Plaque ◽  
Lipid Content ◽  
Plasma Levels ◽  
Cholesterol Efflux ◽  
Density Lipoprotein ◽  
Tanshinone Iia ◽  
Lipoprotein Cholesterol ◽  
Mrna Levels ◽  
Cellular Lipid ◽  
Oil Red O

Background: Tanshinone IIA (Tan IIA) and Omentin-1 have a protective role in the cardiovascular system. However, if and how Tan IIA and Omentin-1 regulate cholesterol metabolism in macrophages has not been fully elucidated. Objective: To investigate the possible mechanisms of Tan IIA and Omentin-1 on preventing macrophage cholesterol accumulation and atherosclerosis development. Methods: The effect of Tan IIA on the protein and mRNA levels of Omentin-1 and ATP-binding cassette transporter A1 (ABCA1) in macrophages was examined by Western blot and qRT-PCR assay, respectively. Cholesterol efflux was assessed by liquid scintillation counting (LSC). Cellular lipid droplet was measured by Oil Red O staining, and intracellular lipid content was detected by high performance liquid chromatography (HPLC). In addition, the serum lipid profile of apoE−/− mice was measured by enzymatic method. The size of atherosclerotic lesion areas and content of lipids and collagen in the aortic of apoE−/− mice were examined by Sudan IV, Oil-red O, and Masson staining, respectively. Results: Tan IIA up-regulated expression of Omentin-1 and ABCA1 in THP-1 macrophages, promoting ABCA1-mediated cholesterol efflux and consequently decreasing cellular lipid content. Consistently, Tan IIA increased reverse cholesterol transport in apoE−/− mice. Plasma levels of high-density lipoprotein cholesterol (HDL-C), ABCA1 expression and atherosclerotic plaque collagen content were increased while plasma levels of low-density lipoprotein cholesterol (LDL-C) and atherosclerotic plaque sizes were reduced in Tan IIA-treated apoE−/− mice. These beneficial effects were, however, essentially blocked by knockdown of Omentin-1. Conclusion: Our results revealed that Tan IIA promotes cholesterol efflux and ameliorates lipid accumulation in macrophages most likely via the Omentin-1/ABCA1 pathway, reducing the development of aortic atherosclerosis.

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