scholarly journals Effects of High Phosphorus Diet on Bone Metabolism-Related Gene Expression in Young and Aged Mice

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Shinichi Katsumata ◽  
Hiroshi Matsuzaki ◽  
Rie Katsumata-Tsuboi ◽  
Mariko Uehara ◽  
Kazuharu Suzuki
Keyword(s):  
Gene Expression ◽  
Mrna Expression ◽  
Bone Metabolism ◽  
Transient Receptor Potential ◽  
Transient Receptor Potential Vanilloid ◽  
Related Gene ◽  
Aged Mice ◽  
High Phosphorus ◽  
Mrna Ratio ◽  
Rankl Mrna

In this study, the effects of high phosphorus (P) diet on bone metabolism-related gene expression were investigated in young and aged mice. Twelve- and 80-week-old ddY male mice were divided into two groups, respectively, and fed a control diet containing 0.3% P or a high P diet containing 1.2% P. After 4 weeks of treatment, serum parathyroid hormone (PTH) concentration was significantly higher in the high P groups than in the control groups in both young and aged mice and was significantly higher in aged mice than in young mice fed the high P diet. High P diet significantly increased receptor activator of NF-κB ligand (RANKL) mRNA in the femur of both young and aged mice and significantly increased the RANKL/osteoprotegerin (OPG) mRNA ratio only in aged mice. High P diet significantly increased mRNA expression of transient receptor potential vanilloid type 6, calbindin-D9k, and plasma membrane Ca2+-ATPase 1b in the duodenum of both young and aged mice. These results suggest that high P diet increased RANKL mRNA expression in the femur and calcium absorption-related gene expression in the duodenum regardless of age. Furthermore, the high P diet-induced increase in PTH secretion might increase the RANKL/OPG mRNA ratio in aged mice.

scholarly journals Analysis of transient receptor potential vanilloid 1 and substance P gene expression in the mouse tongue following oral ginger administration

2016 ◽  
Vol 5 (4) ◽  
pp. 131-134
Author(s):  
Iizuka Michiro ◽  
◽  
Hirata Ayumu ◽  
Abe Noriaki ◽  
Jobu Kohei ◽  
...  
Keyword(s):  
Gene Expression ◽  
Substance P ◽  
Protein Expression ◽  
Mrna Expression ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Transient Receptor Potential Vanilloid ◽  
P Gene ◽  
Glandular Cells ◽  
Transient Receptor

Ginger rhizome (Zingiber officinale) exhibits multiple pharmacological actions. For example, its pungent components target the transient receptor potential vanilloid 1 (TRPV1) ion channel and thus contribute to swallowing reflex recovery by elevating the neuropeptide substance P. However, the precise mechanism underlying this action remains unclear. To examine TRPV1 and substance P gene expression in the mouse tongue in response to stimulation by orally administered ginger, quantitative real-time polymerase chain reaction and immunohistochemistry were performed to evaluate mRNA and protein expression. TRPV1 mRNA expression in the mouse tongue was upregulated 30 min after oral ginger stimulation. In the gingerstimulated mouse, TRPV1 protein expression was increased and concentrated in the plasma membranes of the mucous glandular cells of the tongue epithelium. No significant differences in substance P mRNA expression relative to the control were observed after ginger stimulation. However, immunohistochemistry revealed that the amount of substance P protein expression increased in the mucous glandular cells of the tongue epithelium in ginger-stimulated mice, and this expression appeared to concentrate in the secretory granules of these cells. Activation of TRPV1 promotes the secretion of substance P in saliva, and clinically, saliva levels of substance P can be measured noninvasively and can provide a useful biomarker of the swallowing function. An increased level of substance P in the saliva could indicate improved dysphagia. Our data suggest that ginger activates TRPV1 and promotes the secretion of substance P in saliva. Ginger is therefore expected to serve as a functional agent for improving dysphagia.

Effects of Zinc Supplementation and Deficiency on Bone Metabolism and Related Gene Expression in Rat

2010 ◽  
Vol 143 (1) ◽  
pp. 394-402 ◽  
Author(s):  
Jian-Yi Sun ◽  
Jian-Feng Wang ◽  
Nai-Tao Zi ◽  
Ming-Yan Jing ◽  
Xiao-Yan Weng
Keyword(s):  
Gene Expression ◽  
Bone Metabolism ◽  
Zinc Supplementation ◽  
Related Gene

Oxtr/TRPV1 expression and acclimation of skeletal muscle to cold-stress in male mice

2021 ◽  
Author(s):  
Elena Conte ◽  
Adele Romano ◽  
Michela De Bellis ◽  
Maria Luisa De Ceglia ◽  
Maria Rosaria Carratù ◽  
...  
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Cold Stress ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Transient Receptor Potential Vanilloid ◽  
Male Mice ◽  
Transient Receptor ◽  
Immunohistochemical Studies ◽  
Circulating Levels

We explored the involvement of Oxytocin receptor (Oxtr)/ Transient-receptor-potential-vanilloid-1 (TRPV1) genes and Oxytocin (Oxt) on the adaptation of skeletal muscle to cold stress challenge in mice. Oxtr expression in hypothalamic paraventricular (PVN), supraoptic nuclei (SON), and hippocampus (HIPP) were evaluated by immunohistochemistry in parallel with the measurement of circulating Oxt. The Oxtr and TRPV1 gene expression in Soleus (SOL) and Tibialis Anterior (TA) muscles were investigated by RT-PCR. Histological studies of the cardiac muscle after cold stress were also performed. Male mice (n=15) were divided into controls maintained at room temperature (RT=24°C), exposed to cold stress (CS) at T=4°C for 6 hours (6h), and 5 days (5d). Immunohistochemical studies showed that Oxtr protein expression increased by 2-fold (p=0.01) in PVN and by 1.5-fold (p=0.0001) in HIPP after 6h and 5d CS, but decreased by 2-fold (p=0.026) in SON at 5d. Both Oxtr and TRPV1 gene expression increased after 6h and 5d CS in SOL and TA muscles. Oxtr vs TRPV1 gene expression in SOL and TA muscles evaluated by regression analysis was linearly correlated following CS at 6h and 5d but not at control temperature of 24+1°C, supporting the hypothesis of coupling between these genes. The circulating levels of Oxt are unaffected after 6h CS but decreased by 0.2-fold (p=0.0141) after 5d CS. This is the first report that Oxtr and TRPV1 expression are upregulated in response to cold acclimation in skeletal muscle. The up-regulation of Oxtr in PVN and HIPP balances the decrease of circulating Oxt.

scholarly journals TRPV4 increases cardiomyocyte calcium cycling and contractility yet contributes to damage in the aged heart following hypoosmotic stress

2018 ◽  
Vol 115 (1) ◽  
pp. 46-56 ◽  
Author(s):  
John L Jones ◽  
Deborah Peana ◽  
Adam B Veteto ◽  
Michelle D Lambert ◽  
Zahra Nourian ◽  
...  
Keyword(s):  
Protein Expression ◽  
Transient Receptor Potential ◽  
Pathological Condition ◽  
Left Ventricular ◽  
Left Ventricular Myocardium ◽  
Transient Receptor Potential Vanilloid ◽  
Aged Mice ◽  
Increased Risk ◽  
Hypoosmotic Stress

Abstract Aims Cardiomyocyte Ca2+ homeostasis is altered with aging via poorly-understood mechanisms. The Transient Receptor Potential Vanilloid 4 (TRPV4) ion channel is an osmotically-activated Ca2+ channel, and there is limited information on the role of TRPV4 in cardiomyocytes. Our data show that TRPV4 protein expression increases in cardiomyocytes of the aged heart. The objective of this study was to examine the role of TRPV4 in cardiomyocyte Ca2+ homeostasis following hypoosmotic stress and to assess the contribution of TRPV4 to cardiac contractility and tissue damage following ischaemia–reperfusion (I/R), a pathological condition associated with cardiomyocyte osmotic stress. Methods and results TRPV4 protein expression increased in cardiomyocytes of Aged (24–27 months) mice compared with Young (3–6 months) mice. Immunohistochemistry revealed TRPV4 localization to microtubules and the t-tubule network of cardiomyocytes of Aged mice, as well as in left ventricular myocardium of elderly patients undergoing surgical aortic valve replacement for aortic stenosis. Following hypoosmotic stress, cardiomyocytes of Aged, but not Young exhibited an increase in action-potential induced Ca2+ transients. This effect was mediated via increased sarcoplasmic reticulum Ca2+ content and facilitation of Ryanodine Receptor Ca2+ release and was prevented by TRPV4 antagonism (1 μmol/L HC067047). A similar hypoosmotic stress-induced facilitation of Ca2+ transients was observed in Young transgenic mice with inducible TRPV4 expression in cardiomyocytes. Following I/R, isolated hearts of Young mice with transgenic TRPV4 expression exhibited enhanced contractility vs. hearts of Young control mice. Similarly, hearts of Aged mice exhibited enhanced contractility vs. hearts of Aged TRPV4 knock-out (TRPV4−/−) mice. In Aged, pharmacological inhibition of TRPV4 (1 μmol/L, HC067047) prevented hypoosmotic stress-induced cardiomyocyte death and I/R-induced cardiac damage. Conclusions Our findings provide a new mechanism for hypoosmotic stress-induced cardiomyocyte Ca2+ entry and cell damage in the aged heart. These finding have potential implications in treatment of elderly populations at increased risk of myocardial infarction and I/R injury.

scholarly journals Antinociceptive Effects of Emodin on CFA-Induced Inflammatory Pain in Rats

2020 ◽  
Vol 15 (7) ◽  
pp. 1934578X2094200
Author(s):  
Wan Ni ◽  
Nianyun Wang ◽  
Shenglan Tian ◽  
Qingbang Xu
Keyword(s):  
Mrna Expression ◽  
Inflammatory Pain ◽  
Transient Receptor Potential ◽  
Interleukin 1 ◽  
Receptor Potential ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Transient Receptor Potential Vanilloid ◽  
Tnf Α ◽  
Transient Receptor

The effect of emodin on complete Freund’s adjuvant (CFA)-induced inflammatory pain in rats and its potential molecular mechanism was investigated. For this, a rat model of inflammatory pain induced by CFA was established and rats were treated with emodin by intraperitoneal injection. The pain threshold was evaluated by the von Frey, thermo hyperalgesia, and cold plate tests. The mRNA expression of transient receptor potential channel ankyrin type-1 ( Trpa1) and transient receptor potential vanilloid 1 ( Trpv1) was detected by quantitative reverse transcription polymerase chain reaction, and the level of inflammatory cytokines was determined by enzyme-linked immunosorbent assay. The mechanical and thermal pain thresholds of CFA-treated rats were significantly lower than those of the control rats, while the paw withdrawal responses in response to cold stimulation were higher than that of the control group. Emodin treatment significantly improved CFA-induced hyperalgesia. Further results showed that emodin inhibits the upregulation of Trpa1 and Trpv1 mRNA expression in the dorsal root ganglion (DRG) of rats with inflammatory pain compared with the control group. Emodin also significantly reduced the levels of tumor necrosis factor alpha (TNF-α), interleukin 1 beta (IL-1β), and interleukin 6 (IL-6) in the serum of rats with inflammatory pain. Thus, emodin may inhibit hyperalgesia induced by inflammatory stimulation by downregulating the mRNA expression of Trpa1 and Trpv1 in DRG neurons and reducing the levels of TNF-α, IL-1β, and IL-6.

scholarly journals Inhibition of mucin secretion via glucocorticoid-induced regulation of calcium-related proteins in mouse lung

2018 ◽  
Vol 314 (6) ◽  
pp. L956-L966 ◽  
Author(s):  
Jin Yong An ◽  
Changhwan Ahn ◽  
Hee Young Kang ◽  
Eui-Bae Jeung
Keyword(s):  
Gene Expression ◽  
Transient Receptor Potential ◽  
Periodic Acid ◽  
Mucus Secretion ◽  
Mouse Lung ◽  
Alveolar Type ◽  
Related Gene ◽  
Mucin Secretion ◽  
Calbindin D ◽  
Related Proteins

Calcium is important for physiological functioning in many tissues and is essential in mucus secretion and muscle contraction. Intracellular concentrations of calcium are regulated by calcium-related proteins, such as transient receptor potential cation channel subfamily V member 4 (TRPV 4), TRPV6, Calbindin-D9k (CaBP-9k), sodium-calcium exchanger (NCX1), and plasma membrane Ca2+ ATPase 1 (PMCA1). In this study, the relationship between secretion of pulmonary mucus and calcium regulation was investigated. To confirm the effect of steroid hormones, immature mice were injected with estrogen (E2) or progesterone (P4), and mature mice were injected with dexamethasone (DEX). Subsequently, the location and expression of TRPV4, TRPV6, CaBP-9k, NCX1, and PMCA1 in lung tissue were examined. Periodic acid-Schiff staining was performed to investigate functional aspects of the protein expression. There were no significant differences in calcium-related gene expression in E2- and P4-treated mice, but TRPV4, NCX1, and PMCA1 were increased in DEX-treated mice and were recovered by RU486 treatment. DEX induces the expression of calcium-related proteins through the glucocorticoid receptor-mediated pathway and may involve decreased mucin secretion in the bronchiole. TRPV4, TRPV6, CaBP-9k, NCX1, and PMCA1 were specifically expressed in Clara and alveolar type 2 cells of mouse lung. CC10, a marker of Clara cells, was decreased by DEX. In addition, mucin secretion, which is a functional aspect of this cell, was also decreased by DEX treatment. Control of calcium-related gene expression may affect the control of mucus secretion in the lung. Such a control mechanism can form the basis of studies into diseases such as inflammation attributable to mucus secretion abnormalities, coughing, and respiratory disorders and distress.

scholarly journals Neurotrophic effects of dental pulp stem cells on trigeminal neuronal cells

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Nessma Sultan ◽  
Laila E. Amin ◽  
Ahmed R. Zaher ◽  
Mohammed E. Grawish ◽  
Ben A. Scheven
Keyword(s):  
Gene Expression ◽  
Stem Cells ◽  
Neurotrophic Factors ◽  
Neurotrophic Factor ◽  
Dental Pulp ◽  
Transient Receptor Potential ◽  
Neuronal Cells ◽  
Dental Pulp Stem Cells ◽  
Transient Receptor Potential Vanilloid ◽  
Neuronal Markers

AbstractEvidence indicates that dental pulp stem cells (DPSC) secrete neurotrophic factors which play an important role in neurogenesis, neural maintenance and repair. In this study we investigated the trophic potential of DPSC-derived conditioned medium (CM) to protect and regenerate isolated primary trigeminal ganglion neuronal cells (TGNC). DPSC and TGNC were harvested by enzymatic digestion from Wister-Hann rats. CM was collected from 72 h serum-free DPSC cultures and neurotrophic factors; nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), and glial cell line-derived neurotrophic factor (GDNF) were analysed by specific enzyme-linked immunosorbent assays (ELISAs). Primary co-cultures of DPSC and TGNC were established to evaluate the paracrine effects of DPSC. In comparison, NGF was used to evaluate its neurotrophic and neuritogenic effect on TGNC. Immunocytochemistry was performed to detect the neuronal-markers; neuronal nuclei (NeuN), microtubule-associated protein-2 (MAP-2) and βIII-tubulin. Quantitative real time polymerase chain reaction (qRT-PCR) was used to analyse neuronal-associated gene expression of NeuN, MAP-2, βIII-tubulin in addition to growth-associated protein-43 (GAP-43), Synapsin-I and thermo-sensitive transient receptor potential vanilloid channel-1 (TRPV1). DPSC-CM contained significant levels of NGF, BDNF, NT-3 and GDNF. DPSC and DPSC-CM significantly enhanced TGNC survival with extensive neurite outgrowth and branching as evaluated by immunocytochemistry of neuronal markers. DPSC-CM was more effective in stimulating TGNC survival than co-cultures or NGF treated culture. In comparison to controls, DPSC-CM significantly upregulated gene expression of several neuronal markers as well as TRPV1. This study demonstrated that DPSC-derived factors promoted survival and regeneration of isolated TGNC and may be considered as cell-free therapy for TG nerve repair.

scholarly journals Surgery, Anesthesia and Intensive Care Environment Induce Delirium-Like Behaviors and Impairment of Synaptic Function-Related Gene Expression in Aged Mice

2020 ◽  
Vol 12 ◽  
Author(s):  
Meghana Illendula ◽  
Hari Prasad Osuru ◽  
Bianca Ferrarese ◽  
Navya Atluri ◽  
Elzbieta Dulko ◽  
...  
Keyword(s):  
Gene Expression ◽  
Intensive Care ◽  
Synaptic Function ◽  
Related Gene ◽  
Care Environment ◽  
Aged Mice

Contribution of TRPV4 to enhanced calcium cycling and cardiac arrhythmia following ischemia-reperfusion in aged mouse hearts

2020 ◽  
Author(s):  
◽  
Deborah Peana
Keyword(s):  
Transient Receptor Potential ◽  
Contractile Function ◽  
Ischemia Reperfusion ◽  
Calcium Handling ◽  
Transient Receptor Potential Vanilloid ◽  
Aged Mouse ◽  
Aged Mice ◽  
Hypoosmotic Stress ◽  
Perfused Hearts ◽  
Young Mice

[ACCESS RESTRICTED TO THE UNIVERSITY OF MISSOURI--COLUMBIA AT REQUEST OF AUTHOR.] Cardiomyocyte Ca2+ homeostasis is altered with aging and predisposes the Aged heart to Ca2+ intolerance and arrhythmia. Transient Receptor Potential Vanilloid 4 (TRPV4) is an osmotically-activated cation channel and channel expression is increased in cardiomyocytes of Aged mice. The central goal of this work was to determine the role of TRPV4 in calcium handling and arrhythmogenesis in response to hypoosmotic stress and following ischemia-reperfusion (I/R). Hypoosmotic stress induced an increase in calcium transient amplitude in cardiomyocytes isolated from Aged mice which was followed by an increased incidence of arrhythmic Ca2+ events and Ca2+ waves. This effect was prevented by TRPV4 inhibition and was absent in cardiomyocytes from Young mice. Cardiac contractile function, membrane potential, and cardiac ECG was monitored in Langendorff-perfused hearts during I/R. Aged hearts responded to I/R with an initial increase in contractile function, membrane depolarization, and incidence of ventricular arrhythmia during reperfusion. This effect was attenuated by TRPV4 inhibition and was absent in hearts of Young mice. Also, in hearts of Aged, TRPV4 inhibition decreased the percent of damaged tissue following I/R compared to untreated conditions. Finally, Langendorff-perfused hearts from Aged mice expressing a genetically encoded Ca2+ sensor (GCaMP6f) were subjected to I/R and demonstrated an increased Ca2+ transient amplitude and incidence of arrhythmic Ca2+ waves compared to Aged mice treated with TRPV4 inhibition. These findings suggest that TRPV4 may contribute to initial inotropy followed by pro-arrhythmic cardiomyocyte Ca2+ signaling, arrhythmogenesis, and cell death following I/R in the Aged heart.

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