scholarly journals −254C>G SNP in the TRPC6 Gene Promoter Influences Its Expression via Interaction with the NF-κB Subunit RELA in Steroid-Resistant Nephrotic Syndrome Children

2019 ◽  
Vol 2019 ◽  
pp. 1-7
Author(s):  
Xinyu Kuang ◽  
Qian Zhou ◽  
Zhuying Li ◽  
Yujie Hu ◽  
Yulin Kang ◽  
...  
Keyword(s):  
Nephrotic Syndrome ◽  
Cell Lines ◽  
Transient Receptor Potential ◽  
Gene Promoter ◽  
Receptor Potential ◽  
Pcr Analysis ◽  
Steroid Resistant ◽  
Steroid Resistant Nephrotic Syndrome ◽  
Mutant Sequence ◽  
Transient Receptor

This study is aimed at exploring the mechanism by which the −254C>G single nucleotide polymorphism (SNP) on the transient receptor potential cation channel 6 (TRPC6) gene promoter could increase its activation in steroid-resistant nephrotic syndrome children of China. Plasmids containing the TRPC6 promoter region (with the −254C or G allele) were constructed and then transfected into human embryonic kidney (HEK) 293T cells and human podocytes. Luciferase assays were used to test the promoter activity in both cell lines with or without tumor necrosis factor-α (TNF-α) treatment, and chromatin immunoprecipitation-polymerase chain reaction (ChIP-PCR) analysis was used to verify the transcription factor that could bind to this mutant sequence. Luciferase results indicate that the activity of the mutant promoter was greater than that of the normal promoter of the TRPC6 gene in both cell lines. We further predicted and verified that this variation was mediated by the nuclear factor kappa B (NF-κB) subunit RELA, and TNF-α significantly enhanced the transcription activity of TRPC6 with the −254G allele. In conclusion, the −254C>G SNP is a gain-of-function variation of the TRPC6 gene, and it is also an early and effective factor for predicting steroid-resistant nephrotic syndrome (SRNS) in Chinese children.

scholarly journals Different phospholipase-C-coupled receptors differentially regulate capacitative and non-capacitative Ca2+ entry in A7r5 cells

2005 ◽  
Vol 389 (3) ◽  
pp. 821-829 ◽  
Author(s):  
Zahid Moneer ◽  
Irene Pino ◽  
Emily J. A. Taylor ◽  
Lisa M. Broad ◽  
Yingjie Liu ◽  
...  
Keyword(s):  
Phospholipase C ◽  
Transient Receptor Potential ◽  
Previous Analysis ◽  
Receptor Potential ◽  
Pcr Analysis ◽  
Reciprocal Regulation ◽  
Entry Pathway ◽  
Transient Activation ◽  
A7r5 Cells ◽  
Transient Receptor

Several receptors, including those for AVP (Arg8-vasopressin) and 5-HT (5-hydroxytryptamine), share an ability to stimulate PLC (phospholipase C) and so production of IP3 (inositol 1,4,5-trisphosphate) and DAG (diacylglycerol) in A7r5 vascular smooth muscle cells. Our previous analysis of the effects of AVP on Ca2+ entry [Moneer, Dyer and Taylor (2003) Biochem. J. 370, 439–448] showed that arachidonic acid released from DAG stimulated NO synthase. NO then stimulated an NCCE (non-capacitative Ca2+ entry) pathway, and, via cGMP and protein kinase G, it inhibited CCE (capacitative Ca2+ entry). This reciprocal regulation ensured that, in the presence of AVP, all Ca2+ entry occurred via NCCE to be followed by a transient activation of CCE only when AVP was removed [Moneer and Taylor (2002) Biochem. J. 362, 13–21]. We confirm that, in the presence of AVP, all Ca2+ entry occurs via NCCE, but 5-HT, despite activating PLC and evoking release of Ca2+ from intracellular stores, stimulates Ca2+ entry only via CCE. We conclude that two PLC-coupled receptors differentially regulate CCE and NCCE. We also address evidence that, in some A7r5 cells lines, AVP fails either to stimulate NCCE or inhibit CCE [Brueggemann, Markun, Barakat, Chen and Byron (2005) Biochem. J. 388, 237–244]. Quantitative PCR analysis suggests that these cells predominantly express TRPC1 (transient receptor potential canonical 1), whereas cells in which AVP reciprocally regulates CCE and NCCE express a greater variety of TRPC subtypes (TRPC1=6>2>3).

scholarly journals Expression of multiple Transient Receptor Potential channel genes in murine 3T3-L1 cell lines and adipose tissue

2013 ◽  
Vol 65 (3) ◽  
pp. 751-755 ◽  
Author(s):  
Mahendra Bishnoi ◽  
Kanthi Kiran Kondepudi ◽  
Aakriti Gupta ◽  
Aniket Karmase ◽  
Ravneet K. Boparai
Keyword(s):  
Adipose Tissue ◽  
Cell Lines ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Transient Receptor Potential Channel ◽  
Transient Receptor

scholarly journals Essential Role of Mast Cells in the Visceral Hyperalgesia Induced byT. spiralisInfection and Stress in Rats

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Chang-Qing Yang ◽  
Yan-Yu Wei ◽  
Chan-Juan Zhong ◽  
Li-Ping Duan
Keyword(s):  
Mast Cells ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Pcr Analysis ◽  
Signal Pathways ◽  
Transient Receptor Potential Vanilloid ◽  
Visceral Hyperalgesia ◽  
Cold Restraint Stress ◽  
Transient Receptor ◽  
Extracellular Regulated Kinase

Mast cells (MCs) deficient rats (Ws/Ws) were used to investigate the roles of MCs in visceral hyperalgesia. Ws/Ws and wild control (+/+) rats were exposed toT. spiralisor submitted to acute cold restraint stress (ACRS). Levels of proteinase-activated receptor 2 (PAR2) and nerve growth factor (NGF) were determined by immunoblots and RT-PCR analysis, and the putative signal pathways including phosphorylated extracellular-regulated kinase (pERK1/2) and transient receptor potential vanilloid receptor 1 (TRPV1) were further identified. Visceral hyperalgesia triggered by ACRS was observed only in+/+rats. The increased expression of PAR2 and NGF was observed only in+/+rats induced byT. spiralisand ACRS. The activation of pERK1/2 induced by ACRS occurred only in+/+rats. However, a significant increase of TRPV1 induced byT. spiralisand ACRS was observed only in+/+rats. The activation of PAR2 and NGF via both TRPV1 and pERK1/2 signal pathway is dependent on MCs in ACRS-induced visceral hyperalgesia rats.

scholarly journals Transient Receptor Potential Mucolipin-1 Channels in Glioblastoma: Role in Patient’s Survival

Cancers ◽  
2019 ◽  
Vol 11 (4) ◽  
pp. 525 ◽  
Author(s):  
Maria Beatrice Morelli ◽  
Consuelo Amantini ◽  
Daniele Tomassoni ◽  
Massimo Nabissi ◽  
Antonella Arcella ◽  
...  
Keyword(s):  
Cell Viability ◽  
Cell Lines ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
U251 Cell ◽  
Mediated Effects ◽  
Kaplan Meier ◽  
Negative Prognostic Factor ◽  
Carbonyl Cyanide ◽  
Transient Receptor

A link between mucolipin channels and tumors has been recently suggested. Herein, we aim to investigate the transient receptor potential mucolipin (TRPML)-1 relevance in glioblastoma. The expression of this channel was evaluated via qRT-PCR and immunohistochemistry in biopsies from 66 glioblastoma patients and two human glioblastoma cell lines and compared to normal human brain, astrocytes, and epileptic tissues. The subcellular distribution of TRPML-1 was examined via confocal microscopy in the glioma cell lines. Then, to assess the role of TRPML-1, cell viability assays have been conducted in T98 and U251 cell lines treated with the specific TRPML-1 agonist, MK6-83. We found that MK6-83 reduced cell viability and induced caspase-3-dependent apoptosis. Indeed, the TRPML-1 silencing or the blockage of TRPML-1 dependent [Ca2+]i release abrogated these effects. In addition, exposure of glioma cells to the reactive oxygen species (ROS) inducer, carbonyl cyanide m-chlorophenylhydrazone (CCCP), stimulated a TRPML-1-dependent autophagic cell death, as demonstrated by the ability of the autophagic inhibitor bafilomycin A, the TRPML-1 inhibitor sphingomyelin, and the TRPML-1 silencing to completely inhibit the CCCP-mediated effects. To test a possible correlation with patient’s survival, Kaplan–Meier, univariate, and multivariate analysis have been performed. Data showed that the loss/reduction of TRPML-1 mRNA expression strongly correlates with short survival in glioblastoma (GBM) patients, suggesting that the reduction of TRPML-1 expression represents a negative prognostic factor in GBM patients.

Do Fasudil and Y-27632 affect the level of transient receptor potential (TRP) gene expressions in breast cancer cell lines?

Tumor Biology ◽  
2014 ◽  
Vol 35 (8) ◽  
pp. 8033-8041 ◽  
Author(s):  
Bulent Gogebakan ◽  
Recep Bayraktar ◽  
Ali Suner ◽  
Ozan Balakan ◽  
Mustafa Ulasli ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Cancer Cell Lines ◽  
Breast Cancer Cell Lines ◽  
Gene Expressions ◽  
Transient Receptor

Sequential opening of IP3-sensitive Ca2+channels and SOC during α-adrenergic activation of rabbit vena cava

2002 ◽  
Vol 282 (5) ◽  
pp. H1768-H1777 ◽  
Author(s):  
Cheng-Han Lee ◽  
Roshanak Rahimian ◽  
Tania Szado ◽  
Jasmin Sandhu ◽  
Damon Poburko ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Transient Receptor Potential ◽  
Vena Cava ◽  
Receptor Potential ◽  
Selective Inhibition ◽  
Pcr Analysis ◽  
Release Channel ◽  
Plasmic Reticulum ◽  
Intracellular Ca ◽  
Transient Receptor

α1-Aderenoceptor-mediated constriction of rabbit inferior vena cava (IVC) is signaled by asynchronous wavelike Ca2+ oscillations in the in situ smooth muscle. We have shown previously that a putative nonselective cationic channel (NSCC) is required for these oscillations. In this report, we show that the application of 2-aminoethoxyphenyl borate (2-APB) to antagonize inositol 1,4,5-trisphosphate (InsP3)-sensitive Ca2+ release channels (IP3R channels) can prevent the initiation and abolish ongoing α1-aderenoceptor-mediated tonic constriction of the venous smooth muscle by inhibiting the generation of these intracellular Ca2+ concentration ([Ca2+]i) oscillations. The observed effects of 2-APB can only be attributed to its selective inhibition on the IP3R channels, not to its slight inhibition of the L-type voltage-gated Ca2+ channel and the sarco(endo)plasmic reticulum Ca2+ ATPase. Furthermore, 2-APB had no effect on the ryanodine-sensitive Ca2+ release channel and the store-operated channel (SOC) in the IVC. These results indicate that the putative NSCC involved in refilling the sarcoplasmic reticulum (SR) and maintaining the tonic contraction is most likely an SOC-type channel because it appears to be activated by IP3R-channel-mediated SR Ca2+ release or store depletion. This is in accordance with its sensitivity to Ni2+ and La3+ (SOC blockers). More interestingly, RT-PCR analysis indicates that transient receptor potential (Trp1) mRNA is strongly expressed in the rabbit IVC. The Trp1 gene is known to encode a component of the store-operated NSCC. These new data suggest that the activation of both the IP3R channels and the SOC are required for PE-mediated [Ca2+]i oscillations and constriction of the rabbit IVC.

scholarly journals Mechanism for Regulation of Melanoma Cell Death via Activation of Thermo-TRPV4 and TRPV2

2019 ◽  
Vol 2019 ◽  
pp. 1-14 ◽  
Author(s):  
Jiaojiao Zheng ◽  
Fangyuan Liu ◽  
Sha Du ◽  
Mei Li ◽  
Tian Wu ◽  
...  
Keyword(s):  
Cell Death ◽  
Cell Viability ◽  
Cell Lines ◽  
Melanoma Cell ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Melanoma Cells ◽  
Human Malignant Melanoma ◽  
Transient Receptor ◽  
A375 Cells

Background. Thermo-TRPs (temperature-sensitive transient receptor potential channels) belong to the TRP (transient receptor potential) channel superfamily. Emerging evidence implied that thermo-TRPs have been involved in regulation of cell fate in certain tumors. However, their distribution profiles and roles in melanoma remain incompletely understood. Methods. Western blot and digital PCR approaches were performed to identify the distribution profiles of six thermo-TRPs. MTT assessment was employed to detect cell viability. Flow cytometry was applied to test cell cycle and apoptosis. Calcium imaging was used to determine the function of channels. Five cell lines, including one normal human primary epidermal melanocytes and two human malignant melanoma (A375, G361) and two human metastatic melanoma (A2058, SK-MEL-3) cell lines, were chosen for this research. Results. In the present study, six thermo-TRPs including TRPV1/2/3/4, TRPA1, and TRPM8 were examined in human primary melanocytes and melanoma cells. We found that TRPV2/4, TRPA1, and TRPM8 exhibited ectopic distribution both in melanocytes and melanoma cells. Moreover, activation of TRPV2 and TRPV4 could lead to the decline of cell viability for melanoma A2058 and A375 cells. Subsequently, activation of TRPV2 by 2-APB (IC50 = 150 μM) induced cell necrosis in A2058 cells, while activation of TRPV4 by GSK1016790A (IC50 = 10 nM) enhanced apoptosis of A375 cells. Furthermore, TRPV4 mediated cell apoptosis of melanoma via phosphorylation of AKT and was involved in calcium regulation. Conclusion. Overall, our studies revealed that TRPV4 and TRPV2 mediated melanoma cell death via channel activation and characterized the mechanism of functional TRPV4 ion channel in regulating AKT pathway driven antitumor process. Thus, they may serve as potential biomarkers for the prognosis and are targeted for the therapeutic use in human melanoma.

scholarly journals The TRPA1 Channel Amplifies the Oxidative Stress Signal in Melanoma

Cells ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 3131
Author(s):  
Francesco De Logu ◽  
Daniel Souza Monteiro de Araujo ◽  
Filippo Ugolini ◽  
Luigi Francesco Iannone ◽  
Margherita Vannucchi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Lines ◽  
Cancer Progression ◽  
Melanoma Cell ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Tissue Samples ◽  
Stress Signal ◽  
Transient Receptor ◽  
Melanoma Cell Lines

Macrophages (MΦs) and reactive oxygen species (ROS) are implicated in carcinogenesis. The oxidative stress sensor, transient receptor potential ankyrin 1 (TRPA1), activated by ROS, appears to contribute to lung and breast cancer progression. Although TRPA1 expression has been reported in melanoma cell lines, and oxidative stress has been associated with melanocytic transformation, their role in melanoma remains poorly known. Here, we localized MΦs, the final end-product of oxidative stress, 4-hydroxynonenal (4-HNE), and TRPA1 in tissue samples of human common dermal melanocytic nevi, dysplastic nevi, and thin (pT1) and thick (pT4) cutaneous melanomas. The number (amount) of intratumoral and peritumoral M2 MΦs and 4-HNE staining progressively increased with tumor severity, while TRPA1 expression was similar in all samples. Hydrogen peroxide (H2O2) evoked a TRPA1-dependent calcium response in two distinct melanoma cell lines (SK-MEL-28 and WM266-4). Furthermore, H2O2 induced a TRPA1-dependent H2O2 release that was prevented by the TRPA1 antagonist, A967079, or Trpa1 gene silencing (siRNA). ROS release from infiltrating M2 MΦs may target TRPA1-expressing melanoma cells to amplify the oxidative stress signal that affects tumor cell survival and proliferation.

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