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https://www.readbyqxmd.com/read/28636132/trpc1-and-trpc3-dependent-ca-2-signaling-in-mouse-cortical-astrocytes-affects-injury-evoked-astrogliosis-in-vivo
#1
Thabet Belkacemi, Alexander Niermann, Laura Hofmann, Ulrich Wissenbach, Lutz Birnbaumer, Petra Leidinger, Christina Backes, Eckart Meese, Andreas Keller, Xianshu Bai, Anja Scheller, Frank Kirchhoff, Stephan E Philipp, Petra Weissgerber, Veit Flockerzi, Andreas Beck
Following brain injury astrocytes change into a reactive state, proliferate and grow into the site of lesion, a process called astrogliosis, initiated and regulated by changes in cytoplasmic Ca(2+) . Transient receptor potential canonical (TRPC) channels may contribute to Ca(2+) influx but their presence and possible function in astrocytes is not known. By RT-PCR and RNA sequencing we identified transcripts of Trpc1, Trpc2, Trpc3, and Trpc4 in FACS-sorted glutamate aspartate transporter (GLAST)-positive cultured mouse cortical astrocytes and subcloned full-length Trpc1 and Trpc3 cDNAs from these cells...
June 21, 2017: Glia
https://www.readbyqxmd.com/read/28629808/physiological-and-pathophysiological-role-of-transient-receptor-potential-canonical-channels-in-cardiac-myocytes
#2
REVIEW
Azmi A Ahmad, Molly Streiff, Chris Hunter, Qinghua Hu, Frank B Sachse
Transient receptor potential canonical (TRPC) channels constitute a family of seven Ca(2+) permeable ion channels, named TRPC1 to 7. These channels are abundantly expressed in the mammalian heart, yet mechanisms underlying activation of TRPC channels and their precise role in cardiac physiology remain poorly understood. In this review, we perused original literature regarding TRPC channels in cardiomyocytes. We first reviewed studies on TRPC channel assembly and sub-cellular localization across multiple species and cell types...
June 16, 2017: Progress in Biophysics and Molecular Biology
https://www.readbyqxmd.com/read/28629718/changes-in-podocyte-trpc-channels-evoked-by-plasma-and-sera-from-patients-with-recurrent-fsgs-and-by-putative-glomerular-permeability-factors
#3
Eun Young Kim, Hila Roshanravan, Stuart E Dryer
Primary forms of focal and segmental glomeruloslerosis (FSGS) are driven by circulating factors that cause dysfunction or loss podocytes. Rare genetic forms of FSGS can be caused by mutations in TRPC6, which encodes a Ca(2+)-permeable cationic channel expressed in mesangial cells and podocytes; and NPHS2, which encodes podocin, a TRPC6-binding protein expressed in podocyte slit diaphragm domains. Here we observed that exposing immortalized mouse podocytes to serum or plasma from recurrent FSGS patients for 24h increased the steady-state cell-surface abundance of TRPC6, accompanied by an increase in currents through endogenous TRPC6 channels evoked by a hypoosmotic stretch stimulus...
June 16, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28627661/altered-expression-of-ppar%C3%A2-%C3%AE-and-trpc-in-neonatal-rats-with-persistent-pulmonary-hypertension
#4
Yanna Du, Jianhua Fu, Li Yao, Lin Qiao, Na Liu, Yujiao Xing, Xindong Xue
Persistent pulmonary hypertension of the newborn (PPHN) is a life‑threatening disease that is commonly observed in the neonatal intensive care unit. PPHN is pathologically characterized by pulmonary vascular remodeling and, in particular, pulmonary artery smooth muscle cell (PASMC) proliferation. Decreased expression levels of peroxisome proliferator‑activated receptor γ (PPAR‑γ), which is a member of the nuclear receptor hormone superfamily, in combination with elevated expressions of transient receptor potential cation channel, subfamily C, member 1 (TRPC1) and TRPC6 contributes to the PASMC proliferation and excessive pulmonary vascular remodeling in adult pulmonary hypertension (PH)...
June 9, 2017: Molecular Medicine Reports
https://www.readbyqxmd.com/read/28627017/functional-expression-of-calcium-permeable-canonical-transient-receptor-potential-4-containing-channels-promotes-migration-of-medulloblastoma-cells
#5
Wei-Chun Wei, Wan-Chen Huang, Yu-Ping Lin, Esther B E Becker, Olaf Ansorge, Veit Flockerzi, Daniele Conti, Giovanna Cenacchi, Maike D Glitsch
Aberrant intracellular Ca(2+) signalling contributes to the formation and progression of a range of distinct pathologies including cancers. Rises in intracellular Ca(2+) concentration occur in response to Ca(2+) influx through plasma membrane channels and Ca(2+) release from intracellular Ca(2+) stores, which can be mobilised in response to activation of cell surface receptors. OGR1 (Ovarian cancer G protein coupled Receptor 1, aka GPR68) is a proton-sensing Gq -coupled receptor that is most highly expressed in cerebellum...
June 19, 2017: Journal of Physiology
https://www.readbyqxmd.com/read/28623807/hiv-tat-excites-d1-receptor-like-expressing-neurons-from-rat-nucleus-accumbens
#6
G Cristina Brailoiu, Elena Deliu, Jeffrey L Barr, Linda M Console-Bram, Alexandra M Ciuciu, Mary E Abood, Ellen M Unterwald, Eugen Brailoiu
BACKGROUND: HIV-1 infection and drug abuse are frequently co-morbid and their association greatly increases the severity of HIV-1-induced neuropathology. While nucleus accumbens (NAcc) function is severely perturbed by drugs of abuse, little is known about how HIV-1 infection affects NAcc. METHODS: We used calcium and voltage imaging to investigate the effect of HIV-1 trans-activator of transcription (Tat) on rat NAcc. Based on previous neuronal studies, we hypothesized that Tat modulates intracellular Ca(2+) homeostasis of NAcc neurons...
June 8, 2017: Drug and Alcohol Dependence
https://www.readbyqxmd.com/read/28583863/increasing-extracellular-ca-2-sensitizes-tnf-alpha-induced-vascular-cell-adhesion-molecule-1-vcam-1-via-a-trpc1-erk1-2-nf%C3%AE%C2%BAb-dependent-pathway-in-human-vascular-endothelial-cells
#7
Songtao Li, Hua Ning, Yaxin Ye, Wei Wei, Rui Guo, Qing Song, Lei Liu, Yunyun Liu, Lixin Na, Yuchun Niu, Xia Chu, Rennan Feng, Naima Moustaid-Moussa, Ying Li, Changhao Sun
Increasing circulating Ca(2+) levels within the normal range has been reported to positively correlate with the incidence of fatal cardiovascular diseases (CVDs). However, limited studies have been able to delineate the potential mechanism(s) linking circulating Ca(2+) to CVD. In this study, we exposed primary human umbilical vein endothelial cells (HUVECs) and human umbilical vein cell line (EA.hy926) to different extracellular Ca(2+) to mimic the physiological state. Our data revealed that increasing extracellular Ca(2+) significantly enhanced susceptibility to tumor necrosis factor (TNF)-alpha-stimulated vascular cell adhesion molecule (VCAM)-1 expression and monocytes adhesion...
June 2, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28566634/effect-of-docosahexaenoic-acid-on-voltage-independent-ca-2-entry-pathways-in-cultured-vascular-smooth-muscle-cells-stimulated-with-5-hydroxytryptamine
#8
Takuji Machida, Akina Onoguchi, Kenji Iizuka, Sayuri Ishibashi, Mikiko Yutani, Masahiko Hirafuji
We previously reported that docosahexaenoic acid (DHA) inhibits an increase in intracellular Ca(2+) concentration ([Ca(2+)]i) in cultured rat vascular smooth muscle cells (VSMCs) through a mechanism involving mainly voltage-dependent Ca(2+) channels; however, the effect of DHA on voltage-independent pathways, such as store-operated and receptor-operated Ca(2+) entry, and Ca(2+) entry through Na(+)/Ca(2+) exchanger (NCX), has not been clarified. In the present study, we investigated the effect of DHA treatment on the expression of transient receptor potential canonical (TRPC) channels, capacitative Ca(2+) entry, and Ca(2+) entry through NCX in rat cultured VSMCs stimulated with 5-hydroxytryptamine (5-HT)...
2017: Biological & Pharmaceutical Bulletin
https://www.readbyqxmd.com/read/28526717/major-contribution-of-the-3-6-7-class-of-trpc-channels-to-myocardial-ischemia-reperfusion-and-cellular-hypoxia-reoxygenation-injuries
#9
Xiju He, Shoutian Li, Benju Liu, Sebastian Susperreguy, Karina Formoso, Jinghong Yao, Jinsong Kang, Anbing Shi, Lutz Birnbaumer, Yanhong Liao
The injury phase after myocardial infarcts occurs during reperfusion and is a consequence of calcium release from internal stores combined with calcium entry, leading to cell death by apoptopic and necrotic processes. The mechanism(s) by which calcium enters cells has(ve) not been identified. Here, we identify canonical transient receptor potential channels (TRPC) 3 and 6 as the cation channels through which most of the damaging calcium enters cells to trigger their death, and we describe mechanisms activated during the injury phase...
June 6, 2017: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/28522036/transient-receptor-potential-trp-channel-function-in-the-reproductive-axis
#10
REVIEW
Viktoria Götz, Sen Qiao, Andreas Beck, Ulrich Boehm
Transient receptor potential (TRP) channels play important functional roles in the signal transduction machinery of hormone-secreting cells and have recently been implicated in reproductive physiology. While expression studies have demonstrated TRP channel expression at all levels of the hypothalamic-pituitary-gonadal (hpg) axis, functional details about TRP channel action at the level of the individual cells controlling reproduction are just beginning to emerge. Canonical TRP (TRPC) channels are prominently expressed in the reproductive center of the neuroendocrine brain, i...
May 3, 2017: Cell Calcium
https://www.readbyqxmd.com/read/28508321/trpc-channels-and-glioma
#11
Shanshan Li, Xia Ding
Glioma is the most common type of brain tumors and malignant glioma is extremely lethal, with patients' 5-year survival rate less than 10%. Treatment of gliomas poses remarkable clinical challenges, not only because of their particular localization but also because glioma cells possess several malignant biological features, including highly proliferative, highly invasive, highly angiogenic, and highly metabolic aberrant. All these features make gliomas highly recurrent and drug resistant. Finding new and effective molecular drug targets for glioma is an urgent and critical task for both basic and clinical research...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/28508320/trpc-channels-and-cell-proliferation
#12
Cheng Zhan, Yu Shi
TRPCs have been demonstrated to be widely expressed in different cancers. In recent years, a number of studies closely investigated the roles of TRPCs in cancer cells. Most of the results show that both mRNA and protein levels of TRPCs significantly increase in cancer tissues compared with healthy controls. TRPCs regulate Ca(2+) homeostasis, contribute to cell cycle regulation and the expression/activation of Ca(2+)-related factors, and thus play critical roles in the proliferation of cancer cells. Therefore, TRPCs could act as potential drug targets for cancer diagnosis and therapy...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/28508319/trpc-channels-and-mental-disorders
#13
Karina Griesi-Oliveira, Angela May Suzuki, Alysson Renato Muotri
Transient receptor potential canonical (TRPC) channels mediate the influx of different types of cations through the cell membrane and are involved in many functions of the organism. Evidences of involvement of TRPC channels in neuronal development suggest that this family of proteins might play a role in certain neurological disorders. As reported, knockout mice for different TRPC channels show alterations in neuronal morphological and functional parameters, with behavioral abnormalities, such as in exploratory and social behaviors...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/28508318/trpc-channels-and-epilepsy
#14
Fang Zheng
Accumulating evidence suggest that TRPC channels play critical roles in various aspects of epileptogenesis. TRPC1/4 channels are major contributors to nonsynaptically derived epileptiform burst firing in the CA1 and the lateral septum. TRPC7 channels play a critical role in synaptically derived epileptiform burst firing. The reduction of spontaneous epileptiform bursting in the CA3 is correlated to a reduction in pilocarpine-induced SE in vivo in TRPC7 knockout mice. TRPC channels are also significant contributors to SE-induced neuronal cell death...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/28508317/trpc-channels-and-brain-inflammation
#15
Yoshito Mizoguchi, Akira Monji
Nonresolving low-grade inflammation is supposed to underly the basis of chronic disorders including cardiovascular diseases, cancer, diabetes, obesity, and psychiatric disorders such as depression and Alzheimer's diseases. There is increasing evidence suggesting that pathophysiology of psychiatric disorders is related to the inflammatory responses mediated by microglial cells. Elevation of intracellular Ca(2+) is important for the activation of microglial cell functions, including proliferation, release of NO, cytokines, and BDNF...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/28508316/trpc-channels-and-neuron-development-plasticity-and-activities
#16
Yilin Tai, Yichang Jia
In this chapter, we mainly focus on the functions of TRPC channels in brain development, including neural progenitor proliferation, neurogenesis, neuron survival, axon guidance, dendritic morphology, synaptogenesis, and neural plasticity. We also notice emerging advances in understanding the functions of TRPC channels in periphery, especially their functions in sensation and nociception in dorsal root ganglion (DRG). Because TRPC channels are expressed in all major types of glial cells, which account for at least half of total cells in the brain, TRPC channels may act as modulators for glial functions as well...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/28508315/trpc-channels-and-parkinson-s-disease
#17
Pramod Sukumaran, Yuyang Sun, Anne Schaar, Senthil Selvaraj, Brij B Singh
Parkinson's disease (PD) is a common neurodegenerative disorder, which involves degeneration of dopaminergic neurons that are present in the substantia nigra pars compacta (SNpc) region. Many factors have been identified that could lead to Parkinson's disease; however, almost all of them are directly or indirectly dependent on Ca(2+) signaling. Importantly, though disturbances in Ca(2+) homeostasis have been implicated in Parkinson's disease and other neuronal diseases, the identity of the calcium channel remains elusive...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/28508314/trpc-channels-and-alzheimer-s-disease
#18
Rui Lu, Qian He, Junfeng Wang
Alzheimer's disease (AD) is the most common neurodegenerative disease in the world. The "amyloid hypothesis" is one of the predominant hypotheses for the pathogenesis of AD. Besides, tau protein accumulation, calcium homeostasis disruption, and glial cell activation are also remarkable features in AD. Recently, there are some reports showing that TRPC channels may function in AD development, especially TRPC6. In this chapter, we will discuss the evidence for the involvement of TRPC channels in Alzheimer's disease and the potential of therapeutics for AD based on TRPC channels...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/28508313/trpc-channels-and-stroke
#19
Junbo Huang
TRPC channels play important roles in neuronal death/survival in ischemic stroke, vasospasm in hemorrhagic stroke, thrombin-induced astrocyte pathological changes, and also in the initiation of stroke by affecting blood pressure and atherogenesis. TRPCs' unique channel characters and downstream pathways make them possible new targets for stroke therapy. TRPC proteins have different functions in different cell types. Considering TRPCs' extensive distribution in various tissues and cell types, drugs targeting them could induce more complicated effects...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/28508312/trpc-channels-and-programmed-cell-death
#20
Jian Zhou, Yichang Jia
Neurotrophins, including nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF), bind to their high-affinity receptors to promote neuronal survival during brain development. One of the key downstream pathways is the phospholipase C (PLC) pathway, which not only plays a central role in calcium release from internal store but also in activation of TRPC channels coupled with neurotrophin receptors. TRPC channels are required for the neurotrophin-mediated neuronal protective effects. In addition, activation of TRPC channels is able to protect neurons in the absence of neurotrophin...
2017: Advances in Experimental Medicine and Biology
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