K M Sanders

University of Nevada School of Medicine, Reno, Nevada, United States

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Publications (397)2136.75 Total impact

  • Kenton M. Sanders · Kathleen D. Keef ·

    The Journal of Physiology 10/2015; 593(20). DOI:10.1113/JP271320 · 5.04 Impact Factor
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    Violeta N. Mutafova-Yambolieva · Kenton M. Sanders ·

    AJP Gastrointestinal and Liver Physiology 10/2015; 309(7):G608-G609. DOI:10.1152/ajpgi.00225.2015 · 3.80 Impact Factor
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    Kenton M Sanders · Grant Hennig ·

    Journal of neurogastroenterology and motility 10/2015; 21(4):625-6. DOI:10.5056/jnm15133 · 2.30 Impact Factor
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    ABSTRACT: Background/aims: Smooth muscle cells (SMCs) characteristically express serum response factor (SRF), which regulates their development. The role of SRF in SMC plasticity in the pathophysiological conditions of gastrointestinal (GI) tract is less characterized. Methods: We generated SMC-specific Srf knockout mice and characterized the prenatally lethal phenotype using ultrasound biomicroscopy and histological analysis. We used small bowel partial obstruction surgeries and primary cell culture using cell-specific enhanced green fluorescent protein (EGFP) mouse lines to study phenotypic and molecular changes of SMCs by immunofluorescence, Western blotting, and quantitative polymerase chain reaction. Finally we examined SRF change in human rectal prolapse tissue by immunofluorescence. Results: Congenital SMC-specific Srf knockout mice died before birth and displayed severe GI and cardiac defects. Partial obstruction resulted in an overall increase in SRF protein expression. However, individual SMCs appeared to gradually lose SRF in the hypertrophic muscle. Cells expressing low levels of SRF also expressed low levels of platelet-derived growth factor receptor alpha (PDGFRα(low)) and Ki67. SMCs grown in culture recaptured the phenotypic switch from differentiated SMCs to proliferative PDGFRα(low) cells. The immediate and dramatic reduction of Srf and Myh11 mRNA expression confirmed the phenotypic change. Human rectal prolapse tissue also demonstrated significant loss of SRF expression. Conclusions: SRF expression in SMCs is essential for prenatal development of the GI tract and heart. Following partial obstruction, SMCs down-regulate SRF to transition into proliferative PDGFRα(low) cells that may represent a phenotype responsible for their plasticity. These findings demonstrate that SRF also plays a critical role in the remodeling process following GI injury.
    Journal of neurogastroenterology and motility 10/2015; 21(4):589-602. DOI:10.5056/jnm15063 · 2.30 Impact Factor
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    ABSTRACT: Telokin phosphorylation by cyclic GMP-dependent protein kinase facilitates smooth muscle relaxation. In this study we examined the relaxation of gastric fundus smooth muscles from basal tone, or pre-contracted with KCl or carbachol (CCh), and the phosphorylation of telokin S13, myosin light chain (MLC) S19, MYPT1 T853, T696, and CPI-17 T38 in response to 8-Bromo-cGMP, the NO donor sodium nitroprusside (SNP), or nitrergic neurotransmission. We compared MLC phosphorylation and the contraction and relaxation responses of gastric fundus smooth muscles from telokin-/- mice and their wild-type littermates to KCl or CCh, and 8-Bromo-cGMP, SNP, or nitrergic neurotransmission, respectively. We compared the relaxation responses and telokin phosphorylation of gastric fundus smooth muscles from wild-type mice and W/WV mice which lack ICC-IM, to 8-Bromo-cGMP, SNP, or nitrergic neurotransmission. We found that telokin S13 is basally phosphorylated and that 8-Bromo-cGMP and SNP increased basal telokin phosphorylation. In muscles pre-contracted with KCl or CCh, 8-Bromo-cGMP and SNP had no effect on CPI-17 or MYPT1 phosphorylation, but increased telokin phosphorylation and reduced MLC phosphorylation. In telokin-/- gastric fundus smooth muscles, basal tone and constitutive MLC S19 phosphorylation were increased. Pre-contracted telokin-/- gastric fundus smooth muscles have increased contractile responses to KCl, CCh, or cholinergic neurotransmission and reduced relaxation to 8-Bromo-cGMP, SNP, and nitrergic neurotransmission. However, basal telokin phosphorylation was not increased when muscles were stimulated with lower concentrations of SNP or when the muscles were stimulated by nitrergic neurotransmission. SNP, but not nitrergic neurotransmission, increased telokin Ser13 phosphorylation in both wild-type and W/WV gastric fundus smooth muscles. Our findings indicate that telokin may play a role in attenuating constitutive MLC phosphorylation and provide an additional mechanism to augment gastric fundus mechanical responses to inhibitory neurotransmission.
    PLoS ONE 08/2015; 10(8):e0134876. DOI:10.1371/journal.pone.0134876 · 3.23 Impact Factor
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    ABSTRACT: Genome-scale expression data on the absolute numbers of gene isoforms offers essential clues in cellular functions and biological processes. Smooth muscle cells (SMCs) perform a unique contractile function through expression of specific genes controlled by serum response factor (SRF), a transcription factor that binds to DNA sites known as the CArG boxes. To identify SRF-regulated genes specifically expressed in SMCs, we isolated SMC populations from mouse small intestine and colon, obtained their transcriptomes, and constructed an interactive SMC genome and CArGome browser. To our knowledge, this is the first online resource that provides a comprehensive library of all genetic transcripts expressed in primary SMCs. The browser also serves as the first genome-wide map of SRF binding sites. The browser analysis revealed novel SMC-specific transcriptional variants and SRF target genes, which provided new and unique insights into the cellular and biological functions of the cells in gastrointestinal (GI) physiology. The SRF target genes in SMCs, which were discovered in silico, were confirmed by proteomic analysis of SMC-specific Srf knockout mice. Our genome browser offers a new perspective into the alternative expression of genes in the context of SRF binding sites in SMCs and provides a valuable reference for future functional studies.
    PLoS ONE 08/2015; 10(8). DOI:10.1371/journal.pone.0133751 · 3.23 Impact Factor
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    ABSTRACT: Purines induce transient contraction and prolonged relaxation of detrusor muscles. Transient contraction is likely due to activation of inward currents in smooth muscle cells, and prolonged relaxation may be due to activation of small conductance Ca(2+)-activated K(+) (SK) channels via P2Y1 receptors expressed by detrusor PDGFRα(+) cells. We investigated whether other subtypes of P2Y receptors are involved in the activation of SK channels in PDGFRα(+) cells of detrusor muscles. Quantitative analysis of transcripts revealed that P2ry2, P2ry4 and P2ry14 are expressed in PDGFRα(+) cells of P2ry1-/- /eGFP mice at similar levels as in wild type mice. UTP, a P2Y2/P2Y4 agonist, activated large outward currents in detrusor PDGFRα(+) cells. SK channel blockers and an inhibitor of phospholipase C completely abolished currents activated by UTP. In contrast, UTP activated non-selective cation currents in smooth muscle cells. Under current-clamp (I=0), UTP induced significant hyperpolarization of PDGFRα(+) cells. MRS2500, a P2Y1 antagonist, did not affect the UTP-activated outward currents in PDGFRα(+) cells from wild type, and activation of outward currents by UTP was retained in P2ry1-/-/eGFP mice. As a negative control, we tested the effect of MRS2693, a selective P2Y6 agonist. This compound did not activate outward currents in PDGFRα(+) cells, and currents activated by UTP were unaffected by MRS2578, a selective P2Y6 antagonist. Nonselective P2Y receptor blocker inhibited UTP-activated outward currents in PDGFRα(+) cells. Our data demonstrate that P2Y2 and/or P2Y4 receptors function, in addition to P2Y1 receptors in activating SK currents in PDGFRα(+) cells and possibly in mediating purinergic relaxation in detrusor muscles. Copyright © 2015, American Journal of Physiology - Renal Physiology.
    AJP Renal Physiology 07/2015; 309(6):ajprenal.00156.2015. DOI:10.1152/ajprenal.00156.2015 · 3.25 Impact Factor
  • Kenton M Sanders ·

    Gastroenterology 06/2015; 149(2). DOI:10.1053/j.gastro.2015.06.018 · 16.72 Impact Factor
  • Bernard T. Drumm · Salah A. Baker · Grant W. Hennig · Kenton M. Sanders ·

    19th International Symposium On Calcium Binding Proteins; 05/2015
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    ABSTRACT: In cerebral artery myocytes, close proximity of the sarcoplasmic reticulum (SR) and plasma membrane (PM) creates microdomains where Ca2+ released from the SR attains a concentration sufficient to activate large-conductance Ca2+-activated K+ (BK) and melastatin transient receptor potential 4 (TRPM4) channels; essential regulators of membrane excitability. Microtubules organize the SR in cardiac and skeletal muscle cells, but it is not known if they serve this function in smooth muscle cells. Here, we test the hypothesis that microtubules maintain the SR architecture forming Ca2+ microdomains essential for BK and TRPM4 channel activity. Using membrane- and tubulin-specific fluorescent dyes, we observed distinct microtubule arches beneath the peripheral SR proximal to the PM in contractile cerebral artery smooth muscle cells. Nocodazole, an inhibitor of microtubule polymerization, disrupted these subcellular structures and increased the distance between the SR and PM. Using high-speed, high-resolution confocal Ca2+ imaging, we found that microtubule depolymerization altered the spatiotemporal properties of localized Ca2+ signaling events. Nocodazole treatment also resulted in the loss of Ca2+-dependent TRPM4 and BK channel activity in perforated whole-cell patch clamp recordings and diminished contractility in pressure myography experiments. We conclude that the microtubule network is essential for maintaining the SR architecture and Ca2+ microdomains necessary for the activation of BK and TRPM4 channels in cerebral artery myocytes.
    Experimental Biology 2015; 04/2015
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    Kenton M Sanders · Sean M Ward · Sang Don Koh ·

    Physiological Reviews 04/2015; 95(2):693-4. DOI:10.1152/physrev.00006.2015 · 27.32 Impact Factor
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    ABSTRACT: Gastric peristalsis begins in the orad corpus and propagates to the pylorus. Directionality of peristalsis depends upon orderly generation and propagation of electrical slow waves and a frequency gradient between proximal and distal pacemakers. We sought to understand how chronotropic agonists affect coupling between corpus and antrum. Electrophysiological and imaging techniques were used to investigate regulation of gastric slow wave frequency by muscarinic agonists in mice. We also investigated the expression and role of cholinesterases in regulating slow wave frequency and motor patterns in the stomach. Both acetycholinesterase (Ache) and butyrylcholine esterase (Bche) are expressed in gastric muscles and AChE is localized to var-icose processes of motor neurons. Inhibition of AChE in the absence of stimulation increased slow wave frequency in corpus and throughout muscle strips containing corpus and antrum. CCh caused depolarization and increased slow wave frequency. Stimulation of cholinergic neurons increased slow wave frequency but did not cause depolarization. Neostigmine (1 μM) in-creased slow wave frequency, but uncoupling between corpus and antrum was not detected. Motility mapping of contractile activity in gastric muscles showed similar effects of enteric nerve stimulation on the frequency and propagation of slow waves, but neostigmine (> 1 μM) caused aberrant contractile frequency and propagation and ectopic pacemaking. Our data show that slow wave uncoupling is difficult to assess with electrical recording from a single or double sites and sug-gest that efficient metabolism of ACh released from motor neurons is an extremely important regulator of slow wave frequency and propagation and gastric motility patterns.
    Journal of neurogastroenterology and motility 03/2015; 21(2):200-16. DOI:10.5056/jnm14120 · 2.30 Impact Factor
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    ABSTRACT: Growing evidence suggests important roles for specialized platelet-derived growth factor-alpha-positive (PDGFRalpha(+)) cells in regulating the behaviors of visceral smooth muscle organs. Examination of the female reproductive tracts of mice and monkeys showed that PDGFRalpha(+) cells form extensive networks in ovary, oviduct and uterus. PDGFRalpha(+) cells were located in discrete locations within these organs and their distribution and density was similar in rodents and primates. PDGFRalpha(+) cells were distinct from smooth muscle cells and interstitial cells of Cajal (ICC). This was demonstrated with immunohistochemical techniques and by performing molecular expression studies on PDGFRalpha(+) cells from mice with eGFP driven off the endogenous promoter for Pdgfralpha. Significant differences in gene expression were found in PDGFRalpha(+) cells from ovary, oviduct and uterus. Differences in gene expression were also detected in cells from different tissue regions within the same organ (e.g. uterine myometrium vs. endometrium). PDGFRalpha(+) cells are unlikely to provide pacemaker activity because they lacked significant expression of key pacemaker genes found in ICC (Kit and Ano1). Gja1 encoding connexin 43 was expressed at relatively high levels in PDGFRalpha(+) cells (except ovary) suggesting these cells can form gap junctions to one another and neighboring smooth muscle cells. PDGFRalpha(+) cells also expressed the early response transcription factor and proto-oncogene c-Fos, particularly in the ovary. These data demonstrate extensive distribution of PDGFRalpha(+) cells throughout the female reproductive tract. These cells are a heterogeneous population of cells that are likely to contribute to different aspects of physiological regulation in the various anatomical niches they occupy. Copyright 2015 by The Society for the Study of Reproduction.
    Biology of Reproduction 03/2015; 92(4). DOI:10.1095/biolreprod.114.124388 · 3.32 Impact Factor
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    Mei Hong Zhu · Tae Sik Sung · Kate O'Driscoll · Sang Don Koh · Kenton M Sanders ·
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    ABSTRACT: IInterstitial cells of Cajal (ICC) provide pacemaker activity in gastrointestinal muscles that underlies segmental and peristaltic contractions. ICC generate electrical slow waves that are due to large amplitude inward currents resulting from ANO1 channels, which are Ca(2+)-activated Cl(-) channels. We investigated the hypothesis that the Ca(2+) responsible for the stochastic activation of ANO1 channels during spontaneous transient inward currents (STICs) and synchronized activation of ANO1 channels during slow wave currents comes from intracellular Ca(2+) stores. ICC, obtained from the small intestine of Kit(+/copGFP) mice, were studied under voltage and current clamp to determine the effects of blocking Ca(2+) uptake into stores and release of Ca(2+) via IP3 dependent and ryanodine-sensitive channels. Cyclocpiazonic acid, thapsigargin, 2-APB and xestospongin C inhibited STICs and slow wave currents. Ryanodine and tetracaine also inhibited STICs and slow wave currents. Store-active compounds had no direct effects on ANO1 channels expressed in HEK-293 cells. Under current clamp store-active drugs caused significant depolarization of ICC and reduced spontaneous transient depolarizations (STDs). After block of ryanodine receptors with ryanodine and tetracaine, repolarization did not restore STDs. ANO1 expressed in ICC has limited access to cytoplasmic Ca(2+) concentration, suggesting that pacemaker activity depends upon Ca(2+) dynamics in restricted microdomains. Our data from studies of isolated ICC differ somewhat from studies on intact muscles and suggest that release of Ca(2+) from both IP3 and ryanodine receptors is important in generating pacemaker activity in ICC. Copyright © 2015, American Journal of Physiology - Cell Physiology.
    AJP Cell Physiology 01/2015; 308(8):ajpcell.00360.2014. DOI:10.1152/ajpcell.00360.2014 · 3.78 Impact Factor
  • Salah A. Baker · Grant W. Hennig · Sean M. Ward · Kenton M. Sanders ·
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    ABSTRACT: Key points: Platelet derived growth factor receptor α (PDGFRα(+) ) cells in colonic muscles are innervated by enteric inhibitory motor neurons. PDGFRα(+) cells generate Ca(2+) transients in response to exogenous purines and these responses were blocked by MRS-2500. Stimulation of enteric neurons, with cholinergic and nitrergic components blocked, evoked Ca(2+) transients in PDGFRα(+) and smooth muscle cells (SMCs). Responses to nerve stimulation were abolished by MRS-2500 and not observed in muscles with genetic deactivation of P2Y1 receptors. Ca(2+) transients evoked by nerve stimulation in PDGFRα(+) cells showed the same temporal characteristics as electrophysiological responses. PDGFRα(+) cells express gap junction genes, and drugs that inhibit gap junctions blocked neural responses in SMCs, but not in nerve processes or PDGFRα(+) cells. PDGFRα(+) cells are directly innervated by inhibitory motor neurons and purinergic responses are conducted to SMCs via gap junctions. Abstract: Interstitial cells, known as platelet derived growth factor receptor α (PDGFRα(+) ) cells, are closely associated with varicosities of enteric motor neurons and suggested to mediate purinergic hyperpolarization responses in smooth muscles of the gastrointestinal tract (GI), but this concept has not been demonstrated directly in intact muscles. We used confocal microscopy to monitor Ca(2+) transients in neurons and post-junctional cells of the murine colon evoked by exogenous purines or electrical field stimulation (EFS) of enteric neurons. EFS (1-20 Hz) caused Ca(2+) transients in enteric motor nerve processes and then in PDGFRα(+) cells shortly after the onset of stimulation (latency from EFS was 280 ms at 10 Hz). Responses in smooth muscle cells (SMCs) were typically a small decrease in Ca(2+) fluorescence just after the initiation of Ca(2+) transients in PDGFRα(+) cells. Upon cessation of EFS, several fast Ca(2+) transients were noted in SMCs (rebound excitation). Strong correlation was noted in the temporal characteristics of Ca(2+) transients evoked in PDGFRα(+) cells by EFS and inhibitory junction potentials (IJPs) recorded with intracellular microelectrodes. Ca(2+) transients and IJPs elicited by EFS were blocked by MRS-2500, a P2Y1 antagonist, and absent in P2ry1((-/-)) mice. PDGFRα(+) cells expressed gap junction genes, and gap junction uncouplers, 18β-glycyrrhetinic acid (18β-GA) and octanol blocked Ca(2+) transients in SMCs but not in neurons or PDGFRα(+) cells. IJPs recorded from SMCs were also blocked. These findings demonstrate direct innervation of PDGFRα(+) cells by motor neurons. PDGFRα(+) cells are primary targets for purinergic neurotransmitter(s) in enteric inhibitory neurotransmission. Hyperpolarization responses are conducted to SMCs via gap junctions.
    The Journal of Physiology 01/2015; 593(8). DOI:10.1113/jphysiol.2014.287599 · 5.04 Impact Factor
  • Yoshihiko Kito · Retsu Mitsui · Sean M Ward · Kenton M Sanders ·
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    ABSTRACT: Slow waves (slow wavesICC) were recorded from myenteric interstitial cells of Cajal (ICC-MY) in situ in the rabbit small intestine, and their properties were compared with those of mouse small intestine. Rabbit slow wavesICC consisted of an upstroke depolarization followed by a distinct plateau component. Ni(2+) and nominally Ca(2+)-free solutions reduced the rate-of-rise and amplitude of the upstroke depolarization. Replacement of Ca(2+) with Sr(2+) enhanced the upstroke component, but decreased the plateau component of rabbit slow wavesICC. In contrast, replacing Ca(2+) with Sr(2+) decreased both components of mouse slow wavesICC. The plateau component of rabbit slow wavesICC was inhibited in low[Cl(-)]o solutions and by 4,4'-diisothiocyanostilbene-2,2'-disulphonic acid (DIDS), an inhibitor of Cl(-) channels, cyclopiazonic acid (CPA), an inhibitor of internal Ca(2+) pumps, or bumetanide, an inhibitor of Na(+)-K(+)-2Cl(-) cotransporter (NKCC1). Bumetanide also inhibited the plateau component of mouse slow wavesICC. NKCC1-like immunoreactivity was observed mainly in ICC-MY in the rabbit small intestine. Membrane depolarization with a high-K(+) solution reduced the upstroke component of rabbit slow wavesICC. In cells depolarized with elevated external K(+), DIDS, CPA and bumetanide blocked slow wavesICC. These results suggest that the upstroke component of rabbit slow wavesICC is partially mediated by voltage-dependent Ca(2+) influx, whereas the plateau component is dependent upon Ca(2+)-activated Cl(-) efflux. NKCC1 is likely to be responsible for Cl(-) accumulation in ICC-MY. The results also suggest that the mechanism of the upstroke component differs in rabbit and mouse slow wavesICC in the small intestine. Copyright © 2014, American Journal of Physiology- Gastrointestinal and Liver Physiology.
    AJP Gastrointestinal and Liver Physiology 12/2014; 308(5):ajpgi.00308.2014. DOI:10.1152/ajpgi.00308.2014 · 3.80 Impact Factor
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    Kenton M Sanders · Kate O'Driscoll · Normand Leblanc ·

    Channels (Austin, Tex.) 12/2014; 8(6). DOI:10.4161/19336950.2014.986624 · 2.32 Impact Factor
  • Tae Sik Sung · Heung Up Kim · Jeong Hwan Kim · Hongli Lu · Kenton M. Sanders · Sang Don Koh ·
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    ABSTRACT: Protease-activated receptors (PARs) are G protein-coupled receptors activated by proteolytic cleavage at their amino termini by serine proteases. PAR activation contributes to the inflammatory response in the gastrointestinal (GI) tract and alters GI motility, but little is known about the specific cells within the tunica muscularis that express PARs and the mechanisms leading to contractile responses. Using real time PCR, we found PARs to be expressed in smooth muscle cells (SMCs), interstitial cells of Cajal (ICC) and platelet-derived growth factor receptor α positive (PDGFRα+) cells. The latter cell-type showed dominant expression of F2r (encodes PAR1) and F2rl1 (encodes PAR2). Contractile and intracellular electrical activities were measured to characterize the integrated responses to PAR activation in whole muscles. Cells were isolated and ICC and PDGFRα+ cells were identified by constitutive expression of fluorescent reporters. Thrombin (PAR1 agonist) and trypsin (PAR2 agonist) caused biphasic responses in colonic muscles: transient hyperpolarization and relaxation followed by repolarization and excitation. The inhibitory phase was blocked by apamin, revealing a distinct excitatory component. Patch clamp studies showed that the inhibitory response was mediated by activation of small conductance calcium-activated K+ channels in PDGFRα+ cells, and the excitatory response was mediated by activation of a Cl− conductance in ICC. SMC contributed little to PAR responses in colonic muscles. In summary, PARs regulate the excitability of colonic muscles; different conductances are activated in each cell-type of the SMC/ICC/PDGFRα+ cells (SIP) syncytium. Motor responses to PAR agonists are integrated responses of the SIP syncytium.This article is protected by copyright. All rights reserved
    The Journal of Physiology 12/2014; 593(5). DOI:10.1113/jphysiol.2014.285148 · 5.04 Impact Factor

  • 6th Annual Sierra Nevada Chapter Symposium, Society of Neuroscience, Reno, Nevada, U.S.A.; 11/2014
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    ABSTRACT: Enteric purinergic motor neurotransmission, acting through P2Y1 receptors (P2Y1R), mediates inhibitory neural control of the intestines. Recent studies have shown that NAD+ and ADP ribose better meet criteria for enteric inhibitory neurotransmitters in colon than ATP or ADP. Here we report that human and murine colon muscles also release uridine adenosine tetraphosphate (Up4A) spontaneously and upon stimulation of enteric neurons. Release of Up4A was reduced by tetrodotoxin, suggesting that at least a portion of Up4A is of neural origin. Up4A caused relaxation (human and murine colons) and hyperpolarization (murine colon) that was blocked by the P2Y1R antagonist, MRS 2500, and by apamin, an inhibitor of Ca2+-activated small-conductance K+ (SK) channels. Up4A responses were greatly reduced or absent in colons of P2ry1−/− mice. Up4A induced P2Y1R–SK-channel–mediated hyperpolarization in isolated PDGFRα+ cells, which are postjunctional targets for purinergic neurotransmission. Up4A caused MRS 2500-sensitive Ca2+ transients in human 1321N1 astrocytoma cells expressing human P2Y1R. Up4A was more potent than ATP, ADP, NAD+, or ADP ribose in colonic muscles. In murine distal colon Up4A elicited transient P2Y1R-mediated relaxation followed by a suramin-sensitive contraction. HPLC analysis of Up4A degradation suggests that exogenous Up4A first forms UMP and ATP in the human colon and UDP and ADP in the murine colon. Adenosine then is generated by extracellular catabolism of ATP and ADP. However, the relaxation and hyperpolarization responses to Up4A are not mediated by its metabolites. This study shows that Up4A is a potent native agonist for P2Y1R and SK-channel activation in human and mouse colon.
    Proceedings of the National Academy of Sciences 10/2014; DOI:10.1073/pnas.1409078111 · 9.67 Impact Factor

Publication Stats

17k Citations
2,136.75 Total Impact Points


  • 1986-2015
    • University of Nevada School of Medicine
      • Department of Pharmacology
      Reno, Nevada, United States
  • 1992-2014
    • University of Nevada, Reno
      • • Department of Physiology and Cell Biology
      • • School of Medicine
      Reno, Nevada, United States
    • St. James's Hospital
      • MedEl Directorate
      Dublin, Leinster, Ireland
  • 2009
    • University of Auckland
      Окленд, Auckland, New Zealand
  • 2004
    • Australian National University
      Canberra, Australian Capital Territory, Australia
  • 1996
    • University of Illinois, Urbana-Champaign
      Urbana, Illinois, United States
  • 1995
    • University of California, Davis
      Davis, California, United States
    • Baylor College of Medicine
      Houston, Texas, United States