Glenn D Prestwich

University of Utah, Salt Lake City, Utah, United States

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Publications (573)2300.62 Total impact

  • Glenn D Prestwich, Kevin E Healy
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    ABSTRACT: Regenerative medicine is now coming of age. Many attempts at cell therapy have failed to show significant efficacy, and the umbrella term 'stem cell therapy' is perceived in some quarters as hype or just expensive and unnecessary medical tourism. Here we present a short editorial in three parts. First, we examine the importance of using a semisynthetic extracellular matrix (ECM) mimetic, or sECM, to deliver and retain therapeutic cells at the site of administration. Second, we describe one approach in which biophysical and biochemical properties are tailored to each tissue type, which we call "design for optimal functionality." Third, we describe an alternative approach to sECM design and implementation, called "design for simplicity," in which a deconstructed, minimalist sECM is employed and biology is allowed to perform the customization in situ. We opine that an sECM, whether minimal or instructive, is an essential contributor to improve the outcomes of cell-based therapies.
    Expert opinion on biological therapy. 01/2015; 15(1):3-7.
  • Biomaterials 01/2015; 38:108. · 8.31 Impact Factor
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    ABSTRACT: Significance: Hyaluronic acid (HA, or hyaluronan) is a ubiquitous naturally occurring polysaccharide that plays a role in virtually all tissues in vertebrate organisms. HA-based hydrogels have wound-healing properties, support cell delivery, and can deliver drugs locally. Recent Advances: A few HA hydrogels can be customized for composition, physical form, and biomechanical properties. No clinically approved HA hydrogel allows for in vivo crosslinking on administration, has a tunable gelation time to meet wound-healing needs, or enables drug delivery. Recently, a thiolated carboxymethyl HA (CMHA-S) was developed to produce crosslinked hydrogels, sponges, and thin films. CMHA-S can be crosslinked with a thiol-reactive crosslinker or by oxidative disulfide bond formation to form hydrogels. By controlled crosslinking, the shape and form of this material can be manipulated. These hydrogels can be subsequently lyophilized to form sponges or air-dried to form thin films. CMHA-S films, liquids, and gels have been shown to be effective in vivo for treating various injuries and wounds in the eye in veterinary use, and are in clinical development for human use. Critical Issues: Better clinical therapies are needed to treat ophthalmic injuries. Corneal wounds can be treated using this HA-based crosslinked hydrogel. CMHA-S biomaterials can help heal ocular surface defects, can be formed into a film to deliver drugs for local ocular drug delivery, and could deliver autologous limbal stem cells to treat extreme ocular surface damage associated with limbal stem cell deficiencies. Future Directions: This CMHA-S hydrogel increases the options that could be available for improved ocular wound care, healing, and regenerative medicine.
    Advances in wound care. 11/2014; 3(11):708-716.
  • Aixia Han, Xiaohui Liu, Glenn D. Prestwich, Ling Zang
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    ABSTRACT: A new water-soluble fluorescent perylene sensor was synthesized and compared to the previous non-aqueous sensors. The new sensor, MSI-1-9, exhibits sensitive and selective detection of mercuric ion (Hg2+) directly in aqueous solution through fluorescence quenching. The detection was not affected by the coexistence of other common divalent metal ions. MSI-1-9 possesses the necessary criteria for use in affordable, real-time measurement of Hg2+ in environmental water samples, permitting its incorporation into a portable mercury detection kit.
    Sensors and Actuators B Chemical 07/2014; 198:274–277. · 3.84 Impact Factor
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    ABSTRACT: Ewing sarcoma is a malignant pediatric bone and soft tissue tumor. Although the 5-year survival rate of localized disease approaches 75%, the prognosis of metastatic and/or therapy-resistant disease remains dismal despite the wide use of aggressive therapeutic strategies. We previously reported that high expression of glutathione S-transferase M4 (GSTM4) in primary tumors correlates with poor patient outcomes. GSTM4 is required for oncogenic transformation and mediates resistance to chemotherapeutic drugs in Ewing sarcoma cells. Here, we performed RNA-sequencing analyses of Ewing sarcoma cells and combined our results with publicly available datasets to demonstrate that GSTM4 is a major GST specifically expressed in Ewing sarcoma. Pharmacological inhibition of GSTM4 activity using a pan GST inhibitor, 6-(7-nitro-2,1,3-benzoxadiazol-4-ylthio) hexanol (NBDHEX), significantly limited cellular proliferation and oncogenic transformation of Ewing sarcoma cells. Moreover, combined use of NBDHEX and etoposide synergistically increased cytotoxicity, suggesting a role for GSTM4 as an inhibitor of apoptosis. Mechanistic studies revealed that GSTM4 limits apoptosis owing to its ability to interact with Apoptosis Signal-regulating Kinase 1 (ASK1) and inhibit signaling via the c-Jun N-terminal Kinase axis. To exploit our observation that GSTM4 expression is specifically up-regulated in Ewing sarcoma, we tested the effect of a GSTM4-activated anti-cancer agent, O(2)-(2,4-dinitrophenyl) 1-[(4-ethoxycarbonyl)piperazin-1-yl]diazen-1-ium-1,2-diolate or JS-K, on tumor growth and survival. We found that JS-K robustly decreased Ewing sarcoma cell viability and xenograft tumor growth and improved overall survival of xenograft mice. Our data suggest that GSTM4 is a novel therapeutic target for the treatment of high GSTM4-expressing Ewing sarcoma. Strategies that combine standard chemotherapy with agents that inhibit GSTM4, that are activated by GSTM4, or that block GSTM4/ASK1 interactions, can potentially be more specific and/or efficacious than standard therapeutic approaches.
    Frontiers in Pediatrics 01/2014; 2:83.
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    ABSTRACT: Changes in tissue and organ stiffness occur during development and are frequently symptoms of disease. Many cell types respond to the stiffness of substrates and neighboring cells in vitro and most cell types increase adherent area on stiffer substrates that are coated with ligands for integrins or cadherins. In vivo cells engage their extracellular matrix (ECM) by multiple mechanosensitive adhesion complexes and other surface receptors that potentially modify the mechanical signals transduced at the cell/ECM interface. Here we show that hyaluronic acid (also called hyaluronan or HA), a soft polymeric glycosaminoglycan matrix component prominent in embryonic tissue and upregulated during multiple pathologic states, augments or overrides mechanical signaling by some classes of integrins to produce a cellular phenotype otherwise observed only on very rigid substrates. The spread morphology of cells on soft HA-fibronectin coated substrates, characterized by formation of large actin bundles resembling stress fibers and large focal adhesions resembles that of cells on rigid substrates, but is activated by different signals and does not require or cause activation of the transcriptional regulator YAP. The fact that HA production is tightly regulated during development and injury and frequently upregulated in cancers characterized by uncontrolled growth and cell movement suggests that the interaction of signaling between HA receptors and specific integrins might be an important element in mechanical control of development and homeostasis.
    Biomaterials 10/2013; · 8.31 Impact Factor
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    ABSTRACT: Rationale: Bioactive lipid mediators, derived from membrane lipid precursors, are released into the airway and airspace where they bind high affinity cognate receptors and may mediate asthma pathogenesis. Lysophosphatidic acid (LPA), a bioactive lipid mediator generated by the enzymatic activity of extracellular autotaxin (ATX), binds LPA receptors resulting in an array of biological actions on cell proliferation, migration, survival, differentiation and motility, and therefore could mediate asthma pathogenesis. Objectives: To define a role for the ATX-LPA pathway in human asthma pathogenesis and a murine model of allergic lung inflammation. Methods: We investigated the profiles of LPA molecular species and the level of ATX exoenzyme in BAL fluids of human asthmatics subjected to sub-segmental broncho-provocation with allergen. We interrogated the role of the ATX-LPA pathway in allergic lung inflammation using a murine allergic asthma model in ATX-LPA pathway-specific genetically modified mice. Measurements and Main Results: Sub-segmental broncho-provocation with allergen in mild asthmatics resulted in a remarkable increase in BAL fluid levels of LPA enriched in polyunsaturated 22:5 and 22:6 fatty acids in association with increased concentrations of ATX protein. Using a triple allergen mouse asthma model, we showed that ATX over-expressing transgenic mice had a more severe asthmatic phenotype, whereas blocking ATX activity and knockdown of the LPA2 receptor in mice produced a marked attenuation of Th2 cytokines and allergic lung inflammation. Conclusions: The ATX-LPA pathway plays a critical role in the pathogenesis of asthma. These preclinical data indicate that targeting the ATX-LPA pathway could be an effective anti-asthma treatment strategy.
    American Journal of Respiratory and Critical Care Medicine 09/2013; · 11.04 Impact Factor
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    ABSTRACT: Chondroitin sulfate (CS) proteoglycans (CSPGs) are known to be primary inhibitors of neuronal regeneration at scar sites. However, a variety of CSPGs are also involved in neuronal growth and guidance at other physiological stages. Sulfation patterns of CS chains influence their interactions with various growth factors in the central nervous system (CNS), thus influencing neuronal growth, inhibition and pathfinding. This report demonstrates the use of differentially sulfated CS chains for neuronal navigation. Surface-immobilized patterns of CS glycosaminoglycan chains were used to determine neuronal preference towards specific sulfations of five CS variants: CS-A, CS-B (dermatan sulfate), CS-C, CS-D and CS-E. Neurons preferred CS-A, CS-B and CS-E and avoided CS-C containing lanes. In addition, significant alignment of neurites was observed using underlying lanes containing CS-A, CS-B and CS-E chains. In order to utilize differential preference of neurons towards the CS variants, a binary combinations of CS chains were created by backfilling a neuro-preferred CS variant between the microcontact printed lanes of CS-C stripes, which are avoided by neurons. The neuronal outgrowth results demonstrate for the first time that a combination of sulfation variants of CS chains without any protein component of CSPG is sufficient for directing neuronal outgrowth. Biomaterials with surface immobilized GAG chains could find numerous applications as bridging devices for tackling CNS injuries where directional growth of neurons is critical for recovery.
    Journal of the American Chemical Society 08/2013; · 10.68 Impact Factor
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    ABSTRACT: To elucidate pathways in bladder inflammation, we employed our physiologically relevant LL-37 induced cystitis model. Based on inflammatory studies involving other organ systems implicating the receptor for advanced glycation end-products (RAGE), we first hypothesized that RAGE is critically involved in LL-37 induced cystitis. We further hypothesized a common RAGE ligand - high mobility group box 1 (HMGB1) is up-regulated in bladders challenged with LL-37. Finally, we hypothesized NF-κB dependent inflammatory genes are activated in LL-37 induced cystitis. Testing our first hypothesis, C57Bl/6 mice were challenged with either saline (control) or 320 μM of LL-37 intravesically for 1 hr. After 12 or 24 hours, tissues were examined with immunohistochemistry (IHC) for RAGE, and both mRNA and protein isolation for respective qRT-PCR and Western Blot analysis. Our second hypothesis was tested by employing HMGB1 IHC. Testing our final hypothesis, qRT-PCR was performed investigating five genes: TNFα, IL-6, IL-1β, GM-CSF, COX-2. In control and LL-37 challenged tissues, IHC for RAGE revealed similar qualitative expression. Evaluation with qRT-PCR and Western Blot for RAGE revealed diminished expression at the mRNA and protein level within LL-37 challenged bladders. IHC for HMGB1 revealed a moderate qualitative increase within LL-37 challenged tissues. Finally, with the exception of TNF α, all NF- κB dependent inflammatory genes yielded substantial up-regulation. We have employed our LL-37 induced cystitis model to gain insight towards a possible mechanistic pathway involved in bladder inflammation. This work provides data for future studies involving the inflammatory ligand HMGB1, RAGE, and receptor pathways that activate NF-κB.
    Advances in Bioscience and Biotechnology 08/2013; 4(8B):1-8.
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    ABSTRACT: Bone morphogenetic protein-2 (BMP-2) is known to enhance fracture healing when delivered via a bovine collagen sponge. However, collagen rapidly releases BMP-2 with a high burst phase that is followed by a low sustained phase. As a result, supra-physiological doses of BMP-2 are often required to successfully treat bone defects. High BMP-2 dosing can introduce serious side effects that include edema, bone overgrowth, cyst-like bone formation and significant inflammation. As the release behaviour of BMP-2 carriers significantly affects the efficacy of fracture healing, we sought to compare the influence of two BMP-2 delivery matrices with contrasting release profiles on BMP-2 bioactivity and ectopic bone formation. We compared a thiol-modified hyaluronan (Glycosil(TM)) hydrogel that exhibits a low burst followed by a sustained release of BMP-2 to a collagen sponge for the delivery of three different doses of BMP-2, the bioactivities of released BMP-2 and ectopic bone formation. Analysis of bone formation by micro-computed tomography revealed that low burst followed by sustained release of BMP-2 from a hyaluronan hydrogel induced up to 456% more bone compared to a BMP-2 dose-matched collagen sponge that has a high burst and sustained release. This study demonstrates that BMP-2 released with a low burst followed by a sustained release of BMP-2 is more desirable for bone formation. This highlights the therapeutic potential of hydrogels, particularly hyaluronan-based, for the delivery of BMP-2 for the treatment of bone defects and may help abrogate the adverse clinical effects associated with high dose growth factor use.
    Acta biomaterialia 07/2013; · 5.68 Impact Factor
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    ABSTRACT: The interfacial physical properties of bis(monoacylglycero)phosphate (BMP) and its derivatives with three oleoyl chains (hemi-BDP) and four oleoyl chains (bis(diacylglycero)phosphate, BDP) were investigated using Langmuir monomolecular films. The mean molecular area of BMP at the collapse surface pressure (45mN m(-1)) was similar to those measured with other phospholipids bearing two acyl chains (66 and 59.6Å(2) molecule(-1) at pH 5.5 and 8.0, respectively). In Hemi-BDP and BDP, the mean molecular area increased by 26 and 35Å(2) molecule(-1) per additional acyl chain at pH 5.5 and 8.0, respectively. When BMP was added to a phospholipid mixture mimicking late endosome membrane composition at pH 8.0, the mean phospholipid molecular area increased by 7% regardless of the surface pressure. In contrast, the variation in molecular area was surface pressure-dependent at pH 5.5, a pH value close to that of intra-endosomal content. BMP and hemi-BDP, but not BDP, were hydrolyzed by pancreatic lipase-related protein 2 (PLRP2), which exhibits phospholipase A(1) activity. At pH 5.5, the maximum activities of PLRP2 on BMP were recorded at high surface pressures (25-35mN/m). At pH 8.0, the PLRP2 activity vs. surface pressure showed a bell-shaped curve with maximum activities at 15mN/m for both BMP and hemi-BDP. This is a new activity for this enzyme which could degrade cellular BMP since both human PLRP2 (HPLRP2) and BMP were localized in human monocytic THP-1 cells. This is the first report on the cellular localization of HPLRP2 in human monocytes.
    Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids 04/2013; 1811(7-8):419-30. · 4.13 Impact Factor
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    ABSTRACT: OBJECTIVES/HYPOTHESIS: To determine the resorption rate and biocompatibility characteristics of novel cross-linked hydrogel ventilation tubes and varied formulations of polyester ventilation tubes in a Chinchilla model. STUDY DESIGN: Animal Study. METHODS: Three cross-linked glycosaminoglycan hydrogel ventilation tubes fabricated by cross-linking thiol-modified chondroitin sulfate or thiol-modified carboxymethylated hyaluronic acid, four different polyester ventilation tubes (poly L-lactide [PLA], 50/50 poly D,L-lactide-co-glycolide [PLGA], and silver-impregnated versions of PLA and PLGA tubes) were placed into the tympanic membranes of chinchillas. Commercially available fluoroplastic ventilation tubes were placed in the contralateral ear of each animal to serve as a control. Integrity of the tubes was assessed by weekly otoscopy. Biocompatibility was assessed by auditory brainstem response, by otoscopic and histologic examination of the tympanic membrane at the tube site. RESULTS: The hydrogel tubes had very short resorption times that expanded and enlarged the myringotomy site. PLGA and silver-coated PLGA tubes maintained their integrity in the tympanic membrane for similar durations of 18.9 ± 6.4 days and 21.0 ± 6.0 days, respectively. The silver-coated PLGA tubes had lower neutrophil and fibrosis scores than PLGA tubes. PLA tubes demonstrated equivalent findings to commercially available nonresorbable tubes with respect to otoscopic findings, auditory brainstem response thresholds, and histologic inflammatory scores. CONCLUSIONS: Resorbable polyester pressure equalization tubes demonstrate predictable resorption behavior and similar biocompatibility characteristics when compared with nonresorbable tubes. Silver modification may confer some stability to PLGA tubes. Hydrogel tubes have very short resorption times, tend to enlarge the myringotomy site, and show greater inflammatory changes.
    The Laryngoscope 03/2013; · 1.98 Impact Factor
  • Glenn D Prestwich
    Science translational medicine 01/2013; 5(169):169ed2. · 10.76 Impact Factor
  • Guowei Jiang, Asuka Inoue, Junken Aoki, Glenn D Prestwich
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    ABSTRACT: We describe an efficient synthesis of metabolically stabilized sn-2 radyl phosphorothioate analogs of lysophosphatidic acid (LPA), and the determination of the agonist activity of each analog for the six LPA receptors (LPA(1-6)) using a recently developed TGFα shedding assay. In general, the sn-2 radyl OMPT analogs showed similar agonist activities to the previous 1-oleoyl-2-O-methyl-glycerophosphothioate (sn-1 OMPT) analogs for LPA(1-6) receptors. In most cases, the sn-2 radyl-OMPT analogs were more potent agonists than LPA itself. Most importantly, sn-2 alkyl OMPT analogs were very potent LPA(5) and LPA(6) agonists. The availability of sn-2 radyl OPMT analogs further refines the structure-activity relationships for ligand-receptor interactions for this class of GPCRs.
    Bioorganic & medicinal chemistry letters 01/2013; · 2.65 Impact Factor
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    ABSTRACT: PURPOSE: Our aim was to establish the physiologic relevance of LL-37 induced bladder inflammation. We hypothesized human urinary LL-37 levels are elevated in pediatric spina bifida patients. We further hypothesized within our mouse model that LL-37 induced inflammation occurs via urothelial binding and is dose dependent. Finally, we hypothesized LL-37 induced inflammation involves mast cells. METHODS: Testing our first hypothesis, urine samples were obtained from pediatric SB (n=56) and normal (n=22) patients with LL-37 levels measured by ELISA. Our second hypothesis was tested in C57Bl/6 mice challenged with LL-37 intravesically for 1 hr. Seven concentrations of LL-37 were tested. After 24 hours, tissues were examined histologically and myeloperoxidase assay to quantitate inflammation. In separate experiments, fluorescent LL-37 was instilled and tissues obtained immediately (t=0) and at 24 hours (t=24). Testing our final hypothesis, immunohistochemistry for mast cell tryptase was performed and evaluating 5 hpf's for each bladder to yield a mean number of mast cells/mm(2). RESULTS: Urinary LL-37 levels were 89-fold higher in SB patients. Mouse LL-37 dose escalation experiments yielded increased inflammation with higher LL-37 concentrations. Fluorescent LL-37 demonstrated global urothelial binding at t=0, but was not visible at t=24. IHC for tryptase revealed infiltration of mast cells in all tissue layers. Higher concentrations of LL-37 challenge led to significantly higher levels of mast cell infiltration. CONCLUSIONS: Urinary LL-37 levels were significantly elevated in pediatric SB patients. We innovatively demonstrated LL-37 could elicit profound, dose dependent bladder inflammation involving the urothelium. Finally, the propagation of inflammation involves mast cells.
    The Journal of urology 01/2013; · 3.75 Impact Factor
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    ABSTRACT: Compounds, compositions and methods useful for treating ocular diseases are provided. In particular, antagonists of TRPV4, their synthesis, pharmaceutical compositions thereof and methods of treating ocular diseases such as glaucoma, are disclosed. Compounds of the invention include N-(3-(trifluoromethyl)phenyl )-2-methyl-1-(3-morpholinopropyl )-5-phenyl-1 H-pyrrole-3-carboxamide, as well as other 2-phenyl-pyrrole carboxamide derivates and indole carboxamide derivatives.
    Ref. No: WO 2013169396 A1, Year: 01/2013
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    ABSTRACT: Rheumatoid arthritis (RA) is a destructive arthropathy with systemic manifestations, characterized by chronic synovial inflammation. Under the influence of the pro-inflammatory milieu synovial fibroblasts (SFs), the main effector cells in disease pathogenesis become activated and hyperplastic while releasing a number of signals that include pro-inflammatory factors and tissue remodeling enzymes. Activated RA SFs in mouse or human arthritic joints express significant quantities of autotaxin (ATX), a lysophospholipase D responsible for the majority of lysophosphatidic acid (LPA) production in the serum and inflamed sites. Conditional genetic ablation of ATX from SFs resulted in attenuation of disease symptoms in animal models, an effect attributed to diminished LPA signaling in the synovium, shown to activate SF effector functions. Here we show that administration of 1-bromo-3(S)-hydroxy-4-(palmitoyloxy)butyl-phosphonate (BrP-LPA), a metabolically stabilized analog of LPA and a dual function inhibitor of ATX and pan-antagonist of LPA receptors, attenuates collagen induced arthritis (CIA) development, thus validating the ATX/LPA axis as a novel therapeutic target in RA.
    PLoS ONE 01/2013; 8(7):e70941. · 3.53 Impact Factor
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    ABSTRACT: Autotaxin (ATX), an autocrine motility factor that is highly upregulated in metastatic cancer, is a lysophospholipase D enzyme that produces the lipid second messenger lysophosphatidic acid (LPA) from lysophosphatidylcholine (LPC). Dysregulation of the lysolipid signaling pathway is central to the pathophysiology of numerous cancers, idiopathic pulmonary fibrosis, rheumatoid arthritis, and other inflammatory diseases. Consequently, the ATX/LPA pathway has emerged as an important source of biomarkers and therapeutic targets. Herein we describe development and validation of a fluorogenic analog of LPC (AR-2) that enables visualization of ATX activity in vivo. AR-2 exhibits minimal fluorescence until it is activated by ATX, which substantially increases fluorescence in the near-infrared (NIR) region, the optimal spectral window for in vivo imaging. In mice with orthotopic ATX-expressing breast cancer tumors, ATX activated AR-2 fluorescence. Administration of AR-2 to tumor-bearing mice showed high fluorescence in the tumor and low fluorescence in most healthy tissues with tumor fluorescence correlated with ATX levels. Pretreatment of mice with an ATX inhibitor selectively decreased fluorescence in the tumor. Together these data suggest that fluorescence directly correlates with ATX activity and its tissue expression. The data show that AR-2 is a non-invasive and selective tool that enables visualization and quantitation of ATX-expressing tumors and monitoring ATX activity in vivo.
    PLoS ONE 01/2013; 8(11):e79065. · 3.53 Impact Factor
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    Glenn D Prestwich
    Biomatter. 01/2013; 3(1).
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    ABSTRACT: Interstitial cystitis (IC), often referred to in combination with painful bladder syndrome, is a chronic inflammatory disease of the bladder. Current therapies primarily focus on replenishing urothelial glycosaminoglycan (GAG) layer using GAG analogs and managing pain with supportive therapies. However, the elusive etiology of IC and the lack of animal models to study the disease have been major hurdles developing more effective therapeutics. Previously, we showed an increased urinary concentration of antimicrobial peptide LL-37 in spina bifida patients and used LL-37 to develop a mouse model of cystitis that mimics important clinical findings of IC. Here we investigate (1) the molecular mechanism of LL-37 induced cystitis in cultured human urothelial cells and in mice, (2) the protective effects of GM-0111, a modified GAG, within the context of this mechanism, (3) the physiological and molecular markers that correlate with the severity of the inflammation, and (4) the protective effects of several GAGs using these biomarkers in our LL-37 induced cystitis model. We find that LL-37 quickly induces release of ATP and apoptosis in the urothelium. These changes can be inhibited by a chemically-modified GAG, GM-0111. Furthermore, we also find that GAG analogs provide varying degrees of protection against LL-37 challenge in mice. These findings suggest that GM-0111 and possibly GAG molecules prevent the development of cystitis by blocking the apoptosis and the concurrent release of ATP from the urothelium.
    PLoS ONE 01/2013; 8(10):e77854. · 3.53 Impact Factor

Publication Stats

15k Citations
2,300.62 Total Impact Points


  • 1997–2014
    • University of Utah
      • • Department of Medicinal Chemistry
      • • Department of Pharmaceutics and Pharmaceutical Chemistry
      • • Department of Surgery
      Salt Lake City, Utah, United States
  • 2012–2013
    • Biomedical Sciences Research Center Alexander Fleming
      • Institute of Immunology
      Vári, Attiki, Greece
  • 2009–2012
    • University of Wisconsin, Madison
      • • Division of Otolaryngology-Head and Neck Surgery
      • • Department of Surgery
      Madison, MS, United States
  • 1982–2012
    • University of North Carolina at Chapel Hill
      • • Department of Cell Biology and Physiology
      • • Department of Biology
      Chapel Hill, NC, United States
  • 2011
    • North Carolina State University
      Raleigh, North Carolina, United States
    • University of Pennsylvania
      • Department of Bioengineering
      Philadelphia, PA, United States
  • 2010–2011
    • Tufts University
      • Department of Biomedical Engineering
      Medford, MA, United States
    • Salt Lake City Community College
      Salt Lake City, Utah, United States
    • University of Tennessee
      • Department of Chemistry
      Knoxville, TN, United States
  • 2000–2010
    • Simon Fraser University
      • Department of Chemistry
      Burnaby, British Columbia, Canada
  • 1978–2010
    • Stony Brook University
      • • Department of Chemistry
      • • Department of Biomedical Engineering
      • • Department of Biochemistry and Cell Biology
      • • Department of Physiology and Biophysics
      Stony Brook, NY, United States
  • 2008
    • Medical University of South Carolina
      • Department of Regenerative Medicine and Cell Biology
      Charleston, SC, United States
  • 2006–2008
    • Oregon State University
      Corvallis, Oregon, United States
    • University of Denver
      Denver, Colorado, United States
  • 2006–2007
    • University of Toronto
      • Department of Chemical Engineering and Applied Chemistry
      Toronto, Ontario, Canada
  • 1991–2007
    • Johns Hopkins University
      • Department of Neuroscience
      Baltimore, Maryland, United States
  • 2003–2006
    • Echelon Biosciences Incorporated
      Salt Lake City, Utah, United States
  • 2005
    • Utah State University
      • Department of Biology
      Logan, OH, United States
  • 2004
    • Columbia University
      • Department of Biological Sciences
      New York City, NY, United States
    • Brigham Young University - Provo Main Campus
      • Department of Chemical Engineering
      Provo, UT, United States
    • Icahn School of Medicine at Mount Sinai
      Manhattan, New York, United States
  • 1979–2004
    • State University of New York
      New York City, New York, United States
  • 1996–1999
    • University of Alabama at Birmingham
      • Department of Cell, Developmental and Integrative Biology (CDIB)
      Birmingham, Alabama, United States
  • 1975–1999
    • Cornell University
      • New York State Agricultural Experiment Station, Geneva
      Ithaca, New York, United States
  • 1995
    • Stony Brook University Hospital
      Stony Brook, New York, United States
    • York University
      • Department of Biology
      Toronto, Ontario, Canada
  • 1990–1994
    • University of Washington Seattle
      Seattle, Washington, United States
    • Semmelweis University
      Budapeŝto, Budapest, Hungary
  • 1992–1993
    • Johns Hopkins Medicine
      • Department of Neuroscience
      Baltimore, MD, United States
  • 1984–1993
    • Harvard University
      • Museum of Comparative Zoology
      Cambridge, Massachusetts, United States
  • 1988
    • State University of New York College of Environmental Science and Forestry
      • Department of Chemistry
      Syracuse, New York, United States
  • 1981
    • Howard University
      Washington, West Virginia, United States
    • CUNY Graduate Center
      New York City, New York, United States
  • 1980
    • Forest Research Institute Malaysia (FRIM)
      Kuala Lumpor, Kuala Lumpur, Malaysia