About: Transgenic Mice Expressing MCP-1 by the Urothelium Demonstrate Bladder Hypersensitivity, Pelvic Pain and Voiding Dysfunction: A Multidisciplinary Approach to the Study of Chronic Pelvic Pain Research Network Animal Model Study

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About: Transgenic Mice Expressing MCP-1 by the Urothelium Demonstrate Bladder Hypersensitivity, Pelvic Pain and Voiding Dysfunction: A Multidisciplinary Approach to the Study of Chronic Pelvic Pain Research Network Animal Model Study Goto Sponge NotDistinct Permalink

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Transgenic Mice Expressing MCP-1 by the Urothelium Demonstrate Bladder Hypersensitivity, Pelvic Pain and Voiding Dysfunction: A Multidisciplinary Approach to the Study of Chronic Pelvic Pain Research Network Animal Model Study
Creator	Wang, Xu Bradley, Catherine Kreder, Karl Luo, Yi Lutgendorf, Susan Schrepf, Andrew Wang, Yaoqin Xu, Suming O'donnell, Michael
Source	Medline; PMC
abstract	Monocyte chemoattractant protein-1 (MCP-1) is one of the key chemokines that play important roles in diverse inflammatory and chronic pain conditions. Interstitial cystitis/bladder pain syndrome (IC/BPS) is a chronic and debilitating inflammatory condition of the urinary bladder characterized by the hallmark symptoms of pelvic pain and voiding dysfunction. To facilitate IC/BPS research, we used transgenic technology to develop a novel urothelial MCP-1 secretion mouse model (URO-MCP-1). A transgene consisting of the uroplakin II gene promoter and the mouse MCP-1 coding sequence with a secretory element was constructed and microinjected. URO-MCP-1 mice were found to express MCP-1 mRNA in the bladder epithelium and MCP-1 protein in the urine, and developed bladder inflammation 24 hours after intravesical administration of a single sub-noxious dose of lipopolysaccharide (LPS). The inflamed bladders of URO-MCP-1 mice exhibited elevated mRNAs for interleukin (IL)-1ß, IL-6, substance P precursor, and nerve growth factor as well as increased macrophage infiltration. In parallel with these phenotypic changes, URO-MCP-1 mice manifested significant functional changes at days 1 and 3 after cystitis induction. These functional changes included pelvic pain as measured by von Frey filament stimulation and voiding dysfunction (increased urinary frequency, reduced average volume voided per micturition, and reduced maximum volume voided per micturition) as measured by micturition cages. Micturition changes remained evident at day 7 after cystitis induction, although these changes were not statistically significant. Control wild-type C57BL/6 mice manifested no clear changes in histological, biochemical and behavioral features after similar cystitis induction with LPS. Taken together, our results indicate that URO-MCP-1 mice are hypersensitive to bladder irritants such as LPS and develop pelvic pain and voiding dysfunction upon cystitis induction, providing a novel model for IC/BPS research.
has issue date	2016-09-29(xsd:dateTime)
bibo:doi	10.1371/journal.pone.0163829
bibo:pmid	27684718
has license	cc-by
sha1sum (hex)	2ebb6c8bf24d0955f26398dcc7653b0f6fb5c9f7
schema:url	https://doi.org/10.1371/journal.pone.0163829
resource representing a document's title	Transgenic Mice Expressing MCP-1 by the Urothelium Demonstrate Bladder Hypersensitivity, Pelvic Pain and Voiding Dysfunction: A Multidisciplinary Approach to the Study of Chronic Pelvic Pain Research Network Animal Model Study
has PubMed Central identifier	PMC5042429
has PubMed identifier	27684718
schema:publication	PLoS One
resource representing a document's body	covid:2ebb6c8bf24d0955f26398dcc7653b0f6fb5c9f7#body_text
is schema:about of	named entity 'STUDY' named entity 'APPROACH' named entity 'Frey' named entity 'play' named entity 'parallel' named entity 'inflammatory' named entity 'secretion' named entity 'intravesical' named entity 'inflammatory' named entity 'model' named entity 'Pain' named entity 'Animal' named entity 'Pain' named entity 'Mice' named entity 'CHRONIC PAIN' named entity 'CHANGES' named entity 'CONTROL' named entity 'BLADDER INFLAMMATION' named entity 'IRRITANTS' named entity 'OUR' named entity 'CAGES' named entity 'TAKEN' named entity 'MAXIMUM' named entity 'IL-6' named entity 'LPS' named entity 'DIVERSE' named entity 'RESEARCH' named entity 'BEHAVIORAL' named entity 'SIMILAR' named entity 'CONDITION' named entity 'CHARACTERIZED' named entity 'VOLUME' named entity 'REDUCED' named entity 'FREY' named entity 'FILAMENT' named entity 'STATISTICALLY SIGNIFICANT' named entity 'KEY' named entity 'STIMULATION' named entity 'UROPLAKIN II' named entity 'VOIDING' named entity 'CHEMOKINES' named entity 'SECRETION' named entity 'MOUSE MODEL' named entity 'TECHNOLOGY' named entity 'HYPERSENSITIVE' named entity 'MEASURED' named entity 'CHRONIC' named entity 'INFLAMMATORY' named entity 'HISTOLOGICAL' named entity 'SECRETORY' named entity 'AVERAGE' named entity 'MICE' named entity 'BLADDER EPITHELIUM' named entity 'MICTURITION' named entity 'DOSE' named entity 'INFLAMED' named entity 'C57BL' named entity 'MONOCYTE CHEMOATTRACTANT PROTEIN-1' named entity 'ROLES' named entity 'INTRAVESICAL ADMINISTRATION' named entity 'TO EXPRESS' named entity 'PELVIC PAIN' named entity 'DYSFUNCTION' named entity 'NETWORK' named entity 'MODEL' named entity 'PROTEIN ' named entity 'PLAY' named entity 'FOUND' named entity 'CODING SEQUENCE' named entity 'NOVEL' named entity 'SUB-' named entity 'DAY 7' named entity 'FEATURES'

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