Hdl Handle:
http://hdl.handle.net/10675.2/621761
Title:
High glucose treated cells may lead to cellular senescence effecting function of bladder
Authors:
Vincent, Julie; Klee, Nicole; Webb, Clinton
Abstract:
Introduction: Diabetic bladder dysfunctioneffects 30-50% of all diabetespatientsand is characterized by symptoms of overactive and underactive bladder, which greatly effects quality of life.Diabetes is correlated with increased cellular senescence. Senescence is a physiologic phenomenon; however, chronic high levels can lead to tissue dysfunction. Multiple in vitrostudies have shown that high glucose exposure results in an increase in cellular senescent cells.The smooth muscle layer of the bladderis responsible for contraction and relaxation of the bladder; therefore, we hypothesize that primary bladder smooth muscle cells exposed to a high glucose environment will result in an increased number of cellular senescent cells.Methods:Rat primary BSMcells were incubated in normal glucose (4mM), high glucose (22mM), high mannitol (22mM), and bleomycin(+ control). Abeta-galactoside assay was utilized to visualize the presence of senescent cells.Results: Cells treated with high glucose exhibited increased cellular senescent cellscompared to both normal and high mannitol control. Conclusion: We conclude that high glucose exposure increases cellular senescence in primary bladder smooth muscle cells. An increased amount of cellular senescence within the smooth muscle layer of the bladder could contribute to bladder dysfunction as seen with diabetes.
Affiliation:
Department of Physiology; College of Education
Issue Date:
12-Feb-2018
URI:
http://hdl.handle.net/10675.2/621761
Submitted date:
29-JAN-2018 01:34PM
Type:
Poster Presentation
Description:
Presentation given at the 19th Annual Phi Kappa Phi Student Research and Fine Arts Conference
Appears in Collections:
19th Annual PKP Student Research and Fine Arts Conference: Posters

Full metadata record

DC FieldValue Language
dc.contributor.authorVincent, Julieen
dc.contributor.authorKlee, Nicoleen
dc.contributor.authorWebb, Clintonen
dc.date.accessioned2018-02-12T17:19:36Z-
dc.date.available2018-02-12T17:19:36Z-
dc.date.issued2018-02-12-
dc.date.submitted29-JAN-2018 01:34PM-
dc.identifier.urihttp://hdl.handle.net/10675.2/621761-
dc.descriptionPresentation given at the 19th Annual Phi Kappa Phi Student Research and Fine Arts Conferenceen
dc.description.abstractIntroduction: Diabetic bladder dysfunctioneffects 30-50% of all diabetespatientsand is characterized by symptoms of overactive and underactive bladder, which greatly effects quality of life.Diabetes is correlated with increased cellular senescence. Senescence is a physiologic phenomenon; however, chronic high levels can lead to tissue dysfunction. Multiple in vitrostudies have shown that high glucose exposure results in an increase in cellular senescent cells.The smooth muscle layer of the bladderis responsible for contraction and relaxation of the bladder; therefore, we hypothesize that primary bladder smooth muscle cells exposed to a high glucose environment will result in an increased number of cellular senescent cells.Methods:Rat primary BSMcells were incubated in normal glucose (4mM), high glucose (22mM), high mannitol (22mM), and bleomycin(+ control). Abeta-galactoside assay was utilized to visualize the presence of senescent cells.Results: Cells treated with high glucose exhibited increased cellular senescent cellscompared to both normal and high mannitol control. Conclusion: We conclude that high glucose exposure increases cellular senescence in primary bladder smooth muscle cells. An increased amount of cellular senescence within the smooth muscle layer of the bladder could contribute to bladder dysfunction as seen with diabetes.en
dc.subjectdiabetesen
dc.subjectsenescenceen
dc.subjectbladderen
dc.titleHigh glucose treated cells may lead to cellular senescence effecting function of bladderen
dc.typePoster Presentationen
dc.contributor.departmentDepartment of Physiologyen
dc.contributor.departmentCollege of Educationen
dc.contributor.sponsorKlee, Nicoleen
dc.contributor.sponsorDepartment of Physiologyen
dc.contributor.sponsorWebb, Clintonen
dc.contributor.affiliationAugusta Universityen
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