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Related Concept Videos

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The urinary bladder is a hollow, muscular sac that temporarily stores urine before it is expelled from the body. It can hold approximately 600 mL of urine prior to micturition. The bladder is retroperitoneal and located behind the pubic symphysis in the pelvic floor.
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Urination, or micturition involves the coordination of the bladder's detrusor muscle and two sphincters to ensure controlled bladder emptying.
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Related Experiment Video

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Urinary bladder mucosal responses to ischemia.

Masataka Sunagawa1, Amanda Wolf-Johnston, Masanori Nomiya

  • 1Departments of Medicine, University of Pittsburgh School of Medicine, A 1217 Scaife Hall, 3550 Terrace Street, Pittsburgh, PA, 15261, USA.

World Journal of Urology
|April 15, 2014
PubMed
Summary
This summary is machine-generated.

Chronic bladder ischemia in rats significantly increases urothelium (UT) and lamina propria (LP) proteins involved in barrier function and cell communication. Increased vimentin in the LP suggests altered cell interactions contribute to bladder changes.

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Area of Science:

  • Urology
  • Cell Biology
  • Ischemic Medicine

Background:

  • Chronic bladder ischemia can lead to significant physiological changes in the urinary bladder.
  • Understanding protein expression alterations is crucial for elucidating the mechanisms of bladder dysfunction following ischemia.

Purpose of the Study:

  • To investigate the expression of cellular proteins in the urothelium (UT) and lamina propria (LP) of rat urinary bladders after chronic ischemia.
  • To identify proteins involved in barrier function, remodeling, repair, and intercellular communication that are affected by ischemia.

Main Methods:

  • Adult Sprague-Dawley rats underwent chronic bladder ischemia or sham procedures.
  • Immunocytochemistry was used to assess lamina propria (LP) vimentin-immunoreactive (IR) cells and connexins (Cx26, Cx43).
  • Western immunoblotting or ELISA analyzed proteins related to UT barrier and sensory functions, including ZO-1, nerve growth factor, and norepinephrine.

Main Results:

  • Chronic bladder ischemia significantly increased LP-vimentin-IR cells compared to controls.
  • Expression of gap junction proteins Cx26 and Cx43 in the bladder UT was elevated post-ischemia.
  • Increased expression of the junctional marker ZO-1 was observed (p < 0.05).
  • Nerve growth factor and norepinephrine showed non-significant increases.

Conclusions:

  • Chronic ischemia induces alterations in multiple proteins within the UT and LP.
  • These protein changes impact bladder barrier function, remodeling, repair, and intercellular communication.
  • Elevated LP-vimentin-IR cells indicate that modified cell-cell interactions may contribute to ischemia-induced bladder activity changes.