AI Article Synopsis
- Interstitial cystitis/painful bladder syndrome (IC/PBS) causes lower abdominal pain and increased urgency in urination, with research focusing on the role of sphingosine 1-phosphate (S1P) in smooth muscle contractions.
- The study used rat models with cystitis induced by cyclophosphamide, analyzing the contraction of isolated detrusor smooth muscle strips after they were permeabilized.
- Findings revealed that S1P causes increased contractions in cystitis, which can be inhibited by certain chemicals, indicating that sarcoplasmic reticulum and lysosome-related organelles are key players in calcium release for muscle contraction.
Article Abstract
Aims: Interstitial cystitis/painful bladder syndrome (IC/PBS) is characterized by lower abdominal pain and increased frequency and urgency of urine. Sphingosine 1-phosphate (S1P) is a bioactive sphingolipid that plays role in calcium homeostasis in smooth muscle. The intracellular calcium mobilizing secondary messengers are also involved in smooth muscle contraction. The role of intracellular calcium storing depots in S1P-induced contraction was investigated in permeabilized detrusor smooth muscle having cystitis.
Main Methods: IC/PBS was induced by cyclophosphamide injection. The detrusor smooth muscle strips isolated from rats were permeabilized with β-escin.
Key Findings: S1P-induced contraction was increased in cystitis. S1P-induced enhanced contraction was inhibited by cyclopiazonic acid, ryanodine and heparin showing involvement of sarcoplasmic reticulum (SR) calcium stores. Inhibition of S1P-induced contraction by bafilomycin and NAADP suggested the participation of lysosome-related organelles.
Significance: IC/PBS triggers S1P-induced increase in intracellular calcium from SR and lysosome-related organelles in permeabilized detrusor smooth muscle.
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| http://dx.doi.org/10.1016/j.lfs.2023.121651 | DOI Listing |
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