Over expression of smooth muscle thin filament associated proteins in the bladder wall of diabetics
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Published on: August 18, 2014
Anita S Mannikarottu1, Arun K Changolkar, Michael E Disanto
1Division of Urology, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Purpose:
The thin filament associated proteins caldesmon, tropomyosin and calponin have been shown to modulate actin-myosin interaction, actomyosin adenosine triphosphatase and contraction in smooth muscle. This study was performed to determine whether the expression of these proteins is altered in diabetes induced decrease in the contractility of bladder wall smooth muscle.
Materials And Methods:
Detrusor samples were obtained from New Zealand White male rabbits with alloxan induced diabetes, and from age and sex matched control rabbits. In addition, a bladder myocyte cell line, which continues to express smooth muscle phenotype, was exposed to either normal (5 mM) or high (50 mM) concentrations of glucose. The levels of expression of the thin filament associated proteins were determined at the mRNA and protein levels by reverse transcriptase-polymerase chain reaction and Western blotting, respectively.
Results:
Detrusor smooth muscle tissue from rabbits with alloxan induced diabetes showed over expression of thin filament associated proteins, calponin, tropomyosin and caldesmon when compared with that of the control. Similar up-regulation was seen also in bladder myocytes in cultures treated with 50 mM glucose, indicating that the high glucose induced the changes.
Conclusions:
Our results suggest that the increased expression of thin filament proteins, calponin, tropomyosin and caldesmon in diabetic rabbits might alter the contractile and cytoskeletal structure in bladder myocytes. The over expression of these thin filament associated proteins, which suppresses actin-myosin interaction and actomyosin adenosine triphosphatase, and the enhancement of this suppression by tropomyosin are likely to have an effect on the relationship between force and myosin light chain phosphorylation, requiring higher levels of phosphorylation in diabetic detrusor compared with that of control. The downstream effects of high glucose (eg oxidative stress) appear to modulate the transcriptional regulation of thin filament mediated regulatory proteins in bladder smooth muscle.
Insights
Diabetes alters bladder smooth muscle by increasing expression of proteins like calponin, tropomyosin, and caldesmon. This over-expression may reduce contractility and change cytoskeletal structure in bladder myocytes.
Area of Science:
- Urology
- Smooth Muscle Physiology
- Diabetic Complications
Background:
- Thin filament proteins (caldesmon, tropomyosin, calponin) regulate actin-myosin interactions and smooth muscle contractility.
- Diabetes is associated with decreased contractility in bladder smooth muscle.
Purpose of the Study:
- To investigate if diabetes alters the expression of thin filament proteins in bladder smooth muscle.
- To determine the effect of high glucose on these protein levels in bladder myocytes.
Main Methods:
- Detrusor smooth muscle samples from diabetic and control rabbits were analyzed.
- Bladder myocytes were exposed to normal or high glucose concentrations.
- Protein and mRNA expression levels of caldesmon, tropomyosin, and calponin were measured using Western blotting and RT-PCR.
Main Results:
- Diabetic rabbit detrusor showed increased expression of calponin, tropomyosin, and caldesmon compared to controls.
- High glucose (50 mM) treatment of bladder myocytes led to similar up-regulation of these proteins.
- These findings indicate high glucose induces changes in thin filament protein expression.
Conclusions:
- Increased expression of calponin, tropomyosin, and caldesmon in diabetic bladder smooth muscle may alter contractile and cytoskeletal properties.
- Over-expression of these proteins likely suppresses actin-myosin interaction and actomyosin ATPase activity.
- High glucose, potentially via oxidative stress, modulates transcriptional regulation of these key regulatory proteins in bladder smooth muscle.
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