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Calcification of Vascular Smooth Muscle Cells and Imaging of Aortic Calcification and Inflammation

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Published on: May 31, 2016

Ca2+ extrusion in aged smooth muscle cells.

Pedro J Gomez-Pinilla¹, Maria J Pozo, Akemishi Baba

¹Department of Physiology, University of Extremadura, Campus Universitario, Fac Veterinary, 10071 Caceres, Spain.

Biochemical Pharmacology

|July 31, 2007

Summary

Aging impairs calcium extrusion in smooth muscle bladder cells. Reduced plasma membrane Ca(2+) pump (PMCA) activity and altered interactions between Na(+)/Ca(2+) exchanger (NCX) and sarcoendoplasmic Ca(2+) pump (SERCA) contribute to this decline.

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Area of Science:

Physiology
Cell Biology
Aging Research

Background:

Calcium homeostasis is crucial for smooth muscle function.
Age-related changes can affect cellular ion transport mechanisms.
Understanding calcium extrusion in bladder smooth muscle is vital for maintaining function.

Purpose of the Study:

To investigate the impact of aging on calcium extrusion mechanisms in guinea pig bladder smooth muscle cells.
To quantify the contribution of different calcium pumps (PMCA, NCX, SERCA) in young and aged cells.
To explore interactions between these extrusion mechanisms.

Main Methods:

Utilized fluorescence microscopy and fura-2 to measure intracellular calcium levels.
Employed specific inhibitors (La(3+), SEA0400, thapsigargin) for PMCA, NCX, and SERCA.
Compared calcium extrusion in young (4-month) and aged (20-24-month) guinea pigs.

Main Results:

In young cells, NCX contributed 55%, PMCA 27%, and SERCA 31% to calcium extrusion.
Aged cells showed impaired calcium extrusion, evidenced by reduced PMCA activity (loss of La(3+) effect).
Inhibitory interactions between NCX and SERCA were altered in aged cells, accelerating calcium decay.

Conclusions:

Aging significantly decreases overall calcium extrusion capacity in smooth muscle bladder cells.
Age-related decline in PMCA activity and modified NCX-SERCA interactions impair calcium handling.
These findings highlight age-dependent alterations in cellular calcium regulation mechanisms.