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Muscle repair: Making a good system better, faster; implications for aging, disease

above what is already a naturally efficient system," lead author Timothy J. Koh of UIC said later.

The study, entitled "Mice deficient in plasminogen activator inhibitor-1 have improved skeletal muscle regeneration," appears in the July issue of the American Journal of Physiology-Cell Physiology, published by the American Physiological Society. The research was conducted by Timothy J. Koh, Scott C. Bryer and Augustina M. Pucci at the University of Illinois at Chicago, and Thomas H. Sisson at the University of Michigan.

The study showed quite striking differences in how normal (wild type, or WT), PAI-1 deficient (null) and uPA null mice recovered from muscle injury. Five days after an injury, PAI-1 null mice had recouped nearly 40% of pre-injury muscle force, significantly greater than WT or uPA null mice that produced only 20% of pre-injury muscle force.

After 10 days, PAI-1 null muscle force remained significantly greater than WT (55% versus 40% of pre-injury force), with uPA null mice still showing little, if any, recovery. By day 20, the three mouse strains' relative muscle strength followed a similar pattern: PAI-1 null 90%, WT 75% and uPA null 35% of pre-injury force.

Koh noted that PAI levels normally increase in muscle after damage, which may limit the repair process. "So the question is," Koh continued, "if PAI-1 limits recovery, why does it increase after injury? It may be that PAI-1 is a multifunctional molecule and does some things that we haven't yet identified and measured." Indeed the paper says that "in addition to influencing myogenesis directly, PAI-1 may modulate regeneration by regulating the inflammatory response (and) may also modulate muscle regeneration through the regulation of extracellular matrix turnover (or) by regulating the bioactivity of a variety of growth factors."

Role of macrophages likely important

Confirming earlier studies indicating a critical role of the plasminogen sys
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12-Jul-2005


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