Abstract

Skeletal muscle regeneration is a critical process that replaces damaged muscle fibers with new fibers. The regenerative process can be segmented into four main phases: necrosis, inflammation, regeneration, and maturation. While many of the key signaling molecules are known and characterized, there are still gaps in our understanding of how this process is regulated. While it is reported that growth arrest specific 6 (Gas6) and its receptor Axl are expressed in mature muscle tissue, nothing is known about the effect that Gas6 and Axl have on regulating skeletal muscle regeneration. In this study we investigated the regenerative process in a Gas6/Axl double knockout (dKO) mouse model. The tibialis anterior (TA) muscle was chemically injured with BaCl2 and allowed to recover for 3, 7, or 14 days. We investigated satellite cell (SC) activation and muscle growth. We found that the dKO injured muscle has fewer SCs at 3-days post-injury, but the percentage of mitotically active SCs were no different between WT and dKO injured muscle. Interestingly, basal and injured dKO muscle has an increased cross-sectional area compared to wild type in male mice. Together this may suggest that in the absence of Gas6/Axl signaling may lead to impaired regeneration and compensatory fiber hypertrophy. The mechanism behind the hypertrophy remains unknown, but ultimately our findings suggest that Gas6/Axl signaling has an effect on skeletal muscle regeneration.

Degree

College and Department

Life Sciences; Physiology and Developmental Biology

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