Fig. 7: ADAMTSL2-deficiency in myogenic progenitor cells attenuates muscle regeneration.
From: Myoblast-derived ADAMTS-like 2 promotes skeletal muscle regeneration after injury
ADAMTSL2 regulates muscle regeneration by accelerating myoblast-to-myocyte differentiation, a critical step in the regeneration of contractile myofibers. Our data are consistent with delayed muscle regeneration of ADAMTSL2-deficient muscle compared the regeneration of wild type muscle (scenario I) or with a delayed and diminished regenerative response that still would result in complete muscle regeneration (scenario II). Scenario II is supported by our data since eMyHC staining continued to decline rapidly through 21 dpi in regenerating CKO-Myf5 TA muscles. In an alternative scenario, muscle regeneration would be delayed and does not fully resolve resulting in incomplete “chronic” muscle regeneration (scenario III). Graphics were generated using CorelDRAW and OriginPro.
