Spinal cord injury (SCI) is one of the major central nervous system damages, in which oligodendrocytes play important roles in protecting axons and functional recovery. Kallikrein 6 (KLK6), a serin protease, is expressed by oligodendrocyte in the central nervous system and the expression is increased in spinal cord injury.
We previously reported that KLK6-deficient mice showed smaller number of oligodendrocytes and lower amount of myelin-related protein, myelin basic protein (MBP) and oligodendrocyte specific protein (OSP)/claudin-11, in their spinal cords at postnatal day 7 (P7) than wild type mice. Moreover, KLK6-deficient mice showed lower amount of MBP in their spinal cords after spinal cord injury than wild type mice. These results suggest that KLK6 have functional roles in oligodendrocyte development and myelin formation in development and pathological condition.
In this study, we report a new KLK6 variant derived from 129Sv mice. C57BL/6 mice, BALB/c mice and ICR mice did not have this variant KLK6. Messenger RNA of this variant has six nucleotide mutations compared to C57BL/6 mice-derived (database-reported) KLK6 mRNA, leading to six amino acid mutations. In SDS-PAGE, this variant proteins showed different mobility from C57BL/6 mice-derived KLK6 proteins. We also investigated the enzymatic activity of this variant KLK6 proteins, using Boc-Val-Pro-Arg-MCA as substrates. This variant protein showed 449 % higher Kcat and 26 % lower Km than C57BL/6 mice-derived KLK6 proteins. This finding might give us some new informations about KLK6 function, leading to drug discoveries.