科研之友
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摘要
In an effort to identify factors that contribute to age-related deficits in the undamaged and injured peripheral nervous system (PNS), we noted that Brady and colleagues found that mice null for a small heat shock protein called alphaB-crystallin (alpha BC) developed abnormalities early in life that are reminiscent of aging pathologies. Because of our observation that alpha BC protein levels markedly reduce as wildtype mice age, we investigated whether the crystallin plays a role in modulating age-related deficits in the uninjured and damaged PNS. We show here that the presence of alpha BC correlates with maintenance of myelin sheath thickness, reducing macrophage presence, sustaining lipid metabolism, and promoting remyelination following peripheral nerve injury in an age-dependent manner. More specifically, animals null for alpha BC displayed a higher frequency of thinly myelinated axons, enhanced presence of Iba1 + macrophages, and fewer immunoreactive profiles of the cholesterol biosynthesis enzyme, squalene monooxygenase, before and after sciatic nerve crush injury. These findings thus suggest that alpha BC plays a protective and beneficial role in the aging PNS.
- 出版日期2017-5
