Disrupting protein XXXX phosphatase    does not prevent sympathetic axonal dieback following myocardial infarction.

@entity63 @entity19 @entity52874 @entity299 @entity4149 @entity597
UNASSIGNED: The neuronal receptor protein @entity4149 phosphatase receptor    ( @entity52874  ) inhibits axonal extension upon binding to chondroitin @entity597 proteoglycans (CSPGs) in scar tissue. We recently demonstrated that modulating or deleting @entity52874   promoted re-innervation of the CSPG-containing @entity299 after @entity63 -reperfusion (I-R). However, it remains unknown if the lack of @entity52874   or early treatment with the @entity52874   modulator, intracellular sigma peptide (ISP), prevents the initial injury-induced axonal dieback. To address this, we carried out I-R in @entity52874   -/- @entity19 or control littermates treated with ISP or vehicle immediately at the time of I-R, and then assessed sympathetic innervation of the scar and surrounding myocardium 3days later. Vehicle-treated WT controls displayed sympathetic denervation within the scar and viable tissue adjacent to the scar, as well as distal myocardium farther from the scar. @entity52874   -/- and ISP-treated animals also displayed denervation of the scar and adjacent tissue, but regions distal to the scar were innervated normally. This suggests that @entity52874   does not mediate axonal dieback but its disruption enhances axonal regrowth in the heart. CSPG digestion alters the macrophage response to prevent axonal dieback in spinal neurons, so we investigated whether targeting @entity52874   might alter the macrophage response in the heart. The macrophage response after I-R was similar in vehicle and ISP-treated groups. @entity19 lacking @entity52874   trended toward an increased M2 response, but were not significantly different than the other groups. These data suggest that @entity52874   is not involved in axonal dieback or the early macrophage response following cardiac I-R.
