Figure 6. PNS disautonomy is responsible for deregulation of CXCL12 gradient.

(A) Representative pictures from whole mounting of calvaria of controls (left picture) and STZ-treated mice (right picture). Red signal: tyrosine hydroxilase. Scale bar: 50 μm. Nerve terminal quantification in terms of perimeter (B) in calvaria of STZ-treated versus controls mice n=5 *p<0.05. Fold changes in the expression of mRNA levels of CXCL12 in (C) nestin+ cells (D) bone marrow from control and STZ-treated mice in baseline conditions and 2 hrs after injection of isoproterenol (5 mg/kg i.p) relative to control cells in baseline and normalised to GAPDH (ΔΔCTmethod). n=6, *p<0.5. (E) Left: Western blot showing the amount of phospho-PKA (pPKA) in sorted nestin+ cells from control (+/− isoproterenol) and STZ-treated (+/− isoproterenol) mice. Right: Histogram plot showing ratio in pPKA. (F) Fold changes in the expression of mRNA levels of Cxcl12 in nestin+ cells from diabetic saline treated and diabetic β3 -blocker treated (5 mg/kg/day for 10 days) animals relative to non-diabetic controls. Data are normalized to GAPDH (ΔΔCTmethod). n=6, *p<0.5. Percentage of donor cell engraftment 4 weeks after transplantation of 150 μL of mobilized-PB from STZ-treated and control mice (along with whole bone marrow support cells) in congenic lethally irradiated recipients. Mice were mobilized with single dose of AMD3100 (G) or single dose of AMD3100 at the end of the G-CSF mobilization regimen (H), n=5.