Bone marrow (BM)-derived hematopoietic stem/progenitor cells, such as CD34+ cells (HSPC) have an important role in the process of vascular injury repair. We have showed that CXCL12/CXCR4 and FGF signaling may remodel BM niche during post-stoke recovery in exercise SHRSP, a model of chronic vascular inflammation with severe hypertension. The aim of this study was to examine FGF physiological signaling by in vivo challenge of CXCL12.
Recombinant CXCL12 and Diprotin A were administered at day 2 to 5 post-stroke in SHRSP. A variety of cell types in BM or brain, and FGF and ROS production of BM cells were examined.
CXCL12-treated SHRSP significantly prolonged the survival. The CD34+ cells and GFAP+-, Nestin+-neural progenitor cells (NPC) were increased in the penumbra, and tightened BBB. Increases in BDNF production and DCX+ NPC migration were not detected in SVZ. CXCL12 treatment increased the production of FGF1/FGF2, but not VEGF, in mesenchymal stromal cells (MSC), endothelium, and megakaryocytes (MK) of BM, and the numbers of CD34+ HSPC, MSC and MK in BM vascular niche following stroke injury. ROS production of BM cells reduced in CXCL12-treated SHRSP. FGF signaling in response to CXCL12/CXCR4 in BM niche may regulate CD34+ HSPC migration for stroke repair.

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