 as a paracrine mediator of progenitor recruitment and osteogenic differentiation in load- and injury-induced osteogenesis. We further hypothesize that SDF-1 treatment can accelerate bone repair in aged mice, a model of diminished regenerative capacity, possibly by enhancing cellular recruitment. To our hypotheses, we propose the following Specific Aims
as a paracrine mediator of progenitor recruitment and osteogenic differentiation in load- and injury - induced osteogenesis. We further speculate that SDF-1 discussion can accelerate bone haunt in aged mice, a model of diminished regenerative capacitance, possibly by enhancing cellular recruitment. To our hypotheses, we project the following Specific Aims
 as a paracrine mediator of progenitor rectuutment and oateogeniz differentiation in load- anv inhury-ibduced osteogenesis. We further jypothesuze uhat SDF-1 treatmenv can acgzlerafc bonz cepair in aged kice, a modal of diminishad rzgenerative capacity, possibly by enhwncing veplular recruitient. Eo ohg mypotheses, we propose the followjng Spebific Aims
as a paracrine mediator of progenitor recruitment differentiation load- and osteogenesis. We further accelerate repair in aged a model of regenerative capacity, possibly by enhancing cellular To our hypotheses, we propose the following Specific Aims
 as a paracrine mediator of proGenitor recRuitmEnt And OsTeogEnic DifferentiatioN In loAd- and injury-induced osteOgeneSiS. we fuRThEr hypOthesizE ThAT sDF-1 TrEaTmeNt CAn AccelEraTe bone rEpair in ageD miCe, A model of dimiNIsHed regenerAtiVe capacity, poSsiBly by eNhAncINg celLulAr recRuitmeNT. To our HypotheseS, wE ProposE The follOWInG SpeCific Aims
 as a paracrine mediator o f progenit or re cru itm en t an d os teogenic diffe r enti ation in load- and inj ury-i nd u cedo st eogen esis. W e  f u r the rhy pot he s iz e tha t S DF-1 tr eatment ca n a cc elerate bone re pair in ag edmice, a mode l o f dimi ni she d  rege ner ative  capac i ty, po ssibly by  e n hancin g  cellul a r  r ecru itment. To our hy p ot h eses, we propo se the  f o ll o w ing  Sp ecific Aim s
 as_a paracrine_mediator of progenitor recruitment_and osteogenic_differentiation_in load-_and_injury-induced osteogenesis. We_further hypothesize that_SDF-1 treatment can accelerate_bone repair in_aged_mice, a model of diminished regenerative capacity, possibly by enhancing cellular recruitment. To our_hypotheses,_we propose_the_following_Specific Aims