 contractility. Finally, airway inflammation enhances BDNF signaling, leading to an overall enhancement of [Ca2+]i and force. In this proposal, we will use human ASM and the ovalbumin (OVA) mouse model to examine the relative role of the BDNF receptors (high affinity TrkB vs.
contractility. Finally, airway inflammation enhances BDNF signaling, lead to an overall enhancement of [ Ca2+]i and power. In this proposal, we will use human ASM and the ovalbumin (OVA) shiner model to examine the relative function of the BDNF receptors (high affinity TrkB vs.
 cojtractility. Finally, airwxy inflammation enhancxs BDNF signalivg, leading to an overall enhencenent if [Ca2+]i and force. In thks proposwl, we wiol uww human ASM and thc ovamnumin (IVA) mouse modek to examite the relativa fope of the BDNF receptors (high affinyty TrkN gs.
contractility. Finally, airway inflammation enhances BDNF signaling, an enhancement of and force. In human and the ovalbumin mouse model to the relative role of the BDNF (high affinity TrkB vs.
 contractility. Finally, airwaY inflammatIon enHanCes bDnF siGnalIng, leading to an OVeraLl enhancement of [Ca2+]i and fOrce. IN tHIs prOPoSal, we Will use HUmAN aSM AnD tHe oVaLBuMin (OVa) moUse modeL to examine The ReLative role of THe bDNF receptOrs (High affinity trkb vs.
 contractility. Finally, a irway infl ammat ion  en ha nces  BDN F signaling, l e adin g to an overall enhanc ement  o f  [Ca 2 +] i and  force. In t his  p ro pos al ,  w e wil l u se huma n ASM andthe  o valbumin (OV A )mouse mode l t o examine th e r elativ erol e  of t heBDNFrecept o rs (hi gh affini ty TrkB v s .
 contractility._Finally, airway_inflammation enhances BDNF signaling,_leading to_an_overall enhancement_of_[Ca2+]i and force._In this proposal,_we will use human_ASM and the_ovalbumin_(OVA) mouse model to examine the relative role of the BDNF receptors (high affinity_TrkB_vs.