Calcium Signaling in Airway Smooth Muscle Remodeling

摘要: Asthma is characterized by airway remodeling. One of the most important manifestations remodeling an increased mass smooth muscle cells (ASMCs), which mainly due to hyperplasia (increased cell number). Hyperplasia can result from increase in proliferation, migration, or a decrease apoptosis. Understanding mechanisms underlying ASMC may give rise novel avenues for therapy asthma and other respiratory diseases. Recent studies our group others suggest that Ca2+ signaling Gene protein expression pump sarco/endoplasmic reticulum ATPase 2 (SERCA2) has been shown be reduced ASMCs patients with moderately severe asthma. Conversely, transient receptor potential canonical 3 (TRPC3) channel activity are significantly asthmatic ASMCs, resulting extracellular influx, activation tyrosine kinase (PTK2)/nuclear factor kappa-light-chain-enhancer activated B (NF-κB)/calcineurin axis, cyclin D1 transcription and, ultimately, Orai1-encoded Ca2+-release-activated (CRAC) channels stromal interacting molecule 1 (STIM1) also appear participate mediating platelet-derived grow (PDGF)-dependent store-operated entry (SOCE) proliferation migration This augment Ca2+/calmodulin-dependent II (CaMKII) phosphorylate cyclic adenosine monophosphate (cAMP) response element binding (CREB) activate various genes regulate cycle, thereby leading Airway associated size (hypertrophy). cellular mediated phosphoinositide 3-kinase (PI3K)/mammalian target rapamycin (mTOR)/eukaryotic translation initiation 4E (eIF-4F), ribosomal S6 (RSK)/S6-related kinase, glycogen synthase 3β (GSK3β) pathways, all dependent. Evidently, continual field will improve current knowledge regarding molecular disorders.