The Role Of Hyaluronic Acid And CD44during The Airway Remodeling In Chronic Asthma

Part1Airway smooth muscle cells up-regulate expression ofHyaluronan-CD44in chronic asthmatic rat modelPurposeto observe the expression of hyaluronic acid and CD44in chronic asthmatic ASMCsand the expression of hyaluronan synthase and hyaluronidase.Materials and MethodsRats were divided into2groups:1) control group;2) chronic asthma group. PrimaryASMCs were cultured by tissue adherent. The content of HA in cell culture fluid wasdetected by ELISA. Realtime-PCR was applied to detect the expressions of CD44,HAS1,2,3and HYAL1,2mRNA. Western-blotting was applied to detect theexpression of CD44protein.Results1、Compared to control group, the expressions of mRNA and protein of CD44wasincreased in chronic asthma group（p＜0.05）.2、Compared to control group, the content of HA in cell culture fluid was significantincreased in chronic asthma group（p＜0.01）.3、Compared to control group, the expressions of mRNA of HAS1,2and HYAL1,2was increased in chronic asthma group（p＜0.05）.ConclusionsCompared to control group, our results revealed an increased secretion of HA fromASMCs, an increased mRNA and protein expressions of CD44and an increasedmRNA of HAS and HYAL in ASMCs of chronic asthma group. Part2LMW-HA regulated proliferation and apotosis of ASMCs throughERK signaling pathway during airway remodeling in chronic asthmaPurposeTo observe the role of HA and CD44on ASMCs proliferation and apoptosis duringthe airway remodeling in chronic asthma, and determine the mechanism thatHA-CD44regulated ASMCs proliferation and apoptosis.Materials and MethodsASMCs were divided into6groups:1) normal control group;2)normal control+LMW-HA group;3)normal control+LMW-HA+PD98059group;4) asthma controlgroup;5) asthma control+LMW-HA group;6) asthma control+LMW-HA+PD98059group. The levels of p-ERK and ERK protein were detected by Western blot.Apoptosis and proliferation of airway smooth muscle cells were evaluated by MTTand Flow Cytometry.Results1、Compared to normal control group, the level of ASMCs proliferation wassignificant increased (p＜0.01) in asthma control group, and the level of ASMCsapoptosis was also dropped (p＜0.05).2、Compared to control groups, with the LMW-HA interfered, the level of ASMCsproliferation was significantl increased in both normal control+LMW-HA groupand asthma control+LMW-HA ygroup (p＜0.01). Meanwhile, compared withcontrol groups and control+HA groups, after blocked with PD98059, the levels ofASMCs proliferation were both significantly dropped (p＜0.01).3、Compared to control groups, with the LMW-HA interfered, the level of ASMCsapoptosis was dropped in both normal control+LMW-HA group and asthmacontrol+LMW-HA group (p＜0.05). Meanwhile, compared with control groupand control+HA group, after blocked with PD98059, the levels of ASMCsapoptosis were both increased (p＜0.05).4、Compared to control groups, the expressions of p-ERK1/2, ERK protein and theratio of p-ERK1/2to ERK were increased in normal control+LMW-HA groupand asthma control+LMW-HA group(p＜0.05). Meanwhile, compared withcontrol group and control+HA group, after blocked with PD98059, the level ofp-ERK1/2and p-ERK1/2to ERK were significantly dropped (p＜0.01).ConclusionsDuring the airway remodeling in chronic asthma, the level of ASMCs proliferationrevealed an increased trend. Meanwhile, the level of ASMCs apoptosis showed a dropped trend. With LMW-HA interfered, the level of ASMCs proliferation wasincreased, and apoptosis of ASMCs was inhibited. And these increased proliferationand dropped apoptosis were activating through the pathway of ERK1/2.