重庆医学
重慶醫學
중경의학
CHONGQING MEDICAL JOURNAL
2014年
12期
1416-1418
,共3页
地诺前列酮%力学刺激%成骨细胞%力学敏感性
地諾前列酮%力學刺激%成骨細胞%力學敏感性
지낙전렬동%역학자격%성골세포%역학민감성
dinoprostone%mechanical stimulation%osteoblasts%mechanosensitivity
目的:探讨前列腺素E2(PGE2)与成骨细胞力学敏感性的关系,并对其细胞水平的作用机制进行分析。方法使用16,16-二甲基PGE2(dmPGE2)对成骨细胞株(MC3T3-E1)进行预处理,随后观察其对细胞内钙离子信号的调控作用;并采用蛋白激酶A(PKA)信号通路的激活剂与阻滞剂检验PKA信号通路在此调控过程中的参与作用。结果相对于空白处理组,dmPGE2预处理显著提升了细胞中由水肿胀刺激引起的钙离子信号强度。该作用被 PK A信号通路的激活剂8-溴腺苷-3,5-环单磷酸钠(8br-cAMP)所模拟;且被PKA多肽阻滞剂(PKI)阻断。结论 dmPGE2通过激活PKA信号通路上调MC3T3-E1细胞中由水肿胀刺激引起的钙离子响应,为解释PGE2在骨组织中的促合成作用提供了重要的细胞学基础。
目的:探討前列腺素E2(PGE2)與成骨細胞力學敏感性的關繫,併對其細胞水平的作用機製進行分析。方法使用16,16-二甲基PGE2(dmPGE2)對成骨細胞株(MC3T3-E1)進行預處理,隨後觀察其對細胞內鈣離子信號的調控作用;併採用蛋白激酶A(PKA)信號通路的激活劑與阻滯劑檢驗PKA信號通路在此調控過程中的參與作用。結果相對于空白處理組,dmPGE2預處理顯著提升瞭細胞中由水腫脹刺激引起的鈣離子信號彊度。該作用被 PK A信號通路的激活劑8-溴腺苷-3,5-環單燐痠鈉(8br-cAMP)所模擬;且被PKA多肽阻滯劑(PKI)阻斷。結論 dmPGE2通過激活PKA信號通路上調MC3T3-E1細胞中由水腫脹刺激引起的鈣離子響應,為解釋PGE2在骨組織中的促閤成作用提供瞭重要的細胞學基礎。
목적:탐토전렬선소E2(PGE2)여성골세포역학민감성적관계,병대기세포수평적작용궤제진행분석。방법사용16,16-이갑기PGE2(dmPGE2)대성골세포주(MC3T3-E1)진행예처리,수후관찰기대세포내개리자신호적조공작용;병채용단백격매A(PKA)신호통로적격활제여조체제검험PKA신호통로재차조공과정중적삼여작용。결과상대우공백처리조,dmPGE2예처리현저제승료세포중유수종창자격인기적개리자신호강도。해작용피 PK A신호통로적격활제8-추선감-3,5-배단린산납(8br-cAMP)소모의;차피PKA다태조체제(PKI)조단。결론 dmPGE2통과격활PKA신호통로상조MC3T3-E1세포중유수종창자격인기적개리자향응,위해석PGE2재골조직중적촉합성작용제공료중요적세포학기출。
Objective To explore the relation between prostaglandin E2(PGE2) and the mechanosensitivity of osteoblasts and to analyze its action mechanism in cellular level .Methods Osteoblasts cell line MC3T3-E1 cells were performed the pre-treatment by using 16 ,16-dimethyl prostaglandin E2(dmPGE2) .Then the regulating effect of PGE2 on intracellular calcium ion signal was ob-served;the activator agent and inhibitor of the protein kinase A (PKA) signal path were adopted to detect the participating effect of the PKA signal path in the regulating process .Results Compared with the blank treatment group ,dmPGE2 pre-treatment signifi-cantly increased the calcium ion signal intensity induced by hypotonic swelling stimulation in MC 3T3-E1 cells .This effect of dmPGE2 was mimicked by 8-bromo-cAMP(8br-cAMP) ,an activator of PKA pathway ;but blocked by PKI ,an inhibitor of PKA pathway .Conclusion dmPGE2 is able to up-regulate the calcium response induced by hypotonic swelling stimulation by activating PKA pathway ,which provides an important cellular mechanism for explaining PGE2′s anabolic effect in bone tissue .