第四军医大学学报
第四軍醫大學學報
제사군의대학학보
JOURNAL OF THE FOURTH MILITARY MEDICAL UNIVERSITY
2003年
3期
193-195
,共3页
钙%离子通道%心肌细胞
鈣%離子通道%心肌細胞
개%리자통도%심기세포
Ca2+%ion channel%cardiomyocytes
目的:研究Annexin A7在早期胚胎发育过程中对钙平衡调节的作用. 方法: 利用钙成像技术和膜片钳技术检测敲除Annexin A7小鼠的早期胚胎心肌细胞的钙平衡以及相应的离子通道的特性. 结果: 在胚胎心肌细胞发育的早期,敲除Annexin A7小鼠胚胎心肌细胞的静息钙(340/380荧光比例 0.78±0.02)、钙峰值(340/380荧光比例1.28±0.05)和正常细胞的值相似;动作电位(APD90 242.7±43.7 ms、最大去极化电位56.8±1.7 mV)以及L-型钙电流密度(14.1±2.5 pA/pF)和正常细胞的相似,并且钙电流能被碳酰胆碱减小(51.7±8)%,也和正常细胞相似. 结论: 敲除Annexin A7基因的小鼠早期胚胎心肌细胞具有正常的钙稳态以及正常的离子通道.
目的:研究Annexin A7在早期胚胎髮育過程中對鈣平衡調節的作用. 方法: 利用鈣成像技術和膜片鉗技術檢測敲除Annexin A7小鼠的早期胚胎心肌細胞的鈣平衡以及相應的離子通道的特性. 結果: 在胚胎心肌細胞髮育的早期,敲除Annexin A7小鼠胚胎心肌細胞的靜息鈣(340/380熒光比例 0.78±0.02)、鈣峰值(340/380熒光比例1.28±0.05)和正常細胞的值相似;動作電位(APD90 242.7±43.7 ms、最大去極化電位56.8±1.7 mV)以及L-型鈣電流密度(14.1±2.5 pA/pF)和正常細胞的相似,併且鈣電流能被碳酰膽堿減小(51.7±8)%,也和正常細胞相似. 結論: 敲除Annexin A7基因的小鼠早期胚胎心肌細胞具有正常的鈣穩態以及正常的離子通道.
목적:연구Annexin A7재조기배태발육과정중대개평형조절적작용. 방법: 이용개성상기술화막편겸기술검측고제Annexin A7소서적조기배태심기세포적개평형이급상응적리자통도적특성. 결과: 재배태심기세포발육적조기,고제Annexin A7소서배태심기세포적정식개(340/380형광비례 0.78±0.02)、개봉치(340/380형광비례1.28±0.05)화정상세포적치상사;동작전위(APD90 242.7±43.7 ms、최대거겁화전위56.8±1.7 mV)이급L-형개전류밀도(14.1±2.5 pA/pF)화정상세포적상사,병차개전류능피탄선담감감소(51.7±8)%,야화정상세포상사. 결론: 고제Annexin A7기인적소서조기배태심기세포구유정상적개은태이급정상적리자통도.
AIM: To study the involvement of Annexin A7 in the regulation of Ca2+ homeostasis in embryonic development stage. METHODS: Single cell Ca2+ imaging techniques and patch clamp technique were used to test the current of ion channel and action potential of Annexin A7 knock out mice embryonic heart cells. RESULTS: During early embryonic development (E11.5/E12.5) resting Ca2+ (ratio 0.78±0.02), values of peak Ca2+ concentration (ratio 1.28±0.05, n=30) were quite same to control cells. Anxa7-/- cardiomyocytes displayed normal action potentials (APD90 242.7±43.7 ms, a maximum diastolic potential of 56.8±1.7 mV) , and the density of L-type Ca2+-currents in Anxa7-/- cardiomyocytes (14.1±2.5 pA/pF) were quite same to control cells. Especially basal ICa was depressed by CCh (1 μmol*L-1) by (51.7±8)%. CONCLUSION: Early embryonic cardiomyocytes of Anxa7-/- mice display intact Ca2+ homeostasis and express all the components required for excitation contraction coupling.