整合素连接激酶对含成纤维细胞胶原网格收缩的影响

目的 探讨整合素连接激酶(ILK)对含成纤维细胞胶原网格(FPCL)收缩的影响和机制.方法 (1)运用人皮肤成纤维细胞(Fb)构建FPCL,观察ILK-AKT信号通路特异性抑制剂LY294002对FPCL收缩的影响.(2)运用Western blot印迹法检测ILK小干扰RNA(siRNA)转染和LY294002对Fb中ILK和α-平滑肌肌动蛋白(α-SMA)表达的影响.结果 第24小时和第48小时LY294002组FPCL收缩率[(20.23±9.57)％、(22.47±10.93)％]明显低于对照组[(48.73±6.60)％、( 54.33±12.88)％](P＜0.05),第72、96和120小时FPCL收缩率为(25.58±7.40)％、(26.67±13.76)％、(28.82±3.48)％明显低于对照组(58.00 ±7.54)％、(59.67±11.29)％、(66.95±9.98)％和DMSO组(47.34±12.41)％、(52.26±10.90)％、(56.38±10.75)％ (P＜0.05).LY294002组和ILK siRNA转染组α-SMA蛋白表达(0.992 ±0.255、1.225 ±0.323)与各对照组(2.009 ±0.820、2.190 ±0.577、1.758±0.732)比较均显著降低(P＜0.05).结论 阻断ILK信号通路可明显抑制Fb构建的FPCL收缩和Fb中α-SMA的表达.     

透明质酸对胚胎成纤维细胞胶原网架收缩的影响

目的　探讨羊水中抑制胚胎伤口收缩的成分是否为透明质酸 (HA)以及HA对胚胎伤口收缩是否有直接的抑制作用。方法　使用一种体外胚胎伤口收缩模型含成纤维细胞的胶原网架FPCL) ,观察HA浓度为 1μg/ml～ 10mg/ml时对FPCL收缩的影响。 结果　低浓度组 ( 1、5、2 0、5 0、10 0、10 0 0 μg/ml)的HA对FPCL的收缩指数 (CI)与对照组比较 ,差异无显著意义 (P >0 .0 5 ) ;高浓度组 ( 2、6、10mg/ml)的HA对FPCL的CI与对照组比较 ,差异有显著意义 (P <0 .0 5 )。结论　羊水中抑制胚胎伤口收缩的成分并非为HA ,可能胚胎伤口中高浓度的HA与羊水共同参与了胚胎伤口收缩的抑制作用。     

高糖对肾小球系膜细胞间通讯功能的影响

目的研究高糖对肾小球系膜细胞间隙连接蛋白（connexin 43）表达和细胞间通讯功能的影响。方法分离培养大鼠肾小球系膜细胞，调整培养液葡萄糖浓度为以下3组：正常葡萄糖组（5．5mmol／L葡萄糖）、高糖组（30mmol／L葡萄糖）和渗透压对照组（5．5mmol／L葡萄糖加24．5mmol／L甘露醇），于37℃5％CO2条件下培养24、48h后．利用激光共聚焦显微镜和荧光漂白恢复（FRAP）技术检测细胞间通讯功能，并应用Northern印迹和细胞免疫化学、Western印迹方法检测connexin 43 mRNA和蛋白质表达，比较3组之间的差异。结果正常葡萄糖浓度培养下系膜细胞表达丰富的connexin 43，细胞间通讯功能良好。高糖培养的系膜细胞细胞间通讯功能下降，荧光淬灭后的恢复比例和速度显著低于正常糖组（P〈0．05）。同时高糖环境下培养的系膜细胞connexin 43 mRNA和蛋白质表达均较正常糖组显著下降（P〈0．05）。渗透压对照组与正常糖组之间差异无统计学意义（P〉0．05）。结论高糖可抑制connexin 43的基因和蛋白质表达及细胞间通讯功能，可能是糖尿病肾病系膜细胞表型和功能异常的重要原因之一。     

Human marrow stromal cells enhance connexin43 gap junction intercellular communication in cultured astrocytes

Human marrow stromal cells (hMSCs) provide functional benefit in rats subjected to stroke. Astrocytes are coupled into a cellular network via gap junction channels, predominantly composed of connexin-43 (Cx43) proteins. Astrocytes are believed to play a vital role in neuroprotection by providing energy substrates to neurons and by regulating the concentrations of K+ and neurotransmitters via gap junctions. We therefore investigated the effect of factors secreted by hMSCs on gap junction intercellular communication (GJIC), expression of Cx43, and phosphorylation of Cx43 in an astrocyte cell culture system. Exposing rat cortical astrocytes to various concentrations of hMSC conditioned medium, we demonstrate that hMSCs produce soluble factors that significantly increase astrocytic GJIC, measured by the scrape-loading dye transfer method. Immunohistochemistry and Western blot showed increased Cx43 expression concomitant with altered GJIC. As the PI3K/Akt signaling pathway has been demonstrated to alter gap junction expression and GJIC, we selectively blocked phosphoinositide 3-kinase (PI3K). Addition of the PI3K inhibitor LY294002 decreased GJIC and Cx43 expression in astrocytes. These inhibitory effects of LY294002 were countered by the addition of hMSC conditioned media. Furthermore, coculturing hMSCs with rat astrocytes increased astrocyte GJIC in a manner dependent upon the hMSC/astrocyte ratio. These findings demonstrate that hMSCs secrete soluble factors that increase GJIC of astrocytes through upregulation of Cx43, and indicate a mechanistic role for PI3K.     

A study to the fibroblast—populated collagen lattices

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Fetal rat amniotic fluid: transforming growth factor beta and fibroblast collagen lattice contraction

BACKGROUND: In several mammalian animal models, early-gestational-age fetal wounds heal without scar, but wounds of late gestational age heal with scar. This change in wound healing phenotype can be a result of both intrinsic (i.e., cellular characteristics) and extrinsic (i.e., environmental) factors. Our question was: Does amniotic fluid (AF) influence the change from scarless to scar-forming repair in the rat? METHODS: Rat AF was investigated for its modulation of fibroblast-populated collagen lattice (FPCL) contraction and morphological changes of adult fibroblasts. AF was also assayed for transforming growth factor beta (TGF-beta) levels. Adult rat dermal fibroblasts in monolayer and incorporated into FPCLs were incubated with AF additions from gestational age 14, 16, 18, and 21 days at 10% (v/v). RESULTS: Day 14 AF significantly stimulated FPCL contraction, but AF of 16, 18, and 21 days inhibited FPCL contraction. Fluorescence histology identified microtubules and microfilaments in AF treated adult rat dermal fibroblasts. The staining pattern of microtubules in Day 14 AF-treated fibroblasts showed denser structures at the cell center. Cells incubated with Day 16 or 18 AF showed fine peripheral microtubules. A mink lung epithelial cell bioassay was used to analyze concentrations of TGF-beta in AF. TGF-beta levels were greatly elevated in Day 14 AF, but were relatively low in Day 16, 18 and 21 AF. The inhibitor of FPCL contraction from AF of Days 16, 18, and 21 was not identified. CONCLUSION: It is proposed that the robust expression of TGF-beta or cytoskeletal changes induced by Day 14 AF contributes to enhanced FPCL contraction.     

不稳定逼尿肌中Cx43的表达及其对细胞间通讯的影响

目的研究Cx43在不稳定逼尿肌细胞中的表达及其对不稳定逼尿肌细胞间缝隙连接通讯的影响,探讨Cx43与逼尿肌不稳定（DI）的关系。方法采用Western blot法检测正常及不稳定逼尿肌细胞中Cx43蛋白表达。构建Cx43反义真核表达载体,脂质体介导转染体外培养不稳定逼尿肌细胞（转染组）,空载体做对照转染（空载组）。利用划痕标记荧光染料示踪（SLDT）技术观察Cx43表达降低后不稳定逼尿肌细胞间缝隙连接通讯改变。结果不稳定逼尿肌细胞中Cx43表达显著增高（P〈0．01）,转染反义Cx43组不稳定逼尿肌细胞间缝隙连接通讯较空载组明显减弱（P〈0．05）。结论抑制Cx43表达可明显降低不稳定逼尿肌细胞间缝隙连接通讯功能,Cx43表达增高可能是不稳定逼尿肌发生的重要原因。     

Increased intercellular communication through gap junctions may contribute to progression of osteoarthritis

Our aim was to support the hypothesis of a specific association between gap junctions in synovial tissue and the presence of osteoarthritis, as evidenced by differences between osteoarthritis and non-osteoarthritis synovia in the number of gap junctions, the amount of gap-junction protein, and the amount of enzymatic activity produced through a pathway mediated by gap-junction intercellular communication. An average of 4.41 gap junctions were found per 100 cells counted in the osteoarthritis synovia, compared with 1.00 in the controls. The amount of the gap-junction protein connexin 43 in synovial lining cells was approximately 50% greater in patients with osteoarthritis. Synovial lining cells from patients with osteoarthritis produced matrix metalloproteinases constitutively and, at higher levels, in response to stimulation by interleukin-1 beta. In both cases, intercellular communication through gap junctions was shown to be critical to the ability of the cells to secrete matrix metalloproteinases. Overall, the results indicated that gap junctions between synovial lining cells were altered significantly in patients with osteoarthritis, as a consequence of the disease process or as part of the causal chain. In either case, gap junctions seem to be a rational therapeutic target.     

高糖通过蛋白激酶C改变肾小球系膜细胞的间隙连接与细胞表型

目的观察高糖环境下，蛋白激酶C（PKC）活性的变化对肾小球系膜细胞间隙连接与细胞表型的影响。方法将体外培养的大鼠肾小球系膜细胞分为低糖组、高糖组、高糖＋PKC抑制剂十字孢碱（SP）组，测定细胞间隙连接蛋白-43（connexin 43）、α-平滑肌肌动蛋白（α—SMA）的表达。结果①与低糖组相比，高糖组细胞PKC活性、mSMA mRNA表达增高，connexin 43 mRNA表达下降，差异有统计学意义（P〈0．05）；②与高糖组相比，高糖＋SP组细胞PKC活性、α—SMA mRNA表达下降，connexin 43 mRNA表达增高，差异有统计学意义（P〈0．05）。结论高糖通过PKC改变肾小球系膜细胞的间隙连接与细胞表型。     

Inhibiting gap junctional intercellular communication alters expression of differentiation markers in osteoblastic cells

Gap junctional intercellular communication (GJIC) may contribute to cellular differentiation. To examine this possibility in bone cells we examined markers of cellular differentiation, including alkaline phosphatase, osteocalcin, and osteopontin, in ROS17/2.8 cells (ROS), a rat osteoblastic cell line expressing phenotypic characteristics of fully differentiated osteoblasts. We utilized ROS rendered communication deficient either by stable transfection with antisense cDNA to connexin 43 (Cx43), the predominant gap junction protein in bone (RCx16 cells), or by overexpression of Cx45, a gap junction protein not normally expressed in ROS (ROS/Cx45 cells). Both RCx16 and ROS/Cx45 cells displayed reduced dye coupling and Cx43 protein expression relative to ROS, control transfectants, and ROS/Cx45tr, ROS cells expressing carboxylterminal truncated Cx45. Steady-state mRNA levels for osteocalcin as well as alkaline phosphatase activity, two markers of osteoblastic differentiation, were also reduced in poorly coupled RCx16 and ROS/Cx45 cells. On the other hand, steady-state mRNA levels for osteopontin increased slightly in RCx16 and ROS/Cx45 cells. These results suggest that GJIC at least partly contributes to the regulation of expression of markers of osteoblastic differentiation.     

Age‐related changes in gap junctional intercellular communication in osteoblastic cells

Aging demonstrates deleterious effects upon the skeleton which can predispose an individual to osteoporosis and related fractures. Despite the well‐documented evidence that aging decreases bone formation, there remains little understanding whereby cellular aging alters skeletal homeostasis. We, and others, have previously demonstrated that gap junctions—membrane‐spanning channels that allow direct cell‐to‐cell conductance of small signaling molecules—are critically involved in osteoblast differentiation and skeletal homeostasis. We examined whether the capacity of rat osteoblastic cells to form gap junctions and respond to known modulators of gap junction intercellular communication (GJIC) was dependent on the age of the animal from which they were isolated. We observed no effect of age upon osteoblastic Cx43 mRNA, protein or GJIC. We also examined age‐related changes in PTH‐stimulated GJIC. PTH demonstrated age‐dependent effects upon GJIC: Osteoblastic cells from young rats increased GJIC in response to PTH, whereas there was no change in GJIC in response to PTH in osteoblastic cells from mature or old rats. PTH‐stimulated GJIC occurred independently of changes in Cx43 mRNA or protein expression. Cholera toxin significantly increased GJIC in osteoblastic cells from young rats compared to those from mature and old rats. These data demonstrate an age‐related impairment in the capacity of osteoblastic cells to generate functional gap junctions in response to PTH, and suggest that an age‐related defect in G protein‐coupled adenylate cyclase activity at least partially contributes to decreased PTH‐stimulated GJIC. © 2012 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 30:1979–1984, 2012     

The direct effect of halothane on myocardial contraction in rat myocytes with poorly developed gap junctional intercellular communication

Background: The gap junction channel plays an important role in synchronous beating in the heart, and the reduction in the amount of gap junctional intercellular communication (GJIC) is thought to be the main arrhythmogenic factor in diseased heart. However, the effect of halothane on myocardial contraction in heart tissue with less GJIC is not well known. The purpose of the present study is to examine the direct effect of halothane on myocardium with poorly expressed GJIC.
Methods: Ventricular myocytes were obtained from neonatal rats by enzymatic digestion with collagenase and then cultured for 3 or 7 d. We have previously reported that the number of gap junctions at 3 d is approximately 10% of that at 7 d (1). The myocytes were stabilized in serum-free medium, and the spontaneous beating rate and amplitude were measured by a fiberoptic sensor.
Results: Heptanol (2 mM), an inhibitor of GJIC, abolished synchronized beating in myocytes cultured for 7 d. Halothane decreased the beating rate and amplitude in both groups of myocytes in a concentration-dependent manner ( P <0.05). Halothane at 1 and 2 MAC (adult rat MAC) decreased the beating rate more in myocytes cultured for 3 d than in myocytes cultured for 7 d ( P <0.05). Halothane reduced beating amplitude equally in both groups. Asynchronous contraction developed more frequently among myocytes cultured for 3 d than for those at 7 d.
Conclusion: Halothane may block the GJIC channels, and when the number of these channels is reduced, exposure to halothane may cause asynchronous beating and decrease the beating rate. However, the halothane-induced decrease in amplitude is probably not due to blockade of GJIC because reducing the number of GJIC channels did not alter halothane's depressant effect.     

TGF-β1对大鼠睾丸Leydig细胞间连接蛋白43介导缝隙连接通讯功能的影响

目的:观察转化生长因子TGF-β1对成年大鼠睾丸Leydig细胞间连接蛋白Cx43表达以及由Cx43介导的缝隙连接细胞间通讯(GJIC)功能的影响,旨在探讨TGF-β1对Leydig细胞的影响是否与其改变细胞间GJIC功能相关。方法:将原代培养纯化的Leydig细胞分为6组:实验组分别以1、2、5、10 ng/ml的TGF-β1处理细胞20 h,空白对照组以含10%胎牛血清的DMEM/F12培养液处理细胞,部分实验中以GJIC抑制剂甘珀酸(Carbenox-olone)处理细胞作为阳性对照组。采用免疫荧光法和Western印迹观察Cx43在细胞中的定位和表达变化,用荧光漂白恢复实验(FRAP)检测细胞间GJIC功能的改变。结果:Cx43表达呈斑点状散在分布于Leydig细胞的胞质和胞膜中,TGF-β1处理20 h后,Cx43在胞质中的表达强度随着TGF-β1浓度的增加较空白对照组明显增强,而其在胞膜中的表达则无明显改变。Western印迹结果显示磷酸化状态的Cx43随着TGF-β1浓度增加表现出较空白对照明显增强的趋势(P<0.05),而非磷酸化状态则无显著差异。FRAP结果显示经5 ng/ml TGF-β1作用20 h后细胞内荧光强度较空白对照明显减弱,具有显著性差异(P<0.01),且其平均荧光恢复率仅为(43.58±1.87)%。结论:TGF-β1可显著下调Leydig细胞间的GJIC功能,这种抑制作用可能通过增加其连接蛋白Cx43在细胞质中的表达,提高其磷酸化水平来实现。     

Nitric oxide-mediated regulation of connexin43 expression and gap junctional intercellular communication in mesangial cells

This study investigated a potential role of nitric oxide (NO) in the regulation of gap junctional intercellular communication (GJIC). Incubation of mesangial cells (MC) with NO donor S-nitroso-N-acetylpenicillamine (SNAP) enhanced both basal and 8-bromo-cAMP-stimulated GJIC as well as expression of gap junction protein connexin43 (Cx43). This potentiating action of SNAP on Cx43 expression was mimicked by two other NO donors and significantly blocked by soluble guanylate cyclase inhibitor 1H-[1,2,4]oxadiazolo[4,3,-alpha]quinoxalin-1-1. Guanosine 3',5'-cyclic monophosphate (cGMP) analogue 8-bromo-cGMP exerted an effect similar to NO, whereas another cGMP analogue, 8-pCPT-cGMP, which selectively activates cGMP-dependent kinase without affecting cGMP-inhibited phosphodiesterase (PDE3), had no effect. Moreover, the synergistic action of NO on Cx43 expression was completely prevented by protein kinase A inhibitor H89 but not by cGMP-dependent kinase inhibitor Rp-8-Br-PET-cGMP. These results suggested a possible involvement of NO-cAMP interaction via cGMP-mediated inhibition of PDE3. Indeed, PDE3 inhibitor cilostamide caused potentiation of 8-bromo-cAMP-elicited elevations of Cx43 expression that is similar to the effect of SNAP, and an elevation of intracellular cAMP was detected in SNAP-treated cells. With the use of genetically engineered reporter MC that express secreted alkaline phosphatase under the control of the cAMP response element, significant potentiation of cAMP-elicited activation of cAMP response element by SNAP was found. This effect was abrogated in the presence of PDE3 inhibitor cilostamide. Taken together, the results suggest that NO is involved in the control of GJIC and Cx43 expression. This effect of NO is due to activation of protein kinase A via cGMP-dependent inhibition of PDE3 activity.     

逼尿肌不稳定缝隙连接介导细胞间通讯的研究

目的　研究逼尿肌不稳定 (DI)缝隙连接介导的细胞间通讯 (GJIC)功能 ,探讨DI发病机理以及阻断兴奋传递作为治疗手段的可行性。　方法　采用荧光光漂白恢复技术 (FRAP)检测BOO大鼠模型培养膀胱逼尿肌细胞GJIC功能 ,以荧光恢复率作为比较。　结果　在漂白后第 4min时 ,DI组平均荧光恢复率为 (35 .791± 0 .836 ) % ,正常对照组为 (8.6 4 5± 0 .6 73) % ,DI组显著高于对照组 (P <0 .0 1) ,差异有显著性意义。　结论　细胞间兴奋传递增强是DI发生的重要原因之一。     

缝隙连接在大鼠异丙酚和七氟醚麻醉中的作用

目的 评价缝隙连接在大鼠异丙酚和七氟醚麻醉中的作用.方法 雄性Wistar大鼠80只,体重210～260 g,采用随机数字表法,将大鼠随机分为8组(n=10):空白对照组(C组)、甘珀酸组(CA组)、异丙酚组(P组)、不同剂量甘珀酸+异丙酚组(CA1+P组、CA2+P组、CA3+P组)、七氟醚组(S组)、甘珀酸+七氟醚组(CA+S组).用立体定位仪定位大鼠侧脑室.C组侧脑室注射生理盐水2μl后腹腔注射生理盐水2ml,CA组侧脑室注射甘珀酸200μg后腹腔注射生理盐水2ml,P组、CA1+P组、CA2+P组和CA1+P组分别向侧脑室注射生理盐水2 μl、甘珀酸200、300和400μg后腹腔注射异丙酚5 mg/100 g,S组给予浓度梯度七氟醚,CA+S组侧脑室注射甘珀酸200μg后给予浓度梯度七氟醚,七氟醚初始浓度1%,梯度0.1%,记录翻正反射消失时间、翻正反射消失持续时间和翻正反射消失时七氟醚浓度.结果 C组与CA组大鼠均未出现翻正反射消失的麻醉作用;与P组比较,CA1+P组,CA2+P组,CA3+P组翻正反射消失时间缩短,翻正反射消失持续时间延长(P＜0.01);与CA+P组比较,CA2+P组,CA3+P组翻正反射消失时间缩短(P＜0.05);与S组比较,CA+S组翻正反射消失时七氟醚浓度减小(P＜0.05),翻正反射消失时间和消失持续时间差异无统计学意义(P＞0.05).结论 抑制缝隙连接功能虽然可强化异丙酚和七氟醚的麻醉作用,但不是其麻醉作用的主要机理.

Abstract：

Objective To evaluate the role of intercellular gap junction in the propofol and sevoflurane anesthesia in rats. Methods Eighty male Wistar rats weighing 210-260 g were randomly divided into 8 groups (n = 10 each): control group (group C), carbenoxolone group (group CA), propofol group (group P), different doses of carbenoxolone + propofol groups (groups CA1 + P, CA2 + P, CA3 + P), sevoflurane group (group S) and carbenoxolone + sevoflurane group (group CA + S). The animals ware anesthetized with intraperitoneal 10% chloraldurate 4 mg/kg and placed in a stereotactic apparatus to locate the lateral ventricle. In group C, after normal saline (NS) 2 μl was injected into the latersl ventricle, intraperitoneal NS 2 ml was injected. In group CA, after carbenoxolone 200 μg was injected into the lateral ventricle, intraperitoneal NS 2 ml was injected. In groups P,CA1 + P, CA2 + P and CA3 + P, NS 2 μl, and carbenoxolone 200, 300 and 400 μg were injected into the lateral ventricle respectively and then propofol 5 mg/100 g was injected intraperitoneally. Group S inhaled 1% sevoflurane (in increments of 0. 1% ) until the righting reflex was lost. Group CA + S inhaled 1% sevoflurane (in increments of 0.1% ) until the righting reflex was lost after carbenoxolono 200 μg was injected into the lateral ventricle. The time of loss of righting reflex, duration of loss of righting reflex and the sevoflurane concentration when the righting reflex disappeared were recorded. Results The loss of righting reflex did not appear in groups C and CA. Compared with group P, the time of loss of righting reflex was significantly shortened and duration of loss of righting reflex prolonged in groups CA1 + P, CA2 + P, CA3 + P ( P ＜ 0.01 ). The time of loss of righting reflex was significandy shorter in groups CA2 + P, CA3 + P than in group CA1 + P (P ＜ 0.05). The sevoflurane concentration when the righting reflex disappeared was significantly lower in group CA + S than in group S ( P ＜ 0.05 ). There was no significant difference in the time of loss of righting reflex and duration of loss of righting reflex between CA + S and S groups ( P ＞ 0.05). Conclusion Although inhibition of the function of gap junction can strengthen the anesthetic effects of propofol and sevoflurane, it is not the major mechanism.     

脉冲电磁场影响人骨髓基质干细胞缝隙连接通讯的实验研究

目的研究脉冲电磁场(PEMFs)对人骨髓基质干细胞(hBMSCs)缝隙连接所介导细胞间通讯(GJIC)的影响。方法透射电镜观察BMSCs超微结构,应用荧光漂白恢复(FRAP)技术,通过激光共聚焦显微镜检测hBM-SCs经PEMFs刺激后GJIC的功能变化。结果经PEMFs刺激后的hBMSCs,平均荧光漂白恢复率为(64.12±0.83)%,较对照组犤(35.26±0.76)%犦有显著性增加(P<0.05)。结论PEMFs刺激能促进hBMSCs的缝隙连接通讯功能。