骨髓间充质干细胞介导的血红素氧合酶-1促进大鼠心肌梗死后血管再生

目的探讨骨髓间充质干细胞(MSCs)介导的血红素氧合酶-1(HO-1)对心肌梗死后心脏血管再生及左心室功能的影响。方法取大鼠骨髓,体外分离扩增培养MSCs,HO-1腺病毒转染。结扎左前降支1 h后,分别将HO-1-MSCs、MSCs多点注射到大鼠心肌梗死区周边,对照组注射等量PBS。结果 MSCs介导的HO-1能在体外及体内获得稳定表达;HO-1-MSCs组促血管生长因子VEGF、FGF2的表达及毛细血管密度明显高于MSCs组和对照组(P0.01);但促血管再生的作用可被HO抑制剂阻断。HO-1-MSCs组心肌细胞凋亡及纤维化明显低于MSCs组和对照组(P0.01);HO-1-MSCs组左室收缩功能各项指标明显优于其他两组(P0.01)。HO-1-MSCs组心室壁变厚,心室腔明显缩小。结论 MSCs介导的血红素氧合酶-1能促进心肌梗死后心脏血管再生,改善左心室功能。     

骨髓间充质干细胞介导的血红素氧合酶-1促进大鼠心肌梗死后血管再生简

 目的 探讨骨髓间充质干细胞 (MSCs) 介导的血红素氧合酶-1 (HO-1) 对心肌梗死后心 脏血管再生及左心室功能的影响。方法 取大鼠骨髓,体外分离扩增培养 MSCs,HO-1 腺病毒转染。结扎左前降支 1 h 后,分别将 HO-1-MSCs、MSCs 多点注射到大鼠心肌梗死区周边,对照组注射等量 PBS。 结果 MSCs 介导的HO-1能在体外及体内获得稳定表达;HO-1-MSCs组促血管生长因子VEGF、FGF2的表达及毛细血管密度明显高于 MSCs 组和对照组 (P < 0.01);但促血管再生的作用可被HO抑制剂阻断。HO-1-MSCs组心肌细胞凋亡及纤维化明显低于MSCs 组和对照组 (P < 0.01);HO-1-MSCs组左室收缩功能各项指标明显优于其他两组(P < 0.01)。HO-1-MSCs组心室壁变厚,心室腔明显缩小。结论 MSCs介导的血红素氧合酶-1能促进心肌梗死后心脏血管再生,改善左心室功能。     

血红素氧合酶-1对移植入急性梗死区心肌骨髓间充质干细胞的保护作用

目的:观察血红素氧合酶-1(HO-1)体内外对缺血环境下骨髓间充质干细胞(MSCs)的保护作用及梗死后心脏血流动力学的影响。方法:取大鼠骨髓,体外分离扩增培养MSCs;HO-1腺病毒转染MSCs,荧光显微镜下观察绿色荧光蛋白(GFP)的表达;流式细胞仪检测无氧无血清条件培养的HO-1-MSCs、MSCs的凋亡率。建立心梗模型,分别将DAPI-HO-1-MSCs、DAPI-MSCs多点注射到大鼠心脏梗死区周边,对照组注射等量PBS,比较各组MSCs存活率;4周后测定血流动力学指标。结果:HO-1转染的MSCs可稳定高效地表达GFP;在无氧无血清条件下,HO-1-MSCs的凋亡率显著低于MSCs(P<0.01);细胞移植到梗死后心肌,HO-1-MSCs组存活MSCs计数在第7天明显高于MSCs组(P<0.05),且血流动力学各项指标较MSCs组明显改善(P<0.05)。结论:HO-1可在体内、体外实验中提高缺血环境下MSCs的存活率,并改善心肌梗死后血流动力学和心功能,为优化干细胞治疗提供了新思路。     

血红素氧合酶-1 提高无氧无血清条件下骨髓间充质干细胞的生存

目的： 探讨血红素氧合酶-1(HO-1)是否提高骨髓间充质干细胞(MSCs) 在无氧无血清条件下的存活率。方法：取大鼠骨髓,体外分离扩增培养 MSCs;HO-1腺病毒转染 MSCs,荧光显微镜下观察绿色荧光蛋白 (GFP) 的表达;DAPI 染色观察无氧无血清条件下 HO-1-MSCs、MSCs 细胞核变化;流式细胞仪检测无氧无血清条件下HO-1-MSCs、MSCs 的凋亡率;ELISA 检测无氧无血清条件下 HO-1-MSCs、MSCs 细胞因子的分泌。用无氧无血清条件下 HO-1-MSCs、MSCs 的培养上清液对无氧无血清条件下的心肌细胞进行培养,Western blotting 检测凋亡蛋白 caspase-3 的变化,分光光度计检测 caspase-3 酶活性。结果： HO-1 转染的 MSCs 可稳定高效地表达 GFP; DAPI 染色后,MSCs 细胞核为典型的凋亡形态,HO-1-MSCs 为较均匀蓝色荧光;HO-1-MSCs 在无氧无血清条件下的凋亡率显著低于 MSCs (P<0.01),且在无氧无血清条件下分泌肝细胞生长因子（HGF)、碱性成纤维细胞生长因子 (bFGF)、血管内皮生长因子 (VEGF) 水平显著增高 (P<0.01);HO-1-MSCs、MSCs 培养上清液在无氧无血清条件下分别培养心肌细胞,HO-1-MSCs 组caspase-3 蛋白和 caspase-3 活性都显著降低 (P<0.01)。结论：无氧无血清条件下,HO-1 提高 MSCs 的存活率;HO-1-MSCs 分泌更多的细胞因子,且对无氧无血清条件下的心肌细胞有保护作用。     

血红素氧合酶1提高骨髓间充质干细胞在梗死后心脏的存活

背景：移植骨髓间充质干细胞(bone mesenchymal stem cells,BMSCs)修复梗死后心功能受到围移植期移植细胞大量死亡的限制。因此寻找一种保护因子对移植细胞提供保护至关重要。 目的：观察血红素氧合酶1(heme oxygenase,HO-1)对BMSCs在梗死后心脏生存的影响。 方法：体外分离扩增培养大鼠BMSCs,Adv-hHO-1、Adv-GFP分别转染,移植前DAPI标记。结扎左前降支1 h后,分别将DAPI-hHO-1-BMSCs、DAPI-GFP-BMSCs多点注射到大鼠心脏梗死区周边,对照组注射等量PBS。 结果与结论：Adv-hHO-1转染BMSCs后获稳定表达。仅hHO-1-BMSCs组稳定表达hHO-1 mRNA;hHO-1-BMSCs组血管内皮生长因子、碱性成纤维细胞生长因子、肝细胞生长因子表达均高于其他两组(P < 0.01);存活BMSCs数量在第3,7天均明显高于GFP-BMSCs组(P < 0.05);大鼠心功能各项参数明显优于其他两组(P < 0.01)。移植4周后,HO-1-BMSCs组梗死区周边毛细血管密度明显高于GFP-BMSCs组和对照组(P < 0.01),且胶原蛋白沉积减少,心室壁变厚,梗死面积较其他两组明显缩小(P < 0.01)。提示HO-1提高移植到梗死心脏BMSCs的存活,HO-1协同BMSCs抑制心室重构,改善心功能。     

Livin基因修饰的骨髓间充质干细胞移植治疗对急性心肌梗死大鼠心功能的影响

 目的: 探讨livin修饰的骨髓间充质干细胞(MSCs)移植改善急性心肌梗死大鼠心功能的作用及livin和促凋亡蛋白caspase-3、caspase-7、caspase-9在感染后的表达情况。方法: 通过全骨髓培养法分离培养骨髓间充质干细胞,感染携带livin基因的重组腺病毒后用流式检测其对MSCs凋亡的影响。通过Western blot法分别检测livin、caspase-3、caspase-7和caspase-9的蛋白表达情况。采用冠状动脉左前降支结扎法建立心肌梗死模型,然后实验分4组进行:无胎牛血清的DMEM组;单纯干细胞治疗组(MSCs组);空载腺病毒转染干细胞组(rAd-control/MSCs)组;livin基因转染干细胞组(rAd-livin/MSCs组)。1个月后采用生理仪记录各组大鼠左室收缩压(LVSP)、左室舒张末压(LVEDP)、左室内压最大上升速率(+dp/dt_max)和左室内压最大下降速率(-dp/dt_max)来评价大鼠心功能。结果: rAd-livin/MSCs组凋亡率较MSCs组和rAd-control/MSCs组显著降低(P<0.05);rAd-livin/MSCs组抗凋亡蛋白livin明显上升(P<0.05),促凋亡蛋白caspase-3、caspase-7及caspase-9表达显著下降(P<0.05);细胞移植后1个月,rAd-livin/MSCs组心功能比MSCs组改善更明显(P<0.05)。结论: rAd-livin感染MSCs后可促进抗凋亡蛋白livin的表达,同时降低促凋亡蛋白caspase-3、caspase-7和caspase-9的表达及细胞凋亡率。rAd-livin/MSCs移植能进一步改善心肌梗死大鼠心功能。     

LOX-1在吡格列酮调节高脂血症大鼠主动脉凋亡蛋白表达中的作用

目的:观察吡格列酮对高脂血症大鼠主动脉血凝集素样氧化低密度脂蛋白受体-1(LOX-1)和凋亡蛋白Bax、Bcl-2表达的影响,探讨LOX-1在其中的变化和作用。方法:清洁级SD大鼠26只,随机分为正常组(n=9)、高脂饲料组(n=17),高脂饲料喂养12周后再随机分为高脂血症模型组(n=8)和吡格列酮组(n=9),分别给予生理盐水(正常组和模型组)和药物(吡格列酮组)干预4周后,常规方法检测各组血脂水平,免疫组织化学法检测各组主动脉LOX-1、Bax、Bcl-2蛋白表达,TUNEL染色法观察主动脉内膜细胞凋亡情况,并计算细胞凋亡指数(AI)。结果:高脂饲料喂养12周后,成功复制17只高脂血症模型大鼠。吡格列酮干预4周后,与模型组比较,吡格列酮组甘油三酯(TG)、胆固醇(TC)水平明显降低(P<0.01)。与正常组相比,模型组大鼠主动脉LOX-1、Bax蛋白表达明显增加(P<0.01),Bcl-2蛋白表达及Bcl-2/Bax比值明显降低(P<0.01);与模型组相比,吡格列酮组主动脉LOX-1、Bax蛋白表达明显降低(P<0.01),Bcl-2蛋白表达和Bcl-2/Bax比值明显升高(P<0.01),且吡格列酮组主动脉内膜AI亦较模型组显著降低(P<0.01)。结论:吡格列酮可改善高脂血症大鼠血脂水平,调节凋亡蛋白表达,减少主动脉内皮细胞凋亡,其作用可能与其下调LOX-1蛋白表达有关。     

曲美他嗪与帕瑞昔布联合给药对急性心肌梗死期大鼠心脏的保护作用

目的: 探讨曲美他嗪(TMZ)与帕瑞昔布(parecoxib)联合给药对急性心肌梗死模型大鼠心脏的保护作用及其机制。方法: 66只雄性SD大鼠随机分为假手术组(sham)、急性心肌梗死模型组(AMI)、曲美他嗪治疗组(AMI+TMZ)、帕瑞昔布钠治疗组(AMI+parecoxib)和曲美他嗪与帕瑞昔布钠联合治疗组(AMI+TMZ+parecoxib)。大鼠实施冠状动脉左前降支结扎后,第3 d开始给药,第8 d检测大鼠心功能(HR、LVSP、LVEDP、+dp/dt_max和-dp/dt_max),测定心脏梗死面积, bax和bcl-2 基因表达, COX-2、Bax、Bcl-2和cleaved caspase-3的蛋白表达,caspase-3活化以及心肌梗死周边区细胞凋亡率。结果: 与假手术组相比,AMI模型组大鼠心肌梗死周边区COX-2蛋白表达明显增高(P<0.01);帕瑞昔布钠治疗组与AMI模型组相比,COX-2表达下降(P<0.01);联合给药治疗组与模型组相比,能显著改善心肌梗死大鼠的心脏收缩功能(LVSP与+dp/dt_max)(P<0.05),并使心肌梗死面积缩小(P<0.05),心肌梗死周边区细胞的凋亡率下降,并且治疗效果优于单独给药。联合给药治疗组与模型组相比,Bax/Bcl-2 mRNA和蛋白表达比例显著降低(P<0.05),caspase-3活性和cleaved caspase-3蛋白表达下降(P<0.05)。结论: 帕瑞昔布钠与曲美他嗪联合给药治疗具有一定的协同保护缺血心肌的作用,其机制可能与共同抑制心肌细胞凋亡有关。     

人受体活性修饰蛋白1基因修饰的骨髓间充质干细胞移植对兔血管成形术后新生内膜的影响

目的: 探讨人受体活性修饰蛋白1( hRAMP1 )基因修饰的骨髓间充质干细胞(MSCs)移植对动脉粥样硬化模型兔颈动脉球囊成形术后新生内膜增殖的影响。方法: 密度梯度离心法加贴壁培养法获得MSCs,并以携带 hRAMP1 的腺病毒转染MSCs获得 hRAMP1 基因修饰的MSCs(hRAMP1-MSCs)。建立动脉粥样硬化狭窄并球囊损伤血管成形术的兔模型,随机分为hRAMP1-MSCs组、MSCs组和对照组,模型建立成功后经耳缘静脉分别注射携带pAd2-EGFP-hRAMP1或pAd2-EGFP的MSCs和PBS,于细胞移植后7 d、14 d和28 d分别处死动物取材, 观察MSCs归巢、血管内皮化程度及内膜增生程度,同时检测血清血管内皮生长因子(VEGF)水平和血管局部内皮型一氧化氮合成酶(eNOS)表达。结果: 细胞移植后不同时点hRAMP1-MSCs组和MSCs组损伤血管增生内膜均有CD31和增强型绿色荧光蛋白(EGFP)分布,但以 hRAMP1-MSCs组内皮化程度明显,MSCs组次之,两者与对照组比较均有显著差异(P<0.05);细胞移植后不同时点hRAMP1-MSCs组和MSCs组内膜增生面积及再狭窄率均低于对照组(P<0.05),尤以hRAMP1-MSCs组降低明显;细胞移植后不同时点hRAMP1-MSCs组和MSCs组血清VEGF水平和血管eNOS表达较对照组增加(P<0.05),而 hRAMP1-MSCs组又明显高于MSCs组(P<0.05);损伤血管新生内膜增殖细胞核抗原(PCNA)阳性表达在hRAMP1-MSCs组最少,对照组最多。结论: hRAMP1 基因修饰的MSCs能更有效促进损伤内膜快速内皮化,重组 hRAMP1 腺病毒载体不影响MSCs向内皮细胞分化潜能。基因联合干细胞治疗能更好地促进损伤动脉快速内皮化,降低血管成形术后再狭窄。     

川芎嗪联合骨髓间充质干细胞移植抑制脑缺血大鼠神经细胞凋亡

目的:研究川芎嗪(tetramethylpyrazine,TMP)联合骨髓间充质干细胞(bone marrow mesenchymal stem cells,BMSCs)对脑缺血大鼠神经细胞凋亡及Bcl-2、Bax表达的影响。方法:采用全骨髓贴壁法体外培养BMSCs,传代至第3代用于尾静脉移植。采用线栓法诱导大鼠右侧大脑中动脉阻塞模型,除假手术组外,大鼠随机分为模型组、BMSCs(1×10~9/L)组、川芎嗪(40 mg/kg)组和联合(川芎嗪+BMSCs)组,每组12只。缺血后第1、7和14天采用改良的神经损伤严重程度评分(modified neurological severity scoring,m NSS)进行神经功能评价。缺血后第14天,甲苯胺蓝染色检测脑梗死体积,HE染色观察脑组织病理学变化,采用原位末端标记(TUNEL)法观察神经细胞凋亡数,采用实时荧光定量PCR法和Western blot法检测Bax和Bcl-2的mRNA及蛋白表达。结果:与BMSCs组和川芎嗪组比较,联合组m NSS评分显著减少(P0.01),梗死体积显著减少(P0.01),缺血引起的脑缺血周边区病理性损伤明显减轻,TUNEL阳性细胞数显著减少(P0.01),Bcl-2的mRNA及蛋白表达显著增加,Bax的mRNA及蛋白表达显著降低(P0.01)。结论:川芎嗪联合BMSCs移植能显著促进脑缺血后大鼠的功能恢复,减少梗死体积,减轻脑组织缺血性损伤,抑制神经细胞凋亡,机制可能与调控Bcl-2和Bax的表达有关。     

血红素氧合酶1修饰骨髓间充质干细胞多点注射梗死灶周围对梗死后心肌结构重塑的影响

背景：研究表明血红素氧合酶1的过表达有抗炎症反应的作用,将血红素氧合酶1修饰的骨髓间充质干细胞(HO-1-BMSCs)移植入梗死心脏周围是否可调节基质金属蛋白酶/组织金属蛋白酶抑制剂的比例而明显改善梗死心肌重构呢？ 目的：观察血红素氧合酶1修饰的骨髓间充质干细胞移植对心肌梗死后心肌胶原的调节及心肌重塑的逆转作用。 方法：利用血红素氧合酶1腺病毒转染体外培养扩增的骨髓间充质干细胞。结扎大鼠左前降支动脉制造心肌梗死模型,1 h后,分别将HO-1-BMSCs、BMSCs多点注射到大鼠心脏梗死区四周,对照组注射等量磷酸盐缓冲液。 结果与结论：Adv-hHO-1转染BMSCs后获稳定表达;hHO-1-mRNA仅在HO-1-BMSCs移植组表达;与对照组相比,HO-1-BMSCs移植组基质金属蛋白酶2/9的表达显著减少(P < 0.05),Null-BMSCs组基质金属蛋白酶2/9的表达虽然减少,但差异无显著性意义(P > 0.05);与对照组相比,细胞移植组金属蛋白酶组织抑制剂2/3的表达显著增加,尤以HO-1-BMSCs组明显(P < 0.05);但金属蛋白酶组织抑制剂1无明显变化(P > 0.05)。金属蛋白酶组织抑制剂2/基质金属蛋白酶2和金属蛋白酶组织抑制剂3/基质金属蛋白酶9的比例在细胞移植的心脏中明显上升。与对照组比较,细胞移植组心室中的胶原蛋白沉积减少,心室腔内径显著缩小。结果表明血红素氧合酶1修饰的骨髓间充质干细胞移植可使基质金属蛋白酶/组织金属蛋白酶抑制剂的比例正常化,并逆转心肌细胞外基质的重构。     

大鼠脂肪干细胞联合碱性成纤维生长因子治疗大鼠心肌梗死

目的 探讨脂肪干细胞（ADSC）联合碱性成纤维生长因子（bFGF）提高心肌梗死大鼠心脏功能的可能机制.方法 SD大鼠50只,先行脂肪干细胞提取手术,分离、培养、鉴定脂肪干细胞,行干细胞成脂、成骨诱导分化,建立大鼠心肌梗死模型,选择缩短分数（FS）＜40％的SD大鼠（36只）,完全随机分4组：单纯注射PBS组（n=9）、单纯注射bFGF组（n=9）、PBS＋ADSC组（n=9）以及ADSC＋bFGF组（n=9）,以bFGF胶为可注射性载体,ADSC为种子细胞,1周后进行大鼠心梗部位移植.移植4周后对心梗面积、左心室室壁厚度、心梗部位微血管密度、ADSC在心梗部位分化情况等指标进行检测,并利用心脏超声对心梗大鼠的心脏功能进行测定.应用免疫组织化学、免疫荧光等方法评价其改善心脏功能可能机制.结果 成功分离ADSC并且通过流式细胞术表明大多数分离的脂肪干细胞CD90抗体阳性、CD29抗体阳性、CD45抗体和CD34抗体阴性.脂肪干细胞能够经过诱导分化成成脂、成骨细胞.PBS＋ADSC组以及ADSC＋bFGF组在室壁厚度、梗死面积、梗死区域微血管形成能力与PBS组相比,差异均有统计学意义,且以ADSC＋bFGF组最为显著（P＜0.01）.ADSC移植到大鼠心脏4周后,可以分化为cTnT阳性细胞、SMA阳性细胞以及vWAg阳性细胞.心功能检测结果表明PBS＋ADSC组同ADSC＋bFGF组一样,具有心梗修复能力.结论 移植ADSC的同时增加bFGF能促进梗死区的心肌再生以及血管化,并能显著改善心脏功能.     

心肌干细胞调控ANG Ⅱ/AT1R/TGF-β1/SMAD/CX43通路改进心电生理学稳定性和室颤阈值

BACKGROUND:Previous studies have demonstrated that the electrophysiological stability and ventricular fibrillation threshold after myocardial infarction in rats are significantly improved in the mid-term of cardiac stem cell transplantation, but relative regulatory mechanism and pathway remain unclear. OBJECTIVE:To explore the relative molecular regulatory mechanism of cardiac stem cells improving the electrophysiological stability and ventricular fibrillation threshold after myocardial infarction in rats.  METHODS:Myocardial infarction was induced in 20 Sprague-Dawley rats by ligation of the left anterior descending coronary, which were then randomized into two groups (n=10 per group) and were subjected to the injection of cardiac stem cells labeled with PKH26 in phosphate buffer solution (cardiac stem cell group) or the same amount of phosphate buffer solution (PBS) alone (PBS group) into the local infarct zone at 2 weeks after modeling, respectively. Six weeks later, relevant signaling molecules involved in the ANGII/AT1R/TGF-β1/SMAD/Cx43 pathway were all examined in myocardial tissues of the left ventricle and harvested blood samples. RESULTS AND CONCLUSION:Compared with the PBS group, expressions of connexin 43 in different zones of the left ventricle were significantly increased in the cardiac stem cell group (P < 0.01); there was a significant reduction of the angiotensin II level in plasma and different regions of the left ventricular (P < 0.05; P < 0.01). Furthermore, in the cardiac stem cell group, expressions of angiotensin II type I receptor, transforming growth factor-β1, SMAD2 and SMAD3 were significantly decreased (P < 0.01). Whereas SMAD7 was significantly elevated (P < 0.05) in different areas of the left ventricle compared with the phosphate buffer solution group. These findings suggest that the cardiac stem cell transplantation can improve the electrophysiological stability and ventricular fibrillation threshold after myocardial infarction by enhancing the expression of connexin 43 via ANGII/AT1R/TGF-beta1/SMAD/CX43 signaling pathway.     

Monocyte chemotactic protein 1 increases homing of mesenchymal stem cell to injured myocardium and neovascularization following myocardial infarction

Objective:To investigate the effect of MCP-1 on mesenchymal stem cells(MSCs) homing to injured myocardium in a rat myocardial infarction(MI) model. Methods:Rat myocardial infarction model was established by permanent left anterior descending branch ligation. Mesenchymal stem cells from donor rats were cultured in IMDM and labeled with BrdU. The Rats were divided into two groups. Monocyte chemotactic protein 1(MCP-1) expression were measured by in situ hybridization and immunohistochemistry in the sham operated or infarcted hearts at 1,2, 4,7,14 and 28 days post operation in MCP-1 detection group. The rats were injected with MCP-1, anti-MCP-1 antibody or saline 4 days after myocardial infarction in intervention group. Then, a total of 5 × 106 cells in 2.5 ml of PBS were injected through the tail vein. The number of the labeled MSCs in the infarcted hearts was counted 3 days post injection. Cardiac function and blood vessel density were assessed 28 days post injection. Results:Self-generating MCP-1 expression was increased at the first day, peaked at the 7th day and decreased thereafter post MI and remained unchanged in sham operated hearts. The MSCs enrichment in the host hearts were more abundant in the MI groups than that in the non-Mi group(P = 0.000), the MSCs enrichment in the host hearts were more abundant in the MCP-1 injected group than that in the anti-MCP-1 antibody and saline injected groups (P = 0.000). Cardiac function was improved more in MCP-1 injected group than anti-MCP-1 antibody and saline injected groups(P= 0.000). Neovascularization in MCP-1 injected group significantly increased compared with that of other groups(P = 0.000). Conclusion: Myocardial MCP-1 expression was increased only in the early phase post MI. MCP-1 may enhance MSCs homing to the injured heart and improve cardiac function by promoting neovascularization.     

Bcl-2 engineered MSCs inhibited apoptosis and improved heart function

Engraftment of mesenchymal stem cells (MSCs) derived from adult bone marrow has been proposed as a potential therapeutic approach for postinfarction left ventricular dysfunction. However, limited cell viability after transplantation into the myocardium has restricted its regenerative capacity. In this study, we genetically modified MSCs with an antiapoptotic Bcl-2 gene and evaluated cell survival, engraftment, revascularization, and functional improvement in a rat left anterior descending ligation model via intracardiac injection. Rat MSCs were manipulated to overexpress the Bcl-2 gene. In vitro, the antiapoptotic and paracrine effects were assessed under hypoxic conditions. In vivo, the Bcl-2 gene-modified MSCs (Bcl-2-MSCs) were injected after myocardial infarction. The surviving cells were tracked after transplantation. Capillary density was quantified after 3 weeks. The left ventricular function was evaluated by pressure-volume loops. The Bcl-2 gene protected MSCs against apoptosis. In vitro, Bcl-2 overexpression reduced MSC apoptosis by 32% and enhanced vascular endothelial growth factor secretion by more than 60% under hypoxic conditions. Transplantation with Bcl-2-MSCs increased 2.2-fold, 1.9-fold, and 1.2-fold of the cellular survival at 4 days, 3 weeks, and 6 weeks, respectively, compared with the vector-MSC group. Capillary density in the infarct border zone was 15% higher in Bcl-2-MSC transplanted animals than in vector-MSC treated animals. Furthermore, Bcl-2-MSC transplanted animals had 17% smaller infarct size than vector-MSC treated animals and exhibited functional recovery remarkably. Our current findings support the premise that transplantation of antiapoptotic gene-modified MSCs may have values for mediating substantial functional recovery after acute myocardial infarction.