Chinese Journal of Tissue Engineering Research ›› 2022, Vol. 26 ›› Issue (25): 4070-4075.doi: 10.12307/2022.416
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Zeng Rui, Hai Bing
Received:
2020-11-20
Accepted:
2021-02-05
Online:
2022-09-08
Published:
2022-01-26
Contact:
Hai Bing, Master, Chief physician, Second Ward, Department of Respiratory and Critical Care Medicine, Second Affiliated Hospital of Kunming Medical University, Kunming 650032, Yunnan Province, China
About author:
Zeng Rui, Master candidate, Second Ward, Department of Respiratory and Critical Care Medicine, Second Affiliated Hospital of Kunming Medical University, Kunming 650032, Yunnan Province, China
Supported by:
CLC Number:
Zeng Rui, Hai Bing. Impact of nicotine on stem cells[J]. Chinese Journal of Tissue Engineering Research, 2022, 26(25): 4070-4075.
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2.1 尼古丁临床知识、生物学影响 尼古丁是烟草及相关产品的主要成瘾成分[11-12]。2015年估计全世界每天有9.331亿吸烟者[13]。2018年最新全球成人烟草调查(GATS)示:在中国15岁及以上人群现在吸烟率为26.6%(现在吸烟人数为3.08亿),其中男性50.5%,女性为2.1%,对比2010年GATS结果显示中国成人吸烟率一直保持稳定,意味着尼古丁暴露也保持稳定。近些年电子烟的使用日益广泛,尤其是在初中生中,2019年初中学生电子烟使用率为2.7%,与2014年相比,分别上升了24.9%和1.5%[14]。使得电子烟成为尼古丁暴露的另一种途径。尼古丁具有导致生长迟缓、生殖功能下降、应激反应过度、新陈代谢异常等许多负面影响[15-17]。在心血管疾病中,尼古丁通过损伤血管内皮细胞、增加内皮通透性、促进人脐静脉内皮细胞增殖、迁移和血液凝固,同时激活血管紧张素Ⅱ受体1引起内皮功能紊乱[18],增加了动脉粥样硬化的发病率[19-20]。尼古丁本身并不致癌,但参与多种癌症的进展。在口腔鳞状细胞癌中,尼古丁通过激活核转录因子κB来促进口腔鳞状细胞癌SCC15细胞增殖并诱导少量正常细胞凋亡[21];在膀胱癌中,尼古丁和β-肾上腺素受体结合后激活STAT3 并下调 ERK1 / 2来介导膀胱癌进展;还有研究表明,尼古丁主要通过旁分泌信号激活细胞与细胞的相互作用驱动癌细胞增殖来参与胰腺癌的进展[22]。 尼古丁的生物学效应是通过神经元烟碱型乙酰胆碱受体(nAChRs)介导的。烟碱型乙酰胆碱受体是变构调节的配体门控离子通道,是由9个α亚基(α2- α10)和3个β亚基(β2-β4)组成的五聚体蛋白。在干细胞中,已经确认了有烟碱型乙酰胆碱受体亚基的表达[23],烟碱型乙酰胆碱受体是一类能改变钠和钙通透性的配体门控离子通道[24] ,一旦受体被激活,中心孔就会打开,以允许钠、钾和钙阳离子进入细胞,使细胞去极化。烟碱型乙酰胆碱受体激活后大量钙离子内流,触发许多细胞内信号转导途径,参与细胞增殖、凋亡、细胞分化、氧化应激和炎症、血管生成等细胞行为[25]。 2.2 尼古丁对各类干细胞的影响 干细胞是一类具有自我更新和多向分化潜能的细胞,在一定条件下可以分化为多种功能细胞。根据干细胞发育潜能可分为全能干细胞、多能干细胞和单能干细胞[26]。由于胚胎干细胞具有强大的多能性,所以大多数研究都集中在胚胎干细胞上,其他类型干细胞研究随着政策支持力度的增加也逐渐得到关注,例如牙周膜干细胞、间充质干细胞和诱导多能性干细胞[27]。下面将深入描述尼古丁暴露对干细胞的影响,着重对胚胎干细胞、间充质干细胞、诱导多能性干细胞和牙周膜干细胞进行描述。 2.2.1 胚胎干细胞 胚胎干细胞具有很强的分化能力,可以发育为内胚层、中胚层和外胚层3个胚层组织,并无限增殖并分化成为全身200多种细胞类型。胚胎干细胞来源于早期胚胎。由于胚胎干细胞具有强大的多能性,它已被用于许多疾病和临床前研究[28-29]。2017年3月,中国启动了两项使用人类胚胎干细胞治疗帕金森病和年龄相关性黄斑变性引起的视力丧失的临床试验(《人民日报》2017-04-12),这两项临床试验研究是国家卫生和计划生育委员会和食品药品监督管理局在中国进行的首次临床试验,也是世界上首次将抗原匹配的人类胚胎干细胞用于临床试验。然而,出于对伦理规范和胚胎干细胞治疗安全性的考虑,人类胚胎干细胞用于再生医学具有很大的限制性。 既往有大量研究表明尼古丁暴露对胚胎干细胞有负面影响。早在2012年LISZEWSKI等[30]对比吸烟母亲与不吸烟母亲的脐带组织发现,尼古丁对人类胚胎干细胞分化具有阶段特异性效应,即尼古丁对中胚层、外胚层和内胚层均有延迟其发育作用,但对中胚层晚期发育影响较大,而对外胚层和内胚层的早期发育影响较大,其主要机制是通过转化生长因子β超家族成员Nodal介导来实现的。LIN等[31]对比未接触烟草烟雾的小鼠胚胎干细胞发现,暴露于主流烟或侧流烟(二手烟)24 h的小鼠胚胎干细胞中均产生更高水平的细胞毒性和黏附性损害。对于小鼠胚胎干细胞的增殖,尼古丁具有双向调节特性,0.01 mmol/L和0.1 mmol/L剂量的尼古丁可促进小鼠胚胎干细胞增殖,而 1 mmol/L和10 mmol/L则可抑制小鼠胚胎干细胞增殖,这种剂量依赖性调节是通过Wnt /β-catenin 途径介导的,Wnt /β-catenin途径调节小鼠胚胎干细胞增殖和细胞周期的进展,会加重或逆转尼古丁的影响[32]。 KIM等[33]将小鼠胚胎干细胞长期暴露于烟草烟雾中,发现尼古丁影响小鼠胚胎干细胞表达HDAC1、HDAC2、GATA4、NKX2-5、 TBX5、HAND1和肌钙蛋白Ⅰ,也会延迟心肌细胞发育并抑制可收缩性,影响心脏的基本功能。HE等[34]用单细胞RNA测序来研究尼古丁暴露对人胚胎干细胞H9系(H9人胚胎干细胞系是国际上最通用胚胎干细胞系之一,该细胞是从人类早期胚胎内细胞团分离出来,具有体外培养无限增殖、自我更新和多向分化的特性,可为细胞遗传发育以及疾病模型研究提供丰富的实验材料)心脏分化的影响,发现尼古丁剂量为 0.1-10 μmol/L时不影响H9系细胞增殖,1 μmol/L尼古丁相对下调了心脏祖细胞、中胚层细胞、平滑肌细胞和神经嵴细胞的细胞活力,在分化的第6天,尼古丁使Gata4、Isl-1和Nkx2.5表达终止,最终使心内膜发育延迟。将人胚胎干细胞来源内皮细胞用尼古丁(10 mmol/L)处理24 h,注射到左前降支结扎小鼠的心脏中,然后对照组给予2%的糖精溶液,实验组饮用含有100 mg/L尼古丁的糖精溶液,以评估尼古丁对人胚胎干细胞来源内皮细胞再生潜能的影响。令人惊讶的是,在第6周时,实验组移植的人胚胎干细胞来源内皮细胞存活率较对照组显著提高,这是首次研究表明短期低剂量的尼古丁可以改善移植人胚胎干细胞来源内皮细胞的生存,并增加体内血管的生成,其中机制可能与烟碱型乙酰胆碱受体被激活后通过MAPK和Akt信号通路使其具有抗凋亡、血管生成和增殖作用有关[35]。 2.2.2 间充质干细胞 间充质干细胞是多能干细胞,具有高增殖速率特性,并能在体外分化为各种中胚层细胞谱系[36]。许多研究表明,间充质干细胞的功能受大量信息系统的控制[37]。 已证实间充质干细胞表达烟碱乙酰胆碱受体亚基α3、α5和 β2、β4、β7等[38]。间充质干细胞具有易提取、分离、扩增、纯化和无伦理问题的优点,是临床干细胞治疗研究中应用最多的干细胞类型,尤其自2000年以来间充质干细胞临床试验迅速增加。 尼古丁对间充质干细胞的体外作用已被广泛研究,尼古丁对间充质干细胞增殖、迁移、凋亡、分化均会产生影响。尼古丁影响间充质干细胞的增殖,并且具有双峰效应,国外学者研究发现暴露于浓度为1.0-2.0 mmol/L尼古丁时牙槽骨髓源性间充质干细胞增殖增加,而当浓度为5 mmol/L时细胞增殖显著下降,这可能与细胞周期蛋白D1或p53信号转导有关[39]。人脐带间充质干细胞显露于质量浓度为0.5-1.5 g/L尼古丁时细胞增殖以剂量依赖性方式被抑制,凋亡细胞比例以剂量依赖性方式显著增加,在尼古丁浓度达到6.2 mmol/L时细胞变为致死性,细胞形态发生变化,即细胞质凝结和细胞核内出现空泡,核边界模糊[40]。KIM等[41]研究发现即使尼古丁浓度低至0.1 mmol/L时,也可观察到间充质干细胞增殖显著降低。WAHL等[42]对人脂肪源性间充质干细胞研究发现,暴露在尼古丁浓度为5%和10%水平时,间充质干细胞均无活性,而在尼古丁浓度低于 1%时间充质干细胞存活率无显著变化,这项研究强调尼古丁剂量超过特定阈值,间充质干细胞可能直接凋亡。研究发现,尼古丁可上调人脐带间充质干细胞中α7烟碱型乙酰胆碱受体的表达,并刺激间充质干细胞释放一氧化氮、升高细胞内Ca2+从而致间充质干细胞凋亡[43]。 间充质干细胞还具有迁移能力。间充质干细胞向损伤部位迁移并通过释放生长因子和细胞因子以及通过直接分化促进伤口愈合,这种间充质干细胞特有的定向迁移形式,称为“干细胞归巢”。尼古丁调控间充质干细胞的迁移存在剂量依赖性。当烟草烟雾浓度小于 1%时人脂肪源性间充质干细胞的迁移潜力在体外不受影响,但当烟草烟雾浓度大于 5%时会直接影响人脂肪源性间充质干细胞迁移[44]。研究发现,当烟草烟雾浓度为100%时不仅诱导了乳腺上皮细胞的上皮向间质转化,也促进间充质干细胞的迁移和转移;在无趋化因子的培养物中,加入1 mmol/L尼古丁可显著促进人骨髓源性间充质干细胞的自发迁移[45]。曾慧兰等[46]认为影响间充质干细胞黏附和迁移的机制可能与尼古丁通过增加一氧化氮、一氧化氮合酶、诱导型一氧化氮合酶和活性氧水平,降低线粒体膜电位,使基质细胞衍生因子1、转化生长因子β1、胰岛素样生长因子1及碱性成纤维细胞生长因子分泌下降,细胞间黏附分子 1、基质金属蛋白酶9 及基质金属蛋白酶抑制物1表达上升有关。 烟碱型乙酰胆碱受体能在软骨细胞中表达,尼古丁作为烟碱型乙酰胆碱受体的激动剂,在软骨分化过程中发挥重要作用,尼古丁对间充质干细胞的软骨分化有不利影响,这可能是通过α7烟碱型乙酰胆碱受体介导而受损的[47]。YING等[48]却有不同的看法,他们认为尼古丁在浓度为1 mmol/L时对Ⅱ型胶原有积极作用,Ⅱ型胶原是关节软骨主要组成成分,同期研究发现单层培养 14 d的骨髓间充质干细胞暴露在尼古丁中不影响聚集蛋白聚糖的表达,聚集蛋白聚糖是软骨形成分化最广泛认可的标志。ZHAO等[49]对比3名吸烟者和3名非吸烟者的牙槽骨骨髓间充质干细胞,发现吸烟对人牙槽骨骨髓间充质干细胞的增殖和成骨具有有害的遗传作用,而人牙槽骨骨髓间充质干细胞的生物学功能下降与骨骼愈合呈正相关,吸烟减少了体内和体外人牙槽骨骨髓间充质干细胞的成骨和增殖能力。总之,目前尼古丁对间充质干细胞软骨形成分化的影响尚存在争议,是否与尼古丁剂量不同或者实验条件等因素有关,将来需要更多的研究来证实。 2.2.3 诱导多能干细胞 诱导多能干细胞是通过在已分化的体细胞中表达特定的基因或特定基因产物等方式,以诱导体细胞的重编程而获得可不断自我更新且具有多向分化潜能的细胞。2006年,日本科学家将分化的小鼠体细胞在特定诱导因子Oct4、Sox2、c-Myc和Klf4(即OSKM体系)过表达作用下,逆转去分化重回多能干细胞,并命名为诱导多能干细胞[50]。目前诱导多能干细胞的临床应用可以分为3类:疾病模型(用于疾病机制的研究和罕见病药物筛查的研究)、干细胞疗法和组织器官再生。 有研究报道诱导多能干细胞表达烟碱型乙酰胆碱受体亚基α4、α7和α6,而这些亚基都是激活乙酰胆碱途径所必需的[51]。与其他类型干细胞一样,尼古丁对诱导多能干细胞的增殖和分化有影响。LEE等[52]利用诱导多能干细胞作为筛选模型来评估市场上流行的电子烟的毒性,发现人诱导多能干细胞暴露在尼古丁浓度为 0.1%或更高时,细胞增殖能力显著降低,将人诱导多能干细胞来源内皮细胞暴露于电子烟使用者的血清后,观察到与内皮功能障碍有关的活性氧水平升高,使促血管生成特性受损,且往往尼古丁浓度越高会产生越高水平的活性氧和越多的细胞凋亡。ISHIZUKA等[53]发现用300 nmol/L烟碱处理小鼠诱导多能干细胞会显著增加细胞DNA合成,导致细胞增殖速率显著增加,用α4烟碱型乙酰胆碱受体和α7烟碱型乙酰胆碱受体拮抗剂或CaMKⅡ抑制剂进行预处理可以显著抑制这种情况,此外,在小鼠诱导多能干细胞中Ca2+水平会随着尼古丁剂量的增加而升高,他们认为这可能是尼古丁促进小鼠诱导多能干细胞增殖的主要原因。通过比较诱导多能干细胞源性间充质干细胞与骨髓源性间充质干细胞治疗烟草烟雾接触引起的心脏损伤的疗效,发现诱导多能干细胞源性间充质干细胞在心脏功能结局方面比骨髓源性间充质干细胞更好,诱导多能干细胞源性间充质干细胞表现出左心室射血分数增加,还减轻了氧化应激、炎性细胞因子分泌和纤维化反应。尽管尚不清楚这些作用的潜在机制,但结果表明,诱导多能干细胞源性间充质干细胞对烟草烟雾暴露和相关生理环境有更强的抵抗力[54]。 2.2.4 牙周膜干细胞 牙周膜干细胞是一类牙周膜组织来源的间充质干细胞,文章涉及尼古丁暴露对间充质干细胞的影响主要描述了人脐带、牙槽、脂肪来源的间充质干细胞,此处单独对牙周膜干细胞进行描述的原因有以下几点:第一,香烟烟雾中含有7 000多种化学物质和250种已知毒素,吸入烟雾是吸烟者的主要尼古丁暴露方式。实际上,唾液尼古丁的含量几乎是血浆中的87倍[55]。暴露于这种剂量的尼古丁对口腔中的间充质干细胞亚群(牙周膜干细胞)是十分危险的,所以单独对牙周膜组织来源间充质干细胞进行研究是很有必要的;第二,牙周膜干细胞易从牙周组织中分离出来,并且最能在体内再生典型的牙周膜样结构,这使其在牙周组织工程和细胞治疗中成为了极好的细胞来源;第三,不同于其他类型干细胞,牙周膜干细胞具有独特的衍生自神经细胞的免疫调节和神经源性分化特性,使其在组织再生和疾病治疗中都有更广泛的应用。 牙周膜干细胞存在牙周膜中,并产生牙齿支撑结构,例如牙槽骨、牙周膜和牙骨质。尼古丁抑制牙周膜干细胞的增殖、迁移和成骨分化。周志斐[56]发现牙周膜干细胞中存在α7烟碱型乙酰胆碱受体基因和蛋白的表达,不同浓度尼古丁均可抑制牙周膜干细胞早期和终末期成骨分化且具有浓度依赖性,这可能与尼古丁抑制成骨相关因子碱性磷酸酶、骨涎蛋白、骨钙素、Runt相关转录因子2基因及蛋白的表达和尼古丁激活α7烟碱型乙酰胆碱受体后下游存在Wnt信号通路相关转录因子蛋白的表达有关。为评估体内牙周膜干细胞的增殖变化,从慢性吸烟者中分离出牙周膜干细胞,在分离后没有体外暴露于任何额外的烟草或尼古丁的情况下,与非吸烟者的牙周膜干细胞对比,观察到了牙周膜干细胞增殖速率降低,这些细胞的增殖速率降低了2.53倍,甚至在传代培养3-5次后,仍然观察到增殖减少,这表明尼古丁暴露对牙周膜干细胞增殖的影响可能是永久性的[57]。牙周膜干细胞已被证实表达CD90和CD105,与空白对照组相比,尼古丁实验组牙周膜干细胞培养3 d后,尼古丁浓度为10-4 mol/L时牙周膜干细胞的增殖能力受到明显抑制。尼古丁使牙周膜干细胞的碱性磷酸酶、骨钙素、Runt相关转录因子2的基因及蛋白表达量均降低,加入Toll样受体4抑制剂TAK-242后,尼古丁的抑制效应减弱[58]。吴贾涵等[59]对120例患者牙周膜干细胞进行体外培养,用不同浓度(10-4,10-3,10-2 mol/L)尼古丁培养液刺激牙周膜干细胞,对照组为不含尼古丁的培养液,发现尼古丁可导致牙周膜干细胞形态改变,并降低细胞增殖、成骨分化能力,随着浓度增高、作用时间延长,产生的影响越大,这可能与其自身的毒性作用及其影响线粒体、Toll样受体4表达有关。"
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