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中国临床康复 2006年第13期10卷 87-89,i0005页

作者：章培标侯宜武汉周余来贾晓晶龚守良侯立中吉林大学再生医学科学研究所吉林大学中日联谊医院骨科吉林省长春市130032 吉林大学公共卫生学院放射生物实验室吉林省长春市130021

目的:观察外源性人血管内皮细胞生长因子基因导入正常真皮成纤维细胞后,能否表达及分泌血管内皮细胞生长因子,为进一步构建转VEGF165基因组织工程皮肤在创伤修复中的应用提供新移植物。方法:实验于2001-06/2005-06在长春吉林大学完成。... 详细信息

目的:观察外源性人血管内皮细胞生长因子基因导入正常真皮成纤维细胞后,能否表达及分泌血管内皮细胞生长因子,为进一步构建转VEGF165基因组织工程皮肤在创伤修复中的应用提供新移植物。方法:实验于2001-06/2005-06在长春吉林大学完成。①真核表达载体pcDNA3.0-hVEGF165的扩增、纯化和鉴定过程为大肠杆菌DH5a感受态细胞的制备→pcDNA3.0-hVEGF165质粒DNA细菌转化→pcDNA3.0-hVEGF165质粒大量制备(碱裂解法)→质粒纯化→质粒含量纯度测定。提取的质粒载体用EcoRⅠ和XbaⅠ双酶切,琼脂糖凝胶电泳鉴定。②选取清洁级新生日本大耳白兔2只,无菌条件下取新生兔皮肤,尽量去除皮下组织,切成宽0.3cm小条块,Ⅰ型胶原酶消化,进行真皮成纤维细胞的分离与培养。脂质体介导真核表达质粒pcDNA3.0-hVEGF165转染体外培养的兔皮肤成纤维细胞,经G418筛选,获得阳性转染细胞克隆,并进行传代扩增。③酶联免疫吸附法检测转染后不同时间段的血管内皮细胞生长因子蛋白表达水平;原位杂交显示转基因细胞内VEGF165mRNA的表达情况;流式细胞仪检测细胞周期和凋亡情况;透射电子显微镜观察转染后真皮成纤维细胞的超微结构。结果:①质粒酶切鉴定结果:提取的质粒经双酶切、琼脂糖凝胶电泳鉴定后可得到5.4kb和0.57kb两个片段,与原质粒图谱符合,表明所提取的质粒为重组质粒pcDNA3.0-VEGF165。②pcDNA3-hVEGF165基因转染真皮成纤维细胞情况:共进行15次转染试验,35孔(皿)均有G418抗性集落形成,表明pcDNA3.0-hVEGF165经脂质体介导可有效转染正常皮肤成纤维细胞。③血管内皮细胞生长因子蛋白的表达:pcDNA3.0-hVEGF165转染成纤维细胞后,24h即有较高水平的血管内皮细胞生长因子蛋白表达,高达(3280±2054)ng/L,并于48,72h呈下降趋势。④血管内皮细胞生长因子cDNA原位杂交检测结果:转染后成纤维细胞可见散在的阳性细胞表达hVEGFmRNA。G418应用2～4周后,可成功筛选出转基因成纤维细胞克隆,筛选后可见大量阳性的转染细胞表达hVEGFmRNA。⑤成纤维细胞的细胞周期分布及凋亡检测:转染后成纤维细胞S期细胞比例增加,G1和G2期细胞减少,表明细胞DNA的合成以及细胞的增殖活动加强。但细胞凋亡率逐渐升高,转染前为1.26%,转染后2d为2.64%,至12代时高达17.35%。⑥转染后成纤维细胞超微结构观察:细胞表面有较多微绒毛,核呈不规则形,胞质内可见较多的粗面内质网、线粒体,沿膜可见一些膜包被颗粒。结论:真核表达质粒pcDNA3.0-hVEGF165成功导入家兔皮肤成纤维细胞,在短时期内可高水平地表达分泌血管内皮细胞生长因子,在治疗缺血性疾病和促进创伤修复及以其作为种子细胞构建转基因组织工程皮肤治疗皮肤缺损等方面显示出较好的应用前景。

关键词：生物医学工程内皮血管/代谢内皮生长因子/生物合成细胞培养的基因转染成纤维细胞皮肤人工

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组织因子在纤维肉瘤细胞血管外游走中的作用

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浙江大学学报（医学版） 2011年第2期40卷 184-188页

作者：韩春山辛华韩振国高忠礼吉林大学中日联谊医院胸外科吉林长春130033 吉林大学中日联谊医院骨科吉林长春130033

目的:评价组织因子对纤维肉瘤细胞血管外游走的影响,明确组织因子与纤维肉瘤细胞血行转移的相关性。方法:应用流式细胞仪检测组织因子在纤维肉瘤细胞(HT1080)的表达情况;在体外模拟肿瘤细胞血管外游走过程,构建充分融合的单层血管内皮... 详细信息

目的:评价组织因子对纤维肉瘤细胞血管外游走的影响,明确组织因子与纤维肉瘤细胞血行转移的相关性。方法:应用流式细胞仪检测组织因子在纤维肉瘤细胞(HT1080)的表达情况;在体外模拟肿瘤细胞血管外游走过程,构建充分融合的单层血管内皮细胞及血管外基质,定量评价HT1080向血管外游走的状况。结果:应用流式细胞仪检测出组织因子在HT1080上有强表达;HT1080可以穿过单层血管内皮细胞游走至血管外基质,具有时间依赖性;抗组织因子抗体能够抑制HT1080的血管外游走,并且高浓度的抗TF抗体(20 mg/L)较低浓度的抗TF抗体(5 mg/L)的抑制作用更为明显,差异有显著意义(P<0.05),具有浓度依赖性。结论:组织因子能够促进纤维肉瘤细胞的血管外游走,从而加速纤维肉瘤细胞的血行转移。

关键词：纤维肉瘤/病理学血管/代谢肿瘤转移组织因子纤维肉瘤细胞血管外游走

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胸腔积液中TGF-β_1、VEGF、bFGF、PA I-1的检测及其临床意义

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陕西医学杂志 2006年第1期35卷 100-101,104页

作者：邵景韫戚好文刘安董玉西安市中心医院呼吸内科西安710003 第四军医大学西京医院呼吸内科

目的:探讨胸腔积液中转化生长因子-1β(TGF-1β)、血管内皮细胞生长因子(VEGF)、碱性成纤维细胞生长因子(bFGF)、纤溶酶原激活物抑制剂-1(PA I-1)与胸膜纤维化的关系。方法:采用酶联免疫检测仪检测20例结核性渗出液和20例漏出液中TGF-1... 详细信息

目的:探讨胸腔积液中转化生长因子-1β(TGF-1β)、血管内皮细胞生长因子(VEGF)、碱性成纤维细胞生长因子(bFGF)、纤溶酶原激活物抑制剂-1(PA I-1)与胸膜纤维化的关系。方法:采用酶联免疫检测仪检测20例结核性渗出液和20例漏出液中TGF-1β、VEGF、bFGF、PA I-1的水平。结果:结核性胸液中TGF-1β、VEGF、PA I-1水平均高于漏出液(P<0.05),bFGF两组之间无显著性差异(P>0.05)。结论:TGF-1β、VEGF、PA I-1在胸膜纤维化的形成过程中起重要作用。

关键词：胸腔积液/诊断转化生长因子β/代谢纤溶酶原灭活剂/代谢内皮血管/代谢

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Endothelial heme oxygenase-1 induction by hypoxia -: Modulation by inducible nitric-oxide synthase and S-nitrosothiols

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第18期275卷 13613-13620页

作者： Motterlini, R Foresti, R Bassi, R Calabrese, V Clark, JE Green, CJ Northwick Pk Inst Med Res Dept Surg Res Vasc Biol Unit Harrow HA1 3UJ Middx England Univ Catania Fac Med Dept Biochem I-95125 Catania Italy

The stress protein heme oxygenase-1 (HO-1) is induced in endothelial cells exposed to nitric oxide (NO)releasing agents, and this process is finely modulated by thiols (Foresti, R,, Clark, J, E,, Green, C, J,, and Motterlini Il, (1997) J. Biol, Chem, 272, 18411-18417), Here, we report that up-regulation of HO-1 in aortic endothelial cells by severe hypoxic conditions (pO(2) less than or equal to 2 mm Hg) is preceded by increased inducible NO synthase and NO synthase activity. This effect is accompanied by oxidation of intracellular glutathione and formation of S-nitrosothiols, Incubation of cells with a selective inhibitor of inducible NO synthase (S-(2-aminoethyl)-isothiourea) or a NO scavenger ([2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide]) significantly attenuated the increase in heme oxygenase activity caused by reduced oxygen availability. A series of antioxidant agents did not prevent the elevation in heme oxygenase activity by hypoxia;however, the precursor of glutathione synthesis and thiol donor, N-acetylcysteine, completely abolished HO-1 induction. We also found that the hypoxia-mediated increase in endothelial heme oxygenase activity was potentiated by the presence of S-nitrosoglutathione. These results indicate that intracellular interaction of thiols with NO is an important determinant in the mechanism leading to HO-1 induction by reduced oxygen levels. We suggest that in addition to oxidative stress, HO-1 gene expression can be regulated by redox reactions involving NO and S-nitrosothiols (nitrosative stress), emphasizing a versatile role for the heme oxygenase pathway in the cellular adaptation to a variety of stressful conditions.

关键词：细胞培养的内皮血管/代谢酶诱导血红素氧化酶(脱环)/代谢血红素加氧酶-1 巯基乙醇一氧化氮合酶/代谢一氧化氮合酶Ⅱ型亚硝基化合物/代谢 S-亚硝基硫醇动物牛

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Genes expressed in human tumor endothelium

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SCIENCE 2000年第5482期289卷 1197-1202页

作者： St Croix, B Rago, C Velculescu, V Traverso, G Romans, KE Montgomery, E Lal, A Riggins, GJ Lengauer, C Vogelstein, B Kinzler, KW Johns Hopkins Univ Sch Med Johns Hopkins Oncol Ctr Baltimore MD 21231 USA Johns Hopkins Univ Sch Med Howard Hughes Med Inst Baltimore MD 21231 USA Johns Hopkins Univ Sch Med Dept Pathol Baltimore MD 21231 USA Duke Univ Med Ctr Dept Pathol Durham NC 27710 USA

To gain a molecular understanding of tumor angiogenesis, we compared gene expression patterns of endothelial cells derived from blood vessels of normal and malignant colorectal tissues. Of over 170 transcripts predominantly expressed in the endothelium, 79 were differentially expressed, including 46 that were specifically elevated in tumor-associated endothelium. Several of these genes encode extracellular matrix proteins, but most are of unknown function. Most of these tumor endothelial markers were expressed in a wide range of tumor types, as well as in normal vessels associated with wound healing and corpus Luteum formation. These studies demonstrate that tumor and normal endothelium are distinct at the molecular Level, a finding that may have significant implications for the development of anti-angiogenic therapies.

关键词：细胞分离细胞培养的结肠/血液供给结肠/代谢结直肠肿瘤/血液供给结直肠肿瘤/遗传学结直肠肿瘤/代谢结直肠肿瘤/病理学黄体/血液供给黄体/代谢内皮血管/细胞学内皮血管/代谢内皮血管/病理学细胞外基质蛋白质类/遗传学基因表达基因表达谱肠黏膜/血液供给肠黏膜/细胞学肠黏膜/病理学肿瘤/血液供给肿瘤/遗传学肿瘤/代谢新生血管化病理性/遗传学新生血管化生理性/遗传学 RNA 信使/遗传学 RNA 信使/代谢直肠/血液供给直肠/代谢肿瘤细胞培养的女(雌)性人类

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Phosphorylation of osteopontin is required for inhibition of vascular smooth muscle cell calcification

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第26期275卷 20197-20203页

作者： Jono, S Peinado, C Giachelli, CM Univ Washington Dept Bioengn Seattle WA 98195 USA Osaka City Univ Sch Med Dept Internal Med 2 Osaka 545 Japan

Osteopontin (OPN) is a non-collagenous, glycosylated phosphoprotein associated with biomineralization in osseous tissues, as well as ectopic calcification. We previously reported that osteopontin was co-localized with calcified deposits in atherosclerotic lesions, and that osteopontin potently inhibits calcium deposition in a human smooth muscle cell (HSMC) culture model of vascular calcification. In this report, the role of phosphorylation in osteopontin's mineralization inhibitory function was examined, The ability of OPN to inhibit calcification completely depended on post-translational modifications, since bacteria-derived recombinant OPN did not inhibit HSMC mineralization, Following casein kinase II treatment, phosphorylated OPN (P-OPN) dose-dependently inhibited calcification of HSMC cultured in vitro about as effectively as native OPN. The inhibitory effect of osteopontin depended on the extent of phosphorylation. To determine the specific structural domains of OPN important for inhibition of calcification, we compared OPN fragments (N-terminal, C-terminal, and full-length), and compared the inhibitory effect of both phosphorylated and non-phosphorylated fragments. While none of the non-phosphorylated OPN fragments effected calcification, P-OPN caused dose dependent inhibition of HSMC calcification. P-OPN was treated with alkaline phosphatase to create dephosphorylated OPN. Dephosphorylated OPN did not have an inhibitory effect on calcification. The expression of OPN mRNA and P-OPN secretion by HSMC were decreased in a time-dependent manner during culture calcification. These results indicate that phosphorylation is required for the inhibitory effect of OPN on HSMC calcification, and that regulation of OPN phosphorylation represents one way in which mineralization may be controlled by cells.

关键词：碱性磷酸酶/药理学动物新生印迹法 RNA 钙/代谢酪蛋白激酶Ⅱ 细胞培养的剂量效应关系药物肌平滑血管/代谢骨桥蛋白质磷酰化质粒/代谢沉淀素试验蛋白质丝氨酸苏氨酸激酶/药理学 RNA 信使/代谢重组蛋白质类/代谢唾液糖蛋白类/代谢唾液糖蛋白类/药理学唾液糖蛋白类/生理学时间因素动物人类大鼠

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Cyclic strain stress-induced mitogen-activated protein kinase (MAPK) phosphatase 1 expression in vascular smooth muscle cells is regulated by Ras/Rac-MAPK pathways

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JOURNAL OF BIOLOGICAL CHEMISTRY 1999年第36期274卷 25273-25280页

作者： Li, CH Hu, YH Mayr, M Xu, QB Austrian Acad Sci Inst Biomed Aging Res A-6020 Innsbruck Austria

Recently, we demonstrated that mechanical stress results in rapid phosphorylation or activation of platelet-derived growth factor receptors in vascular smooth muscle cells (VSMCs) followed by activation of mitogen-activated protein kinases (MAPKs) and AP-1 transcription factors (Hu, Y,, Beck, G,, Wick, G., and Xu, Q, (1998) FASEB J. 12, 1135-1142). Herein, we provide evidence that VSMC responses to mechanical stress also include induction of MAPK phosphatase-1 (MKP-1), which may serve as a negative regulator of MAPK signaling pathways. When rat VSMCs cultivated on a flexible membrane were subjected to cyclic strain stress (60 cycles/ min, 5-30% elongation), induction of MKP-1 proteins and mRNA was observed in time- and strength-dependent manners. Concomitantly, mechanical forces evoked rapid and transient activation of all three members of MAPKs, i.e. extracellular signal-regulated kinases (ERKs), c-Jun NH2-terminal protein kinases (JNKs), or stress-activated protein kinases (SAPKs), and p38 MAPKs. Suramin, a growth factor receptor antagonist, completely abolished ERK activation, significantly blocked MKP-1 expression, but not JNK/SAPKs and p38 MAPK activation, in response to mechanical stress. Interestingly, VSMC lines stably expressing dominant negative Ras (Ras N17) or Rac (Rac N17) exhibited a marked decrease in MKP-1 expression;the inhibition of ERK kinases (MEK1/2) by PD 98059 or of p38 MAPKs by SE 202190 resulted in a down-regulation of MKP-1 induction. Furthermore, overexpressing MKP-1 in VSMCs led to the dephosphorylation and inactivation of ERKs, JNKs/SAPKs, and p38 MAPKs and inhibition of DNA synthesis. Taken together, our findings demonstrate that mechanical stress induces MKP-1 expression regulated by two signal pathways, including growth factor receptor-Ras-ERK and Rac-JNK/SAPK or p38 MAPK, and that MKP-1 inhibits VSMC proliferation via MAPK inactivation. These results suggest that MKP-1 plays a crucial role in mechanical stress-stimulated signaling le

关键词：钙-钙调素依赖性蛋白激酶类/代谢细胞周期蛋白质类细胞培养的双特异性磷酸酶1 GTP结合蛋白质类/代谢即早蛋白质类/生物合成肌平滑血管/代谢肌平滑血管/病理学磷蛋白磷酸酶类磷酰化蛋白质磷酸酶1 蛋白质酪氨酸磷酸酶类/生物合成信号传导应力物理 racGTP结合蛋白质类 ras蛋白质类/代谢动物大鼠

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Ability of Ni-containing biomedical alloys to activate monocytes and endothelial cells in vitro

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JOURNAL OF BIOMEDICAL MATERIALS RESEARCH 1999年第3期45卷 251-257页

作者： Wataha, JC Lockwood, PE Marek, M Ghazi, M Med Coll Georgia Sch Dent Dept Oral Rehabil Augusta GA 30912 USA Georgia Inst Technol Atlanta GA 30332 USA Georgia State Univ Atlanta GA 30303 USA

Nickel-containing alloys commonly are used in medical and dental applications that place them into longterm contact with soft: tissues. The release of Ni ions from these alloys is disturbing because of the toxic, immunologic, and carcinogenic effects that have been documented for some Ni compounds. In particular, Ni ions in solution recently have been shown to cause expression of inflammatory mediators, such as interleukin-1 beta (IL-1 beta), tumor necrosis factor-alpha (TNF-alpha), and intercellular adhesion molecules (ICAMs) from keratinocytes, monocytes, and endothelial cells. However, the ability of the solid alloys themselves to induce these inflammatory effects has not been demonstrated. An in vitro system was used to determine if Ni-containing biomedical alloys could cause secretion of either IL-1 beta or TNF-alpha from monocytes or expression of ICAMs on endothelial cells. Pure nickel, titanium, and three biomedical alloys-18-8 stainless steel, NiTi, and Rexillium III-were evaluated. First, it was determined whether or not the alloys or pure metals could cause cytotoxicity to THP-1 human monocytes or human microvascular endothelial cells (HMVECs) by measuring the succinic dehydrogenase (SDH) activity of the cells. Then, using identical conditions of exposure, the secretion of IL-1 beta or TNP-alpha from monocytes or ICAM-1 expression on the HMVECs was determined. Only pure nickel suppressed (by 48% compared to Teflon controls) the SDH activity of the HMVECs or THT-1 monocytes. No alloy or metal caused the HMVECs to express ICAM-1, but the NiTi alloy caused a significant (ANOVA/Tukey) secretion of IL-1 beta from the THP-1 monocytes. Secretion of TNF-alpha induced by NiTi was detectable but not statistically significant. The levels of IL-1 beta secretion from monocytes were sufficient to induce ICAM-1 expression on HMVECs. The release of Ni from the NiTi was a logical suspect in causing the IL-1 beta secretion by monocytes, but its role was not confirmed since

关键词：合金/毒性毛细血管/细胞学毛细血管/药物作用细胞存活/药物作用细胞培养的内皮血管/细胞学内皮血管/药物作用内皮血管/代谢胞间黏附分子1/生物合成白细胞介素1/代谢巨噬细胞活化/药物作用单核细胞/化学单核细胞/药物作用镍/分析镍/毒性琥珀酸脱氢酶/代谢钛/毒性肿瘤坏死因子α/代谢人类

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Inhibition by extracellular cAMP of phorbol 12-myristate 13-acetate-induced prostaglandin H synthase-2 expression in human pulmonary microvascular endothelial cells - Involvement of an ecto-protein kinase A activity

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第18期275卷 13662-13667页

作者： Elalamy, I Said, FA Singer, M Couetil, JP Hatmi, M Inst Pasteur INSERM U485 Unite Pharmacol Cellulaire F-75724 Paris 15 France Hop Broussais Serv Chirurg Cardiothorac F-75014 Paris France

Exposure of human pulmonary microvascular endothelial cells (HPMECs) to phorbol 12-myristate 13-acetate (PMA) leads to the increase of prostaglandin H synthase (PGHS)-2 protein levels. Under same conditions and according to its constitutive nature, no significant variation of PGHS-1 protein was noted. The elevation of the intracellular cAMP rate is known to enhance PGHS-2 levels through a protein kinase A pathway in various cells. To determine whether the extracellular cAMP also regulates the inducible expression of PGHS, cultured HPMECs were exposed to cAMP alone or in combination with PMA. The PMA-induced PGHS-2 protein was attenuated by the extracellular cAMP, In addition, PGHS-2 activity evaluated through 6-keto-PGF1 alpha generation, which was enhanced by PMA was inhibited by extracellular cAMP. Furthermore, in HPMEC medium, PMA-induced PGHS-2 expression was accompanied by the generation of a transferable activity (TA) able to abolish platelet aggregation. This resulting TA was dependent from PGHS-2 pathway, because NS-398, a selective inhibitor of PGHS-2, suppressed its production. The inhibitory TA released by treated HPMECs was also prevented by extracellular cAMP. The specific protein kinase A (PKA) inhibitor blocked the extracellular cAMP effect on both PMA-induced 6-keto-PGF1 alpha synthesis and inhibitory TA generation, suggesting the involvement of PRA signaling at the outer surface of HPMECs, Accordingly, we established, in phosphorylation experiments, the presence of an endothelial ectoprotein kinase activity, able to phosphorylate the synthetic substrate kemptide in a cAMP-dependent mode. Reverse transcription-polymerase chain reaction analysis showed that PIMA-induced PGHS-2 mRNA was markedly reduced by extracellular cAMP. Together, these findings provide the first experimental evidence that extracellular cAMP is able to reduce HPMEC PGHS-2 expression in terms of mRNA, protein, and enzyme activity through an ecto-PKA pathway. In addition, they outli

关键词：致癌物/药理学环AMP/代谢环AMP/药理学环AMP依赖性蛋白激酶类/代谢环氧化酶2 药物相互作用内皮血管/代谢细胞外基质/代谢同工酶类/生物合成肺/血液供给膜蛋白质类微循环前列腺素内过氧化物合酶类/生物合成十四酰佛波乙酯/药理学人类

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Disruption of the sarcoglycan-sarcospan complex in vascular smooth muscle: A novel mechanism for cardiomyopathy and muscular dystrophy

引用

CELL 1999年第4期98卷 465-474页

作者： Coral-Vazquez, R Cohn, RD Moore, SA Hill, JA Weiss, RM Davisson, RL Straub, V Barresi, R Bansal, D Hrstka, RF Williamson, R Campbell, KP Univ Iowa Coll Med Howard Hughes Med Inst Dept Physiol & Biophys Iowa City IA 52242 USA Univ Iowa Coll Med Dept Neurol Iowa City IA 52242 USA Univ Iowa Coll Med Dept Pathol Iowa City IA 52242 USA Univ Iowa Coll Med Dept Obstet & Gynecol Iowa City IA 52242 USA Dept Vet Affairs Iowa City IA 52242 USA Univ Iowa Dept Anat & Cell Biol Iowa City IA 52242 USA Univ Iowa Dept Internal Med Iowa City IA 52242 USA

To investigate mechanisms in the pathogenesis of cardiomyopathy associated with mutations of the dystrophin-glycoprotein complex, we analyzed genetically engineered mice deficient for either alpha-sarcoglycan (Sgca) or delta-sarcoglycan (Sgcd). We found that only Sgcd null mice developed cardiomyopathy with focal areas of necrosis as the histological hallmark in cardiac and skeletal muscle. Absence of the sarcoglycan-sarcospan (SG-SSPN) complex in skeletal and cardiac membranes was observed in both animal models. Loss of vascular smooth muscle SG-SSPN complex was only detected in Sgcd null mice and associated with irregularities of the coronary vasculature. Administration of a vascular smooth muscle relaxant prevented onset of myocardial necrosis. Our data indicate that disruption of the SG-SSPN complex in vascular smooth muscle perturbs vascular function, which initiates cardiomyopathy and exacerbates muscular dystrophy.

关键词：心肌病扩张型/遗传学心肌病扩张型/代谢心肌病扩张型/病理学载体蛋白质类/生理学冠状血管/病理学细胞支架蛋白质类/缺乏细胞支架蛋白质类/遗传学细胞支架蛋白质类/生理学大分子物质膜糖蛋白类/缺乏膜糖蛋白类/遗传学膜糖蛋白类/生理学膜蛋白质类/生理学小鼠基因敲除肌平滑血管/代谢肌平滑血管/病理学肌营养不良动物/遗传学肌营养不良动物/代谢肌营养不良动物/病理学心肌/病理学坏死肿瘤蛋白质类肌聚糖类动物小鼠

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