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Mechanism of DNA damage tolerance. DNA损伤耐受机制。
Pub Date : 2015-08-26 DOI: 10.4331/wjbc.v6.i3.48
Xin Bi

DNA damage may compromise genome integrity and lead to cell death. Cells have evolved a variety of processes to respond to DNA damage including damage repair and tolerance mechanisms, as well as damage checkpoints. The DNA damage tolerance (DDT) pathway promotes the bypass of single-stranded DNA lesions encountered by DNA polymerases during DNA replication. This prevents the stalling of DNA replication. Two mechanistically distinct DDT branches have been characterized. One is translesion synthesis (TLS) in which a replicative DNA polymerase is temporarily replaced by a specialized TLS polymerase that has the ability to replicate across DNA lesions. TLS is mechanistically simple and straightforward, but it is intrinsically error-prone. The other is the error-free template switching (TS) mechanism in which the stalled nascent strand switches from the damaged template to the undamaged newly synthesized sister strand for extension past the lesion. Error-free TS is a complex but preferable process for bypassing DNA lesions. However, our current understanding of this pathway is sketchy. An increasing number of factors are being found to participate or regulate this important mechanism, which is the focus of this editorial.

DNA损伤可能损害基因组完整性并导致细胞死亡。细胞已经进化出多种过程来应对DNA损伤,包括损伤修复和耐受机制,以及损伤检查点。DNA损伤耐受(DDT)途径促进DNA聚合酶在DNA复制过程中绕过单链DNA损伤。这可以防止DNA复制的停滞。两个机械上不同的滴滴涕分支已被表征。一种是翻译合成(TLS),其中复制性DNA聚合酶暂时被具有跨DNA损伤复制能力的特殊TLS聚合酶所取代。TLS在机制上是简单和直接的,但它本质上容易出错。另一种是无错误模板切换(TS)机制,在这种机制中,停滞的新生链从受损的模板切换到未受损的新合成的姊妹链,以延长通过病变。无差错TS是一种复杂但优选的绕过DNA病变的方法。然而,我们目前对这一途径的理解是粗略的。越来越多的因素正在被发现参与或调节这一重要机制,这是本文的重点。
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引用次数: 39
Essential roles of four-carbon backbone chemicals in the control of metabolism. 四碳主链化学物质在代谢控制中的重要作用。
Pub Date : 2015-08-26 DOI: 10.4331/wjbc.v6.i3.223
Sabrina Chriett, Luciano Pirola

The increasing incidence of obesity worldwide and its related cardiometabolic complications is an urgent public health problem. While weight gain results from a negative balance between the energy expenditure and calorie intake, recent research has demonstrated that several small organic molecules containing a four-carbon backbone can modulate this balance by favoring energy expenditure, and alleviating endoplasmic reticulum stress and oxidative stress. Such small molecules include the bacterially produced short chain fatty acid butyric acid, its chemically produced derivative 4-phenylbutyric acid, the main ketone body D-β-hydroxybutyrate - synthesized by the liver - and the recently discovered myokine β-aminoisobutyric acid. Conversely, another butyrate-related molecule, α-hydroxybutyrate, has been found to be an early predictor of insulin resistance and glucose intolerance. In this minireview, we summarize recent advances in the understanding of the mechanism of action of these molecules, and discuss their use as therapeutics to improve metabolic homeostasis or their detection as early biomarkers of incipient insulin resistance.

全球肥胖及其相关心脏代谢并发症的发病率不断上升是一个紧迫的公共卫生问题。虽然体重增加是由于能量消耗和卡路里摄入之间的负平衡,但最近的研究表明,几种含有四碳骨架的小有机分子可以通过促进能量消耗来调节这种平衡,减轻内质网应激和氧化应激。这些小分子包括细菌产生的短链脂肪酸丁酸,其化学衍生物4-苯基丁酸,主要酮体D-β-羟基丁酸-由肝脏合成-以及最近发现的肌细胞因子β-氨基异丁酸。相反,另一种与丁酸相关的分子,α-羟基丁酸,被发现是胰岛素抵抗和葡萄糖耐受不良的早期预测因子。在这篇综述中,我们总结了这些分子的作用机制的最新进展,并讨论了它们作为改善代谢稳态的治疗药物或作为早期胰岛素抵抗的早期生物标志物的检测。
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引用次数: 11
Effect of paricalcitol and enalapril on renal inflammation/oxidative stress in atherosclerosis. 帕尔卡尼醇和依那普利对动脉粥样硬化患者肾脏炎症/氧化应激的影响。
Pub Date : 2015-08-26 DOI: 10.4331/wjbc.v6.i3.240
Kazim Husain, Edu Suarez, Angel Isidro, Wilfredo Hernandez, Leon Ferder

Aim: To investigate the protective effect of paricalcitol and enalapril on renal inflammation and oxidative stress in ApoE-knock out mice.

Methods: Animals treated for 4 mo as group (1) ApoE-knock out plus vehicle, group (2) ApoE-knock out plus paricalcitol (200 ng thrice a week), (3) ApoE-knock out plus enalapril (30 mg/L), (4) ApoE-knock out plus paricalcitol plus enalapril and (5) normal. Blood pressure (BP) was recorded using tail cuff method. The kidneys were isolated for biochemical assays using spectrophotometer and Western blot analyses.

Results: ApoE-deficient mice developed high BP (127 ± 3 mmHg) and it was ameliorated by enalapril and enalapril plus paricalcitol treatments but not with paricalcitol alone. Renal malondialdehyde concentrations, p22(phox), manganese-superoxide dismutase, inducible nitric oxide synthase (NOS), monocyte chemoattractant protein-1, tumor necrosis factor-alpha and transforming growth factor-β1 levels significantly elevated but reduced glutathione, CuZn-SOD and eNOS levels significantly depleted in ApoE-knock out animals compared to normal. Administration of paricalcitol, enalapril and combined together ameliorated the renal inflammation and oxidative stress in ApoE-knock out animals.

Conclusion: Paricalcitol and enalapril combo treatment ameliorates renal inflammation as well as oxidative stress in atherosclerotic animals.

目的:探讨派卡尔醇和依那普利对apoe敲除小鼠肾脏炎症和氧化应激的保护作用。方法:动物治疗4个月,分为(1)apoe敲除加载药组、(2)apoe敲除加依那普利组(200 ng,每周3次)、(3)apoe敲除加依那普利组(30 mg/L)、(4)apoe敲除加依那普利组和(5)正常组。用尾袖带法记录血压。用分光光度计和Western blot分析分离肾脏进行生化分析。结果:apoe缺陷小鼠出现血压升高(127±3 mmHg),依那普利和依那普利加帕利西醇治疗可改善血压升高,但帕利西醇单独治疗不能改善血压升高。apoe敲除小鼠肾脏丙二醛浓度、p22(phox)、锰-超氧化物歧化酶、诱导型一氧化氮合酶(NOS)、单核细胞化学引诱蛋白-1、肿瘤坏死因子- α和转化生长因子-β1水平显著升高,而还原性谷胱甘肽、CuZn-SOD和eNOS水平显著降低。特立醇、依那普利联合用药可改善apoe敲除动物的肾脏炎症和氧化应激。结论:帕里西醇和依那普利联合治疗可改善动脉粥样硬化动物的肾脏炎症和氧化应激。
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引用次数: 12
Topographic patterns of vascular disease: HOX proteins as determining factors? 血管疾病的地形模式:HOX蛋白是决定因素?
Pub Date : 2015-08-26 DOI: 10.4331/wjbc.v6.i3.65
Richard P Visconti, Alexander Awgulewitsch

Steadily increasing evidence supports the idea that genetic diversities in the vascular bed are, in addition to hemodynamic influences, a major contributing factor in determining region-specific cardiovascular disease susceptibility. Members of the phylogenetically highly conserved Hox gene family of developmental regulators have to be viewed as prime candidates for determining these regional genetic differences in the vasculature. During embryonic patterning, the regionally distinct and precisely choreographed expression patterns of HOX transcription factors are essential for the correct specification of positional identities. Apparently, these topographic patterns are to some degree retained in certain adult tissues, including the circulatory system. While an understanding of the functional significance of these localized Hox activities in adult blood vessels is only beginning to emerge, an argument can be made for a role of Hox genes in the maintenance of vessel wall homeostasis and functional integrity on the one hand, and in regulating the development and progression of regionally restricted vascular pathologies, on the other. Initial functional studies in animal models, as well as data from clinical studies provide some level of support for this view. The data suggest that putative genetic regulatory networks of Hox-dependent cardiovascular disease processes include genes of diverse functional categories (extracellular matrix remodeling, transmembrane signaling, cell cycle control, inflammatory response, transcriptional control, etc.), as potential targets in both vascular smooth muscle and endothelial cells, as well as cell populations residing in the adventitia.

越来越多的证据支持这样一种观点,即除了血液动力学影响外,血管床的遗传多样性是决定区域特异性心血管疾病易感性的主要因素。在系统发育上高度保守的发育调节因子Hox基因家族的成员必须被视为确定脉管系统中这些区域遗传差异的主要候选者。在胚胎形成过程中,HOX转录因子的区域差异和精确编排的表达模式对于位置身份的正确规范至关重要。显然,这些地形模式在某种程度上保留在某些成人组织中,包括循环系统。虽然对成人血管中这些局部Hox活性的功能意义的理解才刚刚开始出现,但可以提出Hox基因一方面在维持血管壁稳态和功能完整性方面的作用,另一方面在调节区域限制性血管病变的发展和进展方面的作用。动物模型的初步功能研究以及临床研究的数据为这一观点提供了一定程度的支持。这些数据表明,已知的hox依赖性心血管疾病过程的遗传调控网络包括多种功能类别的基因(细胞外基质重塑、跨膜信号、细胞周期控制、炎症反应、转录控制等),这些基因在血管平滑肌和内皮细胞以及居住在外膜的细胞群中都是潜在的靶点。
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引用次数: 11
Is erythroferrone finally the long sought-after systemic erythroid regulator of iron? 红细胞铁素是否最终成为人们期待已久的系统性红细胞铁调节剂?
Pub Date : 2015-08-26 DOI: 10.4331/wjbc.v6.i3.78
Alfons Lawen

Iron metabolism is regulated on the cellular and the systemic level. Over the last decade, the liver peptide "hepcidin" has emerged as the body's key irons store regulator. The long postulated "erythroid regulator of iron", however, remained elusive. Last year, evidence was provided, that a previously described myokine "myonectin" may also function as the long sought erythroid regulator of iron. Myonectin was therefore re-named "erythroferrone". This editorial provides a brief discussion on the two functions of erythroferrone and also briefly considers the emerging potential role of transferrin receptor 2 in erythropoiesis.

铁的代谢在细胞和全身水平上受到调节。在过去的十年里,肝脏肽“hepcidin”已经成为人体铁储存的关键调节器。然而,长期假设的“铁的红细胞调节因子”仍然难以捉摸。去年,有证据表明,先前描述的肌因子“肌连接素”也可能作为长期寻找的红系铁调节剂起作用。因此,肌连接蛋白被重新命名为“红细胞铁酮”。这篇社论简要讨论了红铁酮的两种功能,并简要考虑了转铁蛋白受体2在红细胞生成中的潜在作用。
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引用次数: 9
Inflammation, oxidative stress and renin angiotensin system in atherosclerosis. 动脉粥样硬化中的炎症、氧化应激和肾素血管紧张素系统。
Pub Date : 2015-08-26 DOI: 10.4331/wjbc.v6.i3.209
Kazim Husain, Wilfredo Hernandez, Rais A Ansari, Leon Ferder

Atherosclerosis is a chronic inflammatory disease associated with cardiovascular dysfunction including myocardial infarction, unstable angina, sudden cardiac death, stroke and peripheral thromboses. It has been predicted that atherosclerosis will be the primary cause of death in the world by 2020. Atherogenesis is initiated by endothelial injury due to oxidative stress associated with cardiovascular risk factors including diabetes mellitus, hypertension, cigarette smoking, dyslipidemia, obesity, and metabolic syndrome. The impairment of the endothelium associated with cardiovascular risk factors creates an imbalance between vasodilating and vasoconstricting factors, in particular, an increase in angiotensin II (Ang II) and a decrease in nitric oxide. The renin-angiotensin system (RAS), and its primary mediator Ang II, also have a direct influence on the progression of the atherosclerotic process via effects on endothelial function, inflammation, fibrinolytic balance, and plaque stability. Anti-inflammatory agents [statins, secretory phospholipase A2 inhibitor, lipoprotein-associated phospholipase A2 inhibitor, 5-lipoxygenase activating protein, chemokine motif ligand-2, C-C chemokine motif receptor 2 pathway inhibitors, methotrexate, IL-1 pathway inhibitor and RAS inhibitors (angiotensin-converting enzyme inhibitors)], Ang II receptor blockers and ranin inhibitors may slow inflammatory processes and disease progression. Several studies in human using anti-inflammatory agents and RAS inhibitors revealed vascular benefits and reduced progression of coronary atherosclerosis in patients with stable angina pectoris; decreased vascular inflammatory markers, improved common carotid intima-media thickness and plaque volume in patients with diagnosed atherosclerosis. Recent preclinical studies have demonstrated therapeutic efficacy of vitamin D analogs paricalcitol in ApoE-deficient atherosclerotic mice.

动脉粥样硬化是一种慢性炎症性疾病,与心血管功能障碍相关,包括心肌梗死、不稳定型心绞痛、心源性猝死、中风和周围血栓形成。据预测,到2020年,动脉粥样硬化将成为世界上死亡的主要原因。动脉粥样硬化是由氧化应激引起的内皮损伤引起的,这些损伤与心血管危险因素有关,包括糖尿病、高血压、吸烟、血脂异常、肥胖和代谢综合征。与心血管危险因素相关的内皮损伤造成血管舒张因子和血管收缩因子之间的不平衡,特别是血管紧张素II (Ang II)的增加和一氧化氮的减少。肾素-血管紧张素系统(RAS)及其主要介质Ang II也通过对内皮功能、炎症、纤溶平衡和斑块稳定性的影响,直接影响动脉粥样硬化过程的进展。抗炎药[他汀类药物、分泌型磷脂酶A2抑制剂、脂蛋白相关磷脂酶A2抑制剂、5-脂氧合酶激活蛋白、趋化因子基序配体-2、C-C趋化因子基序受体2途径抑制剂、甲氨蝶呤、IL-1途径抑制剂和RAS抑制剂(血管紧张素转换酶抑制剂)]、Ang II受体阻滞剂和ranin抑制剂可减缓炎症过程和疾病进展。几项使用抗炎药和RAS抑制剂的人体研究显示,稳定型心绞痛患者的血管益处和冠状动脉粥样硬化的进展减少;在诊断为动脉粥样硬化的患者中降低血管炎症标志物,改善颈总动脉内膜-中膜厚度和斑块体积。最近的临床前研究已经证明了维生素D类似物特利糖醇对apoe缺乏的动脉粥样硬化小鼠的治疗效果。
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引用次数: 277
Techniques to elucidate the conformation of prions. 阐明朊病毒构象的技术。
Pub Date : 2015-08-26 DOI: 10.4331/wjbc.v6.i3.218
Martin L Daus

Proteinaceous infectious particles (prions) are unique pathogens as they are devoid of any coding nucleic acid. Whilst it is assumed that prion disease is transmitted by a misfolded isoform of the cellular prion protein, the structural insight of prions is still vague and research for high resolution structural information of prions is still ongoing. In this review, techniques that may contribute to the clarification of the conformation of prions are presented and discussed.

蛋白质感染性颗粒(朊病毒)是一种独特的病原体,因为它们没有任何编码核酸。虽然假设朊病毒疾病是由细胞朊病毒蛋白的错误折叠异构体传播的,但对朊病毒的结构认识仍然模糊,对朊病毒高分辨率结构信息的研究仍在进行中。在这篇综述中,提出并讨论了可能有助于澄清朊病毒构象的技术。
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引用次数: 1
Role of ZAC1 in transient neonatal diabetes mellitus and glucose metabolism. ZAC1 在一过性新生儿糖尿病和葡萄糖代谢中的作用
Pub Date : 2015-08-26 DOI: 10.4331/wjbc.v6.i3.95
Anke Hoffmann, Dietmar Spengler

Transient neonatal diabetes mellitus 1 (TNDM1) is a rare genetic disorder representing with severe neonatal hyperglycaemia followed by remission within one and a half year and adolescent relapse with type 2 diabetes in half of the patients. Genetic defects in TNDM1 comprise uniparental isodisomy of chromosome 6, duplication of the minimal TNDM1 locus at 6q24, or relaxation of genomically imprinted ZAC1/HYMAI. Whereas the function of HYMAI, a non-coding mRNA, is still unidentified, biochemical and molecular studies show that zinc finger protein 1 regulating apoptosis and cell cycle arrest (ZAC1) behaves as a factor with versatile transcriptional functions dependent on binding to specific GC-rich DNA motives and interconnected regulation of recruited coactivator activities. Genome-wide expression profiling enabled the isolation of a number of Zac1 target genes known to regulate different aspects of β-cell function and peripheral insulin sensitivity. Among these, upregulation of Pparγ and Tcf4 impairs insulin-secretion and β-cell proliferation. Similarly, Zac1-mediated upregulation of Socs3 may attenuate β-cell proliferation and survival by inhibition of growth factor signalling. Additionally, Zac1 directly represses Pac1 and Rasgrf1 with roles in insulin secretion and β-cell proliferation. Collectively, concerted dysregulation of these target genes could contribute to the onset and course of TNDM1. Interestingly, Zac1 overexpression in β-cells spares the effects of stimulatory G-protein signaling on insulin secretion and raises the prospect for tailored treatments in relapsed TNDM1 patients. Overall, these results suggest that progress on the molecular and cellular foundations of monogenetic forms of diabetes can advance personalized therapy in addition to deepening the understanding of insulin and glucose metabolism in general.

一过性新生儿糖尿病 1(TNDM1)是一种罕见的遗传性疾病,表现为严重的新生儿高血糖,随后在一年半内缓解,半数患者会在青少年时期复发 2 型糖尿病。TNDM1 的遗传缺陷包括 6 号染色体单亲异位、位于 6q24 的最小 TNDM1 基因座重复或基因组印记 ZAC1/HYMAI 松弛。虽然 HYMAI(一种非编码 mRNA)的功能仍未确定,但生化和分子研究表明,调节细胞凋亡和细胞周期停滞的锌指蛋白 1(ZAC1)是一种具有多功能转录功能的因子,它依赖于与特定富含 GC 的 DNA 动机的结合,以及对招募的辅助激活因子活性的相互调节。通过全基因组表达谱分析,分离出了许多已知能调控β细胞功能和外周胰岛素敏感性不同方面的Zac1靶基因。其中,Pparγ和Tcf4的上调会损害胰岛素分泌和β细胞增殖。类似地,Zac1 介导的 Socs3 上调可能会通过抑制生长因子信号来减弱β细胞的增殖和存活。此外,Zac1 还直接抑制 Pac1 和 Rasgrf1,它们在胰岛素分泌和 β 细胞增殖中发挥作用。总之,这些靶基因的协同失调可能会导致 TNDM1 的发病和病程。有趣的是,Zac1 在β细胞中的过表达可避免刺激性 G 蛋白信号对胰岛素分泌的影响,为复发的 TNDM1 患者提供了定制治疗的前景。总之,这些结果表明,在单基因糖尿病的分子和细胞基础方面取得的进展,除了能加深人们对胰岛素和葡萄糖代谢的总体认识外,还能推进个性化治疗。
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引用次数: 0
Effect of agitation speed on the morphology of Aspergillus niger HFD5A-1 hyphae and its pectinase production in submerged fermentation. 搅拌速度对黑曲霉HFD5A-1菌丝形态及深层发酵中果胶酶产量的影响
Pub Date : 2015-08-26 DOI: 10.4331/wjbc.v6.i3.265
Darah Ibrahim, Haritharan Weloosamy, Sheh-Hong Lim

Aim: To investigate the impact of agitation speed on pectinase production and morphological changing of Aspergillus niger (A. niger) HFD5A-1 in submerged fermentation.

Methods: A. niger HFM5A-1 was isolated from a rotted pomelo. The inoculum preparation was performed by adding 5.0 mL of sterile distilled water containing 0.1% Tween 80 to a sporulated culture. Cultivation was carried out with inoculated 1 × 10(7) spores/mL suspension and incubated at 30 °C with different agitation speed for 6 d. The samples were withdrawn after 6 d cultivation time and were assayed for pectinase activity and fungal growth determination. The culture broth was filtered through filter paper (Whatman No. 1, London) to separate the fungal mycelium. The cell-free culture filtrate containing the crude enzyme was then assayed for pectinase activity. The biomass was dried at 80 °C until constant weight. The fungal cell dry weight was then expressed as g/L. The 6 d old fungal mycelia were harvested from various agitation speed, 0, 50, 100, 150, 200 and 250 rpm. The morphological changing of samples was then viewed under the light microscope and scanning electron microscope.

Results: In the present study, agitation speed was found to influence pectinase production in a batch cultivation system. However, higher agitation speeds than the optimal speed (150 rpm) reduced pectinase production which due to shear forces and also collision among the suspended fungal cells in the cultivation medium. Enzyme activity increased with the increasing of agitation speed up to 150 rpm, where it achieved its maximal pectinase activity of 1.559 U/mL. There were significant different (Duncan, P < 0.05) of the pectinase production with the agitation speed at static, 50, 100, 200 and 250 rpm. At the static condition, a well growth mycelial mat was observed on the surface of the cultivation medium and sporulation occurred all over the fungal mycelial mat. However with the increased in agitation speed, the mycelial mat turned slowly to become a single circular pellet. Thus, it was found that agitation speed affected the morphological characteristics of the fungal hyphae/mycelia of A. niger HFD5A-1 by altering their external as well as internal cell structures.

Conclusion: Exposure to higher shear stress with an increasing agitation speed could result in lower biomass yields as well as pectinase production by A. niger HFD5A-1.

目的:研究搅拌速度对黑曲霉(Aspergillus niger) HFD5A-1深层发酵中果胶酶产量及形态变化的影响。方法:从腐烂的柚子中分离黑僵菌hm5a -1。接种准备是在有孢子的培养基中加入5.0 mL含0.1% Tween 80的无菌蒸馏水。接种1 × 10(7)个孢子/mL悬浮液,在30℃不同搅拌速度下培养6 d,培养6 d后取出样品,测定果胶酶活性和真菌生长情况。用滤纸(Whatman No. 1, London)过滤培养液,分离真菌菌丝体。然后测定含粗酶的无细胞培养滤液的果胶酶活性。将生物质在80℃下干燥至恒重。然后用g/L表示真菌细胞干重。分别在0、50、100、150、200和250 rpm的搅拌转速下收获6 d的真菌菌丝。然后在光镜和扫描电镜下观察样品的形态变化。结果:在间歇式发酵系统中,搅拌速度对果胶酶的产量有影响。然而,较高的搅拌速度比最佳速度(150转/分)降低了果胶酶的产量,这是由于剪切力和悬浮真菌细胞之间的碰撞在培养基中。酶活性随着搅拌速度的增加而增加,搅拌速度达到150 rpm时,酶活性达到1.559 U/mL的最大值。在静态、50、100、200和250 rpm的搅拌转速下,果胶酶产量有显著差异(Duncan, P < 0.05)。在静态条件下,培养基表面菌丝席生长良好,菌丝席上布满了孢子。但随着搅拌速度的增加,菌丝席慢慢转向成单个圆形球。因此,我们发现搅拌速度通过改变黑曲霉HFD5A-1菌丝/菌丝的外部和内部细胞结构来影响菌丝/菌丝的形态特征。结论:随着搅拌速度的增加,剪切应力的增加会降低黑曲霉HFD5A-1的生物量产量和果胶酶产量。
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引用次数: 65
Biology of hyaluronan: Insights from genetic disorders of hyaluronan metabolism. 透明质酸生物学:来自透明质酸代谢遗传疾病的见解。
Pub Date : 2015-08-26 DOI: 10.4331/wjbc.v6.i3.110
Barbara Triggs-Raine, Marvin R Natowicz

Hyaluronan is a rapidly turned over component of the vertebrate extracellular matrix. Its levels are determined, in part, by the hyaluronan synthases, HAS1, HAS2, and HAS3, and three hyaluronidases, HYAL1, HYAL2 and HYAL3. Hyaluronan binding proteins also regulate hyaluronan levels although their involvement is less well understood. To date, two genetic disorders of hyaluronan metabolism have been reported in humans: HYAL1 deficiency (Mucopolysaccharidosis IX) in four individuals with joint pathology as the predominant phenotypic finding and HAS2 deficiency in a single person having cardiac pathology. However, inherited disorders and induced mutations affecting hyaluronan metabolism have been characterized in other species. Overproduction of hyaluronan by HAS2 results in skin folding and thickening in shar-pei dogs and the naked mole rat, whereas a complete deficiency of HAS2 causes embryonic lethality in mice due to cardiac defects. Deficiencies of murine HAS1 and HAS3 result in a predisposition to seizures. Like humans, mice with HYAL1 deficiency exhibit joint pathology. Mice lacking HYAL2 have variably penetrant developmental defects, including skeletal and cardiac anomalies. Thus, based on mutant animal models, a partial deficiency of HAS2 or HYAL2 might be compatible with survival in humans, while complete deficiencies of HAS1, HAS3, and HYAL3 may yet be recognized.

透明质酸是脊椎动物细胞外基质的一种快速转化成分。其水平部分由透明质酸合成酶HAS1、HAS2和HAS3以及三种透明质酸酶HYAL1、HYAL2和HYAL3决定。透明质酸结合蛋白也调节透明质酸水平,尽管它们的作用尚不清楚。迄今为止,有两种透明质酸代谢的遗传性疾病在人类中被报道:4例以关节病理为主要表型的人存在透明质酸1缺乏症(粘多糖病IX), 1例有心脏病理的人存在透明质酸2缺乏症。然而,影响透明质酸代谢的遗传疾病和诱导突变在其他物种中也有发现。HAS2产生的透明质酸过多会导致沙佩犬和裸鼹鼠的皮肤折叠和增厚,而HAS2完全缺乏会导致小鼠因心脏缺陷而致胚胎死亡。小鼠缺乏HAS1和HAS3会导致癫痫发作。与人类一样,HYAL1缺乏的小鼠也表现出关节病理。缺乏HYAL2的小鼠具有不同程度的渗透性发育缺陷,包括骨骼和心脏异常。因此,基于突变动物模型,HAS2或HYAL2的部分缺失可能与人类的生存相容,而HAS1、HAS3和HYAL3的完全缺失可能尚未被发现。
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引用次数: 54
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World journal of biological chemistry
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