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C.B-17 SCID小鼠发生心外膜钙化,心功能未改变。

C.B-17 SCID mice develop epicardial calcinosis with unaltered cardiac function.

作者信息

Raghunathan Suchi, Reynolds Corey L, Schwartz Robert J, Stewart M David, McConnell Bradley K

机构信息

Department of Pharmacological and Pharmaceutical Sciences, College of Pharmacy, University of Houston, Houston, 77204, TX, USA.

Mouse Phenotyping Core, Baylor College of Medicine, Houston, 77030, TX, USA.

出版信息

Fundam Clin Pharmacol. 2019 Feb;33(1):25-30. doi: 10.1111/fcp.12398. Epub 2018 Aug 5.

DOI:10.1111/fcp.12398
PMID:29959870
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6311438/
Abstract

Inbred mouse strains are the most widely used mammalian model organism in biomedical research owing to ease of genetic manipulation and short lifespan; however, each inbred strain possesses a unique repertoire of deleterious homozygous alleles that can make a specific strain more susceptible to a particular disease. In the current study, we report dystrophic cardiac calcinosis (DCC) in C.B-17 SCID male mice at 10 weeks of age with no significant change in cardiac function. Acquisition of DCC was characterized by myocardial injury, fibrosis, calcification, and necrosis of the tissue. At 10 weeks of age, 38% of the C.B-17 SCID mice from two different commercial colonies exhibited significant calcinosis on the ventricular epicardium, predominantly on the right ventricle. The frequency of calcinosis was more than 50% for mice obtained from Taconic's Cambridge City colony and 25% for mice obtained from Taconic's German Town colony. Interestingly, the DCC phenotype did not affect cardiac function at 10 weeks of age. No differences in echocardiography or electrocardiography were observed between the calcinotic and non-calcinotic mice from either colony. Our findings suggest that C.B-17 SCID mice exhibit DCC as early as 10 weeks of age with no significant impact on cardiac function. This strain of mice should be cautiously considered for the study of cardiac physiology.

摘要

近交系小鼠由于易于进行基因操作且寿命较短,是生物医学研究中使用最广泛的哺乳动物模式生物;然而,每个近交系都拥有独特的有害纯合等位基因库,这可能使特定品系更容易患某种特定疾病。在本研究中,我们报告了10周龄的C.B-17 SCID雄性小鼠出现营养不良性心脏钙化(DCC),心脏功能无显著变化。DCC的发生以心肌损伤、纤维化、钙化和组织坏死为特征。在10周龄时,来自两个不同商业种群的C.B-17 SCID小鼠中有38%在心室心外膜出现明显钙化,主要在右心室。从Taconic的剑桥市种群获得的小鼠钙化频率超过50%,从Taconic的德国镇种群获得的小鼠钙化频率为25%。有趣的是,DCC表型在10周龄时对心脏功能没有影响。两个种群的钙化小鼠和非钙化小鼠在超声心动图或心电图方面均未观察到差异。我们的研究结果表明,C.B-17 SCID小鼠早在10周龄时就出现DCC,对心脏功能没有显著影响。在心脏生理学研究中应谨慎考虑使用这种品系的小鼠。

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本文引用的文献

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Spontaneous cardiac calcinosis in BALB/cByJ mice.BALB/cByJ小鼠的自发性心脏钙化
Comp Med. 2013 Feb;63(1):29-37.
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Tubercular chronic calcific constrictive pericarditis.结核性慢性钙化性缩窄性心包炎
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Humanized SCID mouse models for biomedical research.用于生物医学研究的人源化重症联合免疫缺陷小鼠模型。
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New Dyscalc loci for myocardial cell necrosis and calcification (dystrophic cardiac calcinosis) in mice.小鼠心肌细胞坏死和钙化(营养不良性心脏钙化)的新骨钙素基因座。
Physiol Genomics. 2001 Aug 28;6(3):137-44. doi: 10.1152/physiolgenomics.2001.6.3.137.
9
Calcific constrictive pericarditis: is it still with us?钙化性缩窄性心包炎:它仍与我们相伴吗?
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10
Chromosomal localization of the loci responsible for dystrophic cardiac calcinosis in DBA/2 mice.DBA/2小鼠中导致营养不良性心脏钙化的基因座的染色体定位。
Genomics. 1999 Jul 1;59(1):105-7. doi: 10.1006/geno.1999.5862.