Abstract
The paper analyzes the distribution of polymorphic loci in rats of different hypertensive strains. When analyzing the transcribed loci of ISIAH rats and the corresponding loci of 11 other hypertensive strains/substrains of rats, the maximum frequency of occurrence of identical SNPs in different strains was 0.58 (i.e., in 7 of 12 hypertensive strains/substrains). The analysis of the genomic sequences of 11 hypertensive strains/substrains of rats, which model different forms of arterial hypertension, also did not reveal a single SNP common to all 11 hypertensive strains/substrains of rats taken in the analysis. Analysis of experimental data suggests that hypertension is a genetically heterogeneous disease.
Similar content being viewed by others
REFERENCES
Ellinor, P.T., Lunetta, K.L., Glazer, N.L., et al., Common variants in KCNN3 are associated with lone atrial fibrillation, Nat. Genet., 2010, vol. 42, no. 3, pp. 240—244. https://doi.org/10.1038/ng.537
Low, S.K., Takahashi, A., Mushiroda, T., Kubo, M., Genome-wide association study: a useful tool to identify common genetic variants associated with drug toxicity and efficacy in cancer pharmacogenomics, Clin. Cancer Res., 2014, vol. 20, no. 10, pp. 2541—2552. https://doi.org/10.1158/1078-0432.CCR-13-2755
Kingsmore, S.F., Lindquist, I.E., Mudge, J., et al., Genome-wide association studies: progress and potential for drug discovery and development, Nat. Rev. Drug Discovery, 2008, vol. 7, no. 3, pp. 221–230. https://doi.org/10.1038/nrd2519
Rapp, J.P., Genetic analysis of inherited hypertension in the rat, Physiol. Rev., 2000, vol. 80, no. 1, pp. 135—172. https://doi.org/10.1152/physrev.2000.80.1.135
Ershov, N.I., Markel, A.L., and Redina, O.E., Strain-specific single-nucleotide polymorphisms in hypertensive ISIAH rats, Biochemistry (Moscow), 2017, vol. 82, no. 2, pp. 224—235. https://doi.org/10.1134/S0006297917020146
Kim, D., Pertea, G., Trapnell, C., et al., TopHat2: accurate alignment of transcriptomes in the presence of insertions, deletions and gene fusions, Genome Biol., 2013, vol. 14, no. 4, p. R36. https://doi.org/10.1186/gb-2013-14-4-r36
McKenna, A., Hanna, M., Banks, E., et al., The genome analysis toolkit: a MapReduce framework for analyzing next-generation DNA sequencing data, Genome Res., 2010, vol. 20, no. 9, pp. 1297—1303. https://doi.org/10.1101/gr.107524.110
Hermsen, R., de Ligt, J., Spee, W., et al., Genomic landscape of rat strain and substrain variation, BMC Genomics, 2015, vol. 16, no. 357. https://doi.org/10.1186/s12864-015-1594-1
Kumar, P., Henikoff, S., and Ng, P.C., Predicting the effects of coding non-synonymous variants on protein function using the SIFT algorithm, Nat. Protoc., 2009, vol. 4, no. 7, pp. 1073—1081. https://doi.org/10.1038/nprot.2009.86
Zheng, X., Levine, D., Shen, J., et al., A high-performance computing toolset for relatedness and principal component analysis of SNP data, Bioinformatics, 2012, vol. 28, no. 24, pp. 3326—3328. https://doi.org/10.1093/bioinformatics/bts606
Sarikonda, K.V., Watson, R.E., Opara, O.C., and Dipette, D.J., Experimental animal models of hypertension, J. Am. Soc. Hypertens., 2009, vol. 3, no. 3, pp. 158—165. https://doi.org/10.1016/j.jash.2009.02.003
Bader, M., Rat models of cardiovascular diseases, Methods Mol. Biol., 2010, vol. 597, pp. 403—414. https://doi.org/10.1007/978-1-60327-389-3_27
Cardenas-Rodriguez, M., Osborn, D.P., Irigoin, F., et al., Characterization of CCDC28B reveals its role in ciliogenesis and provides insight to understand its modifier effect on Bardet—Biedl syndrome, Hum. Genet., 2013, vol. 132, no. 1, pp. 91—105. https://doi.org/10.1007/s00439-012-1228-5
Elbedour, K., Zucker, N., Zalzstein, E., et al., Cardiac abnormalities in the Bardet—Biedl syndrome: echocardiographic studies of 22 patients, Am. J. Med. Genet., 1994, vol. 52, no. 2, pp. 164—169. https://doi.org/10.1002/ajmg.1320520208
Croft, J.B. and Swift, M. Obesity, hypertension, and renal disease in relatives of Bardet—Biedl syndrome sibs, Am. J. Med. Genet., 1990, vol. 36, no. 1, pp. 37—42. https://doi.org/10.1002/ajmg.1320360109
Rahmouni, K., Fath, M.A., Seo, S., et al., Leptin resistance contributes to obesity and hypertension in mouse models of Bardet—Biedl syndrome, J. Clin. Invest., 2008, vol. 118, no. 4, pp. 1458—1467. https://doi.org/10.1172/JCI32357
Oparil, S. and Schmieder, R.E., New approaches in the treatment of hypertension, Circ. Res., 2015, vol. 116, no. 6, pp. 1074—1095. https://doi.org/10.1161/CIRCRESAHA.116.303603
Benjamin, E.J., Blaha, M.J., Chiuve, S.E., et al., Heart disease and stroke statistics—2017 Update: a report from the American Heart Association, Circulation, 2017, vol. 135, no. 10, pp. e146—e603. https://doi.org/10.1161/CIR.0000000000000485
Mann, S.J., Neurogenic essential hypertension revisited: the case for increased clinical and research attention, Am. J. Hypertens., 2003, vol. 16, no. 10, pp. 881—888.
Jazwinska, E.C., Exploiting human genetic variation in drug discovery and development, Drug Discovery Today, 2001, vol. 6, no. 4, pp. 198—205. https://doi.org/10.1016/S1359-6446(00)01642-1
Funding
This work was supported by budget projects 0324-2019-0041 and 0324-2019-0042. The studies were carried out using the equipment of the Center for Genetic Resources of Laboratory Animals at the Institute of Cytology and Genetics, Siberian Branch of the Russian Academy of Sciences, supported by the Russian Ministry of Education and Science (unique project identifier RFMEFI62117X0015). Computational analysis of the data was carried out using the resources of the Siberian Supercomputer Center of the Institute of Computational Mathematics and Mathematical Geophysics, Siberian Branch, Russian Academy of Sciences.
Author information
Authors and Affiliations
Corresponding author
Ethics declarations
The authors declare that they have no conflict of interest. This article does not contain any studies involving animals or human participants performed by any of the authors.
Rights and permissions
About this article
Cite this article
Redina, O.E., Devyatkin, V.A., Ershov, N.I. et al. Genetic Polymorphism of Experimentally Produced Forms of Arterial Hypertension. Russ J Genet 56, 213–225 (2020). https://doi.org/10.1134/S1022795420020106
Received:
Revised:
Accepted:
Published:
Issue Date:
DOI: https://doi.org/10.1134/S1022795420020106