Genetic Analysis of Blood Pressure in 8 Mouse Intercross Populations

Ma, Feng; Deerhake, M. Elizabeth; Keating, Ryan; Thaisz, Jill; Xu, Lingfei; Tsaih, Shirng‐Wern; Smith, R. V.; Ishige, Taiichiro; Sugiyama, Fumihiro; Churchill, Gary A.; DiPetrillo, Keith

doi:10.1161/hypertensionaha.109.134569

Cited by 32 publications

(34 citation statements)

References 23 publications

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“…Eln ϩ/Ϫ rs369822 129 homozygotes, however, have an even higher SBP of 141 mm Hg. A similarly located peak was identified in a C3HxKK intercross by Feng et al (18), but in this case the total pressure difference between homozygous genotypes was only 3 mm Hg.…”

Section: Additive and Interactive Peaks Are Identified For Systolic Bsupporting

confidence: 68%

Genetic Modifiers of Cardiovascular Phenotype Caused by Elastin Haploinsufficiency Act by Extrinsic Noncomplementation

Kozel

Knutsen

et al. 2011

Journal of Biological Chemistry

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Background: Variability in vascular pathology is associated with elastin loss-of-function mutations. Results: Quantitative trait loci and several candidate genes that modify vessel pathology were identified in a mouse model of elastin insufficiency. Conclusion: The effects of elastin insufficiency are determined by interactions between the primary elastin defect and unrelated secondary modifiers. Significance: Identification of modifier genes enhances our understanding of disease mechanisms associated with elastin mutations.

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Section: Additive and Interactive Peaks Are Identified For Systolic Bsupporting

confidence: 68%

Genetic Modifiers of Cardiovascular Phenotype Caused by Elastin Haploinsufficiency Act by Extrinsic Noncomplementation

Kozel

Knutsen

et al. 2011

Journal of Biological Chemistry

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“…For example, a phenotypic screen of 37 strains of mice22 using the VPR tail‐cuff system (same as in this study) reported a 100±2 to 133±3 mm Hg range of SBPs for those animals. Other laboratories had comparable results using the same39 or different tail‐cuff systems 40, 41, 42.…”

Section: Discussionmentioning

confidence: 60%

“…However, a systematic and comprehensive evaluation of these stress‐inducing factors and their effect on hemodynamics in mice is lacking. It is believed that the mice habituate to the tail‐cuff procedure following repeated exposure and there is a common practice to “train” mice before starting an experiment 10, 21, 22. However, there is evidence that this does not happen 23, 24.…”

Section: Introductionmentioning

confidence: 99%

Tail‐Cuff Technique and Its Influence on Central Blood Pressure in the Mouse

Wilde

Aubdool

Thakore

et al. 2017

JAHA

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BackgroundReliable measurement of blood pressure in conscious mice is essential in cardiovascular research. Telemetry, the “gold‐standard” technique, is invasive and expensive and therefore tail‐cuff, a noninvasive alternative, is widely used. However, tail‐cuff requires handling and restraint during measurement, which may cause stress affecting blood pressure and undermining reliability of the results.Methods and ResultsC57Bl/6J mice were implanted with radio‐telemetry probes to investigate the effects of the steps of the tail‐cuff technique on central blood pressure, heart rate, and temperature. This included comparison of handling techniques, operator's sex, habituation, and influence of hypertension induced by angiotensin II. Direct comparison of measurements obtained by telemetry and tail‐cuff were made in the same mouse. The results revealed significant increases in central blood pressure, heart rate, and core body temperature from baseline following handling interventions without significant difference among the different handling technique, habituation, or sex of the investigator. Restraint induced the largest and sustained increase in cardiovascular parameters and temperature. The tail‐cuff readings significantly underestimated those from simultaneous telemetry recordings; however, “nonsimultaneous” telemetry, obtained in undisturbed mice, were similar to tail‐cuff readings obtained in undisturbed mice on the same day.ConclusionsThis study reveals that the tail‐cuff technique underestimates the core blood pressure changes that occur simultaneously during the restraint and measurement phases. However, the measurements between the 2 techniques are similar when tail‐cuff readings are compared with telemetry readings in the nondisturbed mice. The differences between the simultaneous recordings by the 2 techniques should be recognized by researchers.

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“…Mice from 15 inbred strains were purchased from The Jackson Laboratory and bred at Novartis Pharmaceuticals to generate nine populations of male F 2 mice for QTL analysis. Blood pressure was measured in F2 mice at 8 wk of age [QTL results for this phenotype are published (18)] and then spot urine samples were collected at 10 wk of age and analyzed with mouse albumin standards using a Roche Hitachi 917 Clinical Chemistry Autoanalyzer. DNA isolated from each F 2 mouse was genotyped by KBiosciences (Herts, UK) as described previously (18).…”

Section: Methodsmentioning

confidence: 99%

Genetic analysis of albuminuria in collaborative cross and multiple mouse intercross populations

Thaisz

Tsaih

et al. 2012

American Journal of Physiology-Renal Physiology

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Albuminuria is an important marker of nephropathy that increases the risk of progressive renal and chronic cardiovascular diseases. The genetic basis of kidney disease is well-established in humans and rodent models, but the causal genes remain to be identified. We applied several genetic strategies to map and refine genetic loci affecting albuminuria in mice and translated the findings to human kidney disease. First, we measured albuminuria in mice from 33 inbred strains, used the data for haplotype association mapping (HAM), and detected 10 genomic regions associated with albuminuria. Second, we performed eight F(2) intercrosses between genetically diverse strains to identify six loci underlying albuminuria, each of which was concordant to kidney disease loci in humans. Third, we used the Oak Ridge National Laboratory incipient Collaborative Cross subpopulation to detect an additional novel quantitative trait loci (QTL) underlying albuminuria. We also performed a ninth intercross, between genetically similar strains, that substantially narrowed an albuminuria QTL on Chromosome 17 to a region containing four known genes. Finally, we measured renal gene expression in inbred mice to detect pathways highly correlated with albuminuria. Expression analysis also identified Glcci1, a gene known to affect podocyte structure and function in zebrafish, as a strong candidate gene for the albuminuria QTL on Chromosome 6. Overall, these findings greatly enhance our understanding of the genetic basis of albuminuria in mice and may guide future studies into the genetic basis of kidney disease in humans.

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Genetic Analysis of Blood Pressure in 8 Mouse Intercross Populations

Cited by 32 publications

References 23 publications

Genetic Modifiers of Cardiovascular Phenotype Caused by Elastin Haploinsufficiency Act by Extrinsic Noncomplementation

Genetic Modifiers of Cardiovascular Phenotype Caused by Elastin Haploinsufficiency Act by Extrinsic Noncomplementation

Tail‐Cuff Technique and Its Influence on Central Blood Pressure in the Mouse

Genetic analysis of albuminuria in collaborative cross and multiple mouse intercross populations

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