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小鼠氧诱导视网膜病变中无血管区的遗传控制。

The genetic control of avascular area in mouse oxygen-induced retinopathy.

作者信息

O'Bryhim Bliss E, Radel Jeff, Macdonald Stuart J, Symons R C Andrew

机构信息

Department of Ophthalmology, University of Kansas Medical Center, Kansas City, KS, USA.

出版信息

Mol Vis. 2012;18:377-89. Epub 2012 Feb 8.

PMID:22355249
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3283213/
Abstract

PURPOSE

The C57BL/6ByJ and BALB/cByJ inbred strains of mice are, respectively, susceptible and resistant to oxygen-induced retinopathy (OIR). The purpose of this work was to investigate the genetic control of the retinal avascular area in mouse OIR using a mapping cross.

METHODS

The central retinal avascular area was measured on postnatal day 16 (P16) in C57BL/6ByJ, BALB/cByJ, 101 (C57BL/6ByJ x BALB/cByJ)F₂, and 116 (BALB/cByJ x C57BL/6ByJ)F₂ mice that had been subjected to the OIR protocol. A genome-wide scan was performed of selected albino and non-albino mice to determine quantitative trait loci associated with weight and avascular area.

RESULTS

C57BL/6ByJ mice had significantly larger avascular areas than BALB/cByJ ones. Albino mice of the F₂ generation had smaller avascular areas than the non-albino mice. Genotyping was performed at 856 informative single nucleotide polymorphisms approximately evenly distributed across the genome from each of 85 selected F₂ mice. Weight, sex, and the paternal grandmother were found to act as additive covariates associated with the avascular area on P16; mapping analyses that used a model incorporating these covariates found a quantitative trait locus on chromosome 7 related to avascular area. Mapping analyses that used a model that did not incorporate covariates found a quantitative trait locus on chromosome 9 related to avascular area. A quantitative trait locus for bodyweight on P16 was mapped to chromosome 5.

CONCLUSIONS

The retinal avascular area in the mouse OIR model is under genetic control. Revascularization in OIR is related to the weight, strain of paternal grandmother, sex, and albinism. Our data support the existence of a quantitative trait locus on chromosome 5 that influences weight after exposure to hyperoxia, as well as quantitative trait loci on chromosomes 7 and 9 that modify susceptibility to OIR.

摘要

目的

C57BL/6ByJ和BALB/cByJ近交系小鼠分别对氧诱导性视网膜病变（OIR）敏感和耐受。本研究旨在通过杂交定位研究小鼠OIR中视网膜无血管区的遗传控制。

方法

对接受OIR方案的C57BL/6ByJ、BALB/cByJ、101（C57BL/6ByJ×BALB/cByJ）F₂和116（BALB/cByJ×C57BL/6ByJ）F₂小鼠在出生后第16天（P16）测量视网膜中央无血管区。对选定的白化和非白化小鼠进行全基因组扫描，以确定与体重和无血管区相关的数量性状基因座。

结果

C57BL/6ByJ小鼠的无血管区明显大于BALB/cByJ小鼠。F₂代白化小鼠的无血管区比非白化小鼠小。对85只选定的F₂小鼠中的每只，在全基因组中大约均匀分布的856个信息性单核苷酸多态性位点进行基因分型。发现体重、性别和祖母代父系作为与P16无血管区相关的加性协变量；使用包含这些协变量的模型进行的定位分析发现7号染色体上有一个与无血管区相关的数量性状基因座。使用不包含协变量的模型进行的定位分析发现9号染色体上有一个与无血管区相关的数量性状基因座。P16时体重的数量性状基因座定位于5号染色体。

结论

小鼠OIR模型中视网膜无血管区受遗传控制。OIR中的血管再生与体重、祖母代父系品系、性别和白化有关。我们的数据支持5号染色体上存在一个影响高氧暴露后体重的数量性状基因座，以及7号和9号染色体上改变对OIR易感性的数量性状基因座。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f49e/3283213/c4a856528586/mv-v18-377-f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f49e/3283213/5cf127a97012/mv-v18-377-f1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f49e/3283213/ee26deef636b/mv-v18-377-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f49e/3283213/3c6c764026c4/mv-v18-377-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f49e/3283213/5a56b06408ad/mv-v18-377-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f49e/3283213/e31c985d733b/mv-v18-377-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f49e/3283213/c4a856528586/mv-v18-377-f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f49e/3283213/5cf127a97012/mv-v18-377-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f49e/3283213/aec854641070/mv-v18-377-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f49e/3283213/ee26deef636b/mv-v18-377-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f49e/3283213/3c6c764026c4/mv-v18-377-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f49e/3283213/5a56b06408ad/mv-v18-377-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f49e/3283213/e31c985d733b/mv-v18-377-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f49e/3283213/c4a856528586/mv-v18-377-f7.jpg

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