Premium
Inter‐individual Differences in Arteriolar Tree Architecture in the Mouse Spinotrapezius May Suggest a Genetic Basis for Susceptibility to Ischemic Insult
Author(s) -
Bruce Anthony,
Mac Gabhann Feilim,
Peirce Shayn M.
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.973.15
Subject(s) - arteriole , phenotype , strain (injury) , inbred strain , genetic architecture , biology , microcirculation , anatomy , pathology , neuroscience , medicine , gene , genetics
We have previously shown that the arteriolar network architecture of the murine spinotrapezius muscle and lattimus dorsi can be characterized as either highly interconnected or highly dendritic, depending on the strain of inbred mouse. We have also shown that there is a high degree of individual‐to‐individual variability in arteriolar network architecture in outbred CD‐1 mice. Specifically, Balb/c spinotrapezius muscle exhibits a microvascular architecture composed of unconnected dendritic trees, which we hypothesize are susceptible to ischemic injury. In contrast, C57BL/6 spinotrapezius muscle exhibits looped microvasculature architecture that may be protective against ischemic injury. Importantly, outbred CD‐1 mice exhibit either C57BL/6‐like or Balb/c‐like microvasculature architecture in the spinotrapezius muscle and respond to locally‐induced ischemic injury in a manner consistent with the respective inbred strain. We show that differences in microvasculature architecture appear as early as 10 days of age. It is common for CD‐1 littermates to possess either phenotype suggesting a genetic basis for architectural differences, and we have collected microarray data to probe this hypothesis. A method for inducing stable arteriole‐to‐arteriole connections could be very effective at minimizing the effect of ischemic events. Support provided by: NIH‐HL082838‐02 and NIH‐T32‐HL007284.