Dynamic Regulation of Vascular Myosin Light Chain
(MYL9) with Injury and Aging
Lina A. Shehadeh1,2,3*, Keith A. Webster2,3,4, Joshua M. Hare1,3, Roberto I. Vazquez-Padron2,3,5*
1Department of Medicine, Division of Cardiology, University of Miami Leonard M. Miller School of Medicine, Miami, Florida, United States of America, 2Vascular Biology
Institute, University of Miami Leonard M. Miller School of Medicine, Miami, Florida, United States of America, 3Interdisciplinary Stem Cell Institute, University of Miami
Leonard M. Miller School of Medicine, Miami, Florida, United States of America, 4Department of Pharmacology, University of Miami Leonard M. Miller School of Medicine,
Miami, Florida, United States of America, 5Department of Surgery, University of Miami Leonard M. Miller School of Medicine, Miami, Florida, United States of America
Background: Aging-associated changes in the cardiovascular system increase the risk for disease development and lead to
profound alterations in vascular reactivity and stiffness. Elucidating the molecular response of arteries to injury and age will
help understand the exaggerated remodeling of aging vessels.
Methodology/Principal Findings: We studied the gene expression profile in a model of mechanical vascular injury in the
iliac artery of aging (22 months old) and young rats (4 months old). We investigated aging-related variations in gene
expression at 30 min, 3 d and 7 d post injury. We found that the Myosin Light Chain gene (MYL9) was the only gene
differentially expressed in the aged versus young injured arteries at all time points studied, peaking at day 3 after injury (4.6
fold upregulation (p,0.05) in the smooth muscle cell layers. We confirmed this finding on an aging aortic microarray
experiment available through NCBI’s GEO database. We found that Myl9 was consistently upregulated with age in healthy
rat aortas. To determine the arterial localization of Myl9 with age and injury, we performed immunohistochemistry for Myl9
in rat iliac arteries and found that in healthy and injured (30 days post injury) arteries, Myl9 expression increased with age in
the endothelial layers.
Conclusions/Significance: The consistent upregulation of the myosin light chain protein (Myl9) with age and injury in
arterial tissue draws attention to the increased vascular permeability and to the age-caused predisposition to arterial
constriction after balloon angioplasty.
Citation: Shehadeh LA, Webster KA, Hare JM, Vazquez-Padron RI (2011) Dynamic Regulation of Vascular Myosin Light Chain (MYL9) with Injury and Aging. PLoS
ONE 6(10): e25855. doi:10.1371/journal.pone.0025855
Editor: Marcello Rota, Brigham & Women’s Hospital - Harvard Medical School, United States of America
Received May 27, 2011; Accepted September 12, 2011; Published October 7, 2011
Copyright: ? 2011 Shehadeh et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits
unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Funding: This work was supported by awards from the American Heart Association (Scientist Development Grant 0930169N) and American Federation for Aging
Research (M1001096) to LAS; and by the American Heart Association (Scientist Development Award 0535167B) and NIH-NHLBI [1K01HL096413-01] to RIVP. The
funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Competing Interests: The authors have declared that no competing interests exist.
* E-mail: firstname.lastname@example.org (LAS); RVazquez@med.miami.edu (RIV-P)
Vascular diseases remain the most common cause of death in
the world . Aging increases the risk for hypertension, coronary
artery disease, and heart failure. The aging-associated changes in
the cardiovascular system lead to profound alterations in vascular
reactivity and stiffness [2,3]. Aging also increases the risk for
vascular proliferative diseases such atherosclerosis  and
restenosis after percutaneous coronary interventions.
In fact, experimental data suggesting that age increases the risk
for vascular diseases date back to 1982. Using a balloon injury
model Stemerman et al.  showed that VSMCs of aged rats
proliferate more in response to injury than those of young animals.
These results were reproduced in rabbits and primates [4,6] and
extended to a model of vascular injury in mice . We previously
demonstrated that aged mice develop more neointima following
arterial injury than their younger counterparts .
Based on the aforementioned observations, the aim of this study
was to investigate the effects of aging on the early vascular
response to injury in a model of arterial stenosis. Therefore, we
studied the global gene expression profiles in healthy and injured
arteries of aged and young rats at multiple time points. Moreover,
we attempted to verify our results by analysis of a public dataset on
gene expression of aged and young healthy aortas spanning four
different ages . Finally, we studied the localization of the
identified contractility gene, Myl9, within the arterial wall of aged
and young, healthy and injured iliac arteries.
Myl9 is the only gene differentially expressed in all 3
different time-points after wire injury in aged versus
We can start to comprehend the dynamics of vascular injury
only if we examine vascular remodeling with time. Therefore, we
elected to study global gene expression of vascular remodeling in a
3-point time series. Looking at the global gene expression in the
iliac arteries of old versus young rats 30 minutes, 3 days, or 7 days
after balloon injury, we found that Myosin Light Chain, Myl9, was
the only gene that overlapped as differentially expressed in all the
PLoS ONE | www.plosone.org1 October 2011 | Volume 6 | Issue 10 | e25855
three experiments (Figure 1). Myl9, was significantly downregu-
lated at 30 mins (22.2 fold), highly upregulated at 3 days (4.6
fold), and upregulated at 7 days (2.9 fold). 40 other genes
overlapped between 30 minutes and 3-days; 44 other genes
overlapped between 3-day and 7-day injury; 74 genes overlapped
between 3 minutes and 7-day injury. A comprehensive list of the
overlapping genes is provided in Supplemental Table S1.A 2.0
fold change and p,.05 significance cut-offs were used. No
multiple correction was employed.
Age has a profound effect on genes differentially
expressed after 30 minutes of wire injury in rats
Vascular remodeling is highly sensitive to age. Therefore, to
examine the effect of age on vascular remodeling using a common
30 minutes post-injury time, we studied the global gene expression
in the iliac arteries of old versus young, old versus old, and young
versus young rats. While most of the genes did not overlap among
the 3 pairs compared, 12 genes overlapped in all the 3 experiments
(Figure 2AB). These 12 genes can be considered not sensitive to
the age effect but rather unique to the injury process. They include
the Ca2+-dependent activator protein (Cadps2), the RNA binding
motif protein (Rbm39), the neutrophil cytosolic factor (Ncf4), and
the gap junction protein (Gja5). A comprehensive list of the
overlapping genes between any 2 conditions is provided in
Supplemental Table S2.A 2.0 fold change and p,.05 significance
cut-offs were used. No multiple correction was employed.
A common aging transcriptional profile in healthy rat
iliac and aortic arteries includes Myl9
To investigate for a common aging transcriptional profile in
healthy vessels, we compared global gene expression between 1)
aged (22 months) versus young (3 months) rat iliac arteries, and 2)
aged (28 months) versus young (3 months) rat thoracic aortas .
We found that 114 transcripts overlapped in the two studies
(Figure 3A). Among these common transcripts were the contrac-
tion genes Myl9 (Figure 3B) and Itga1 (Integrin alpha 1), which
increased systematically with age in rat thoracic aortas (Figure 3B).
As expected, collagens (Col1a1 and Col3a1) and vascular
endothelial growth factor (Vegfa) were consistently downregulated,
and the aging genes B-cell leukemia/lymphoma 2 (Bcl2) and
vascular cell adhesion molecule 1 (Vcam1) were upregulated in
both iliac and aortic arteries with age. In addition, NADPH
oxidase 4 (Nox4) which is a positive regulator of SMC migration
was also upregulated with age. A 2.0 fold change and p,.05
Figure 1. Differentially expressed genes overlapping in
multiple time points in old versus young injured rat iliac
arteries. A. Venn diagram shows the number of differentially
expressed genes determined by our analysis of 3 different time points
in old versus young injured rat iliac arteries. Gene lists were compared
to find common differentially expressed transcripts. A 2.0 fold change
and p,.05 significance cut-offs were used. No multiple correction was
employed. B. Heat map of Myl9 gene expression levels in multiple time
points in old versus young injured rat iliac arteries. Myosin Light chain 9,
Myl9, was significantly downregulated at 30 mins (22.2 fold), highly
upregulated at 3 days (4.6 fold), and upregulated at 7 days (2.9 fold).
Color bar shown in Log2.
Figure 2. Differentially expressed genes overlapping in
different age groups of 30 min-injured rat iliac arteries. A.
Venn diagram shows lists of differentially expressed genes determined
by our analysis of 3 different pairs of age groups of 30 min-injured rat
iliac arteries. Gene lists were compared to find common differentially
expressed transcripts. A 2.0 fold change and p,.05 significance cut-offs
were used. No multiple correction was employed. B. Heat map of
differentially expressed genes overlapping in different age groups of
30 min-injured rat iliac arteries.12 genes overlapped in old versus
young, old versus old, and young versus young, 30 min-injured rat iliac
arteries. Color bar shown in Log2.
Vascular Myl9 with Injury and Aging
PLoS ONE | www.plosone.org2 October 2011 | Volume 6 | Issue 10 | e25855
significance cut-offs were used. No multiple correction was
Myl9 protein in over-expressed in aged versus young iliac
arteries and is concentrated in the endothelial layer
To confirm the over-expression of Myl9 in aged versus young
arteries, we performed immunohistochemical staining for Myl9 in
young (3 months) and older (22 months) healthy rat iliac arteries.
Results confirm over-expression of Myl9 in the older group and
point to concentration of Myl9 protein expression in the
endothelial layer of the healthy iliac arteries (Figure 4). Arterial
injury also induced Myl9 expression with age. Interestingly, the
localization of Myl9 was dependent on the post-injury time. Myl9
was highly over-expressed in the smooth muscle cell layer of the
injured arteries 3 days post insult (Figure 5), whereas Myl9 was
concentrated in the endothelial layer 30 days post injury (Figure 6).
The present findings show that vascular remodeling is a
dynamic process that is greatly influenced by age and post-injury
time. While we found that the transcriptional programs clearly
vary among age groups and post-injury times, we identified a
common denominator for aging healthy arteries and aging injured
arteries at various post-injury times. The contractile regulatory
gene myosin light chain (Myl9) was consistently upregulated in
healthy aging aortas and was the only differentially expressed gene
Figure 3. Differentially expressed genes overlapping in healthy
aging rat iliac arteries and aortas. A. Venn diagram shows
differentially expressed genes determined by our analysis of healthy
aging rat iliac arteries and healthy aging rat thoracic aortas. The two
gene lists were compared to find common differentially expressed
transcripts. A 2.0 fold change and p,.05 significance cut-offs were
used. No multiple correction was employed. B. Heat map of
differentially expressed genes overlapping in healthy aging rat iliac
arteries and aortas. Selected genes, including Myl9, from the 114
transcripts overlapping in healthy aging iliac arteries and thoracic
aortas, are shown in a heatmap displaying their expression levels in
young and old aortas. Color bar shown in Log2.
Figure 4. Myl9 immunostaining of old (22 months) and young
(3 months) non-injured rat iliac arteries. Shown are representative
images of young and old healthy iliac arteries immunostained for Myl9.
Results confirm over-expression of Myl9 in the older group and point to
concentration of Myl9 expression in the endothelial layer of the iliac
Figure 5. Myl9 immunostaining of old (22 months) and young
(3 months) injured rat iliac arteries. Shown are representative
images of young and old iliac arteries 3 days post injury, immuno-
stained for Myl9. Results confirm over-expression of Myl9 in the older
injured group and point to concentration of Myl9 expression in the
smooth muscle layer of the iliac arteries during this post injury
Vascular Myl9 with Injury and Aging
PLoS ONE | www.plosone.org3 October 2011 | Volume 6 | Issue 10 | e25855
in injured iliac arteries at all 3 post-injury time points explored (30
minutes, 3 days, and 7days).
Myosins are a diverse superfamily of actin-dependent molecular
motors consisting of distinct structural and functional classes and
are implicated in contraction, cell shape, migration, adhesion,
intracellular transport of organelles, and signal transduction .
Conventional myosin II-complexes are hexamers consisting of 2
heavy chains, 2 regulatory MLCs, and 2 essential light chains. The
activity of myosin is regulated by reversible phosphorylation of
specific amino acids in the regulatory MLC . In the vascular
muscle, the interaction of myosin with actin is the primary
determinant of force production (contraction). Arterial vascular
smooth muscle cells contain abundant amounts of smooth muscle
myosin heavy chain (gene MYH11) that are generated by
alternative splicing of exons in the head (SM-A,B) and tail
(SM1,2) of the motor protein .The consequences of the
differential distribution of muscle and non- muscle MLC isoforms
in vascular tissues are unknown though it has been proposed that
MLCs influence myosin ATPase activity and velocity of shortening
. We found that Myl9 expression transiently increased with
age in the smooth muscle cell layers of injured arteries (3 d post-
injury). Our finding is in agreement with previously published
work demonstrating that aging rats showed an increased vascular
negative remodeling (constriction) after balloon dilatation com-
pared with adult animals. This agrees with the aggressive
circumferential coronary constriction (‘recoil’) observed after
balloon angioplasty in patients with coronary artery diseases and
animal models [12,13]. Our observation is also in accordance with
previous findings from the literature reporting that the effect of
phosphorylation and de-phosphorylation of Myl9 protein to be at
the essence of altered vascular contractility .
Interestingly, we found that in healthy and late injured (30
days post injury) iliac arteries, Myl9 expression increased with
age in the endothelial layers. Our findings are in line with those
recently published by Licht et al , describing Jun-b
dependent expression of Myl9 in primary cultures of endothelial
cells (ECs). The effect of contractility proteins on aged-related
vascular remodeling and their localization in the EC versus SMC
layers is not well understood. Zeng et al had also found Myl9
expressed in ECs, which upon phosphorylation regulated
endothelial cytoskeletal remodeling, and increased endothelial
cell contraction resulting in increased paracellular gap formation
and endothelial hyperpermeability
expression causes endothelial dysfunction, it may explain the
increased signs of arterial constriction in the aging vasculature.
For instance, age-related endothelial dysfunction in aged rat
aortas was found associated with decreased vasorelaxation likely
caused by a decline in NO and endothelium-derived hyperpo-
larizing factor [17,18].
Myosin light chain phosphorylation may play an important role
in endothelial function, including reorganization of the cytoskel-
eton, changing cell shape, and controlling endothelial cell
isometric tension [19,20]. Interestingly, endothelial permeability
appears quite early in the progress of aging. In fact aortas of 30-
month-old rats had a 2-fold increase in endothelial permeability to
albumin compared with 10-month-old rats . Endothelial cells
lining blood vessels form a continuous layer that constrains
proteins and blood elements to the vascular lumen. An increase in
endothelial cell isometric tension (contraction) may disrupt the
continuous endothelial barrier leading to an increase in perme-
ability and development of edema, a hallmark of acute and
chronic inflammation. It is believed that elevated permeability of
the endothelium allows entry of lipoproteins into the vessel wall,
which become oxidized and propagate endothelial dysfunction
. The relevance of vascular permeability in the development of
age-related vascular diseases have been extensively discussed
[23,24]. Of note, endothelial leakage favors the passage of plasma
macromolecules across the endothelium and their trapping in the
intima, which could contribute to the development of restenosis
and atherosclerosis. The increased endothelial Myl9 may also
explain the morphological changes of endothelial cells associated
with aging which could account for the altered endothelial
permeability . Conversely, phosphorylation of myosin regula-
tory light chain (MLC) not only increases actomyosin ATPase
activity, but also destabilizes the endothelial cell2cell junctions
leading to increased monolayer cell permeability , [16,27].Our
results are encouraging and they warrant future research on
demonstrating whether ectopic expression of Myl9 in the aged
endothelium causes endothelial dysfunction.
In conclusion, our findings suggest that the amount and
localization of Myl9 is critical in the vascular function and
remodeling process with age. The analysis presented here sets the
basis for future studies in the field of vascular aging, in particular
for those aimed at preventing age-related vascular dysfunction.
Based on the knowledge of the role of Myl9 in endothelium
degeneration, strategies to prevent this process could be designed
and tested. New therapeutic interventions to prevent vascular
aging might have enormous medical consequences given the
strong age dependency of cardiovascular diseases.
Rat Balloon Injury Model
Aged Fisher (.22-month-old, F344) rats were purchased from
the National Institute of Aging (Bethesda, MD). Young (2-month-
old) rats were obtained from Harlan Laboratories (Indianapolis,
IN). Animal work was revised and approved by the Institutional
Committee for Use and Care of Laboratory Animals at the
University of Miami protocol approval ID 05-069 entitled ‘‘The
role of vascular senescence in age-related vasculopathies’’. All
operative procedures were under isoflurane anesthesia (Baxter, IL,
USA). Balloon injury in the right iliac artery was inflicted with a
2F Fogarty catheter (Baxter Corp., Irvine, CA, USA) adapted to a
custom angiographic kit (Boston Scientific, Scimed) . The
balloon catheter was always inflated to yield a constant pressure
between 1.5–1.6 atmospheres. Arterial specimens were collected
30 min, 3, 7 and 30 days after injury, cut in two fragments that
were fixed in 4% formalin-PBS or submerged in RNA later until
RNA isolation. All animal procedures were previously approved
Figure 6. Myl9 immunostatining of old (22 months) and young
(3 months) injured rat iliac arteries. Shown are representative
images of young and old iliac arteries 30 days post injury,
immunostained for Myl9. Results confirm over-expression of Myl9 in
the older injured group and point to concentration of Myl9 expression
in the endothelial layer of the iliac arteries during this post injury period.
Vascular Myl9 with Injury and Aging
PLoS ONE | www.plosone.org4 October 2011 | Volume 6 | Issue 10 | e25855
by the Institutional Committee for Use and Care of Laboratory
Animals at the University of Miami.
RNA Isolation for Gene Arrays
To isolate total RNA from the each of the 40 iliac artery
samples, 0.3 mL of TRI Reagent (Molecular Research Center Cat
#TRI-118) was added per tissue sample. The sample was then
macerated using a Kinematica AG Polytron PT-2100 for 1 min.
After a 5 min incubation at room temperature 0.2 volumes of
chloroform was added and mixed, following by a 3 min incubation
at room temperature and 10 min centrifugation at 12,000 g 4uC.
The top aqueous layer was transferred to a new tube containing
0.5 volume of isopropanol and 2 to 10 ul of polyacryl carrier
(Molecular Research Center, Cat # PC152). After mixing, the
precipitate containing the total RNA was collected by 15 min of
centrifugation at 12,000 g 4uC. The pellet was then washed two
times with 70% ethanol. Total RNA was additionally purified with
RNeasy Mini Kit (Qiagen, Cat # 74106). Total RNA yield was
RNA Qualification by Agilent
To characterize the quality of an RNA sample, it was analyzed
on the Agilent 2100 Bioanalyzer. Briefly, approximately 100 to
200 ng of the sample was placed in an RNA LabChip with the
appropriate sample loading buffer and electrophoresed in parallel
with an RNA standard ladder (Ambion cat # 7152). Agilent
Technologies’ Bioanalyzer software was used to analyze the results
and to create an electropherogram. RNA was considered usable if
ratio of 28S ribosomal peak to 18 S ribosomal peak was above 1.0.
All the 40 RNA samples used in our expression study had RIN
values between 6.4 and 7.2.
Labeling and Hybridization
10 to 20 ug of total RNA were mixed with the 200 pMol of
oligo-dT primer. After 10 min incubation at 70uC and 5 min at
4uC, 20 units of Transcriptor reverse transcriptase (RuC he, Cat #
3531287001), 10 nMol of each dNTP and 4 nMol of aminoallyl-
dUTP (Ambion, Cat # 8439) were added, and this mix was
incubated 2 hours at 42uC. After 30 min RNase treatment cDNA
was purified using QIAquick PCR purification Kit (Qiagen, Cat #
28106). Amount of cDNA was determined spectrophotometrically,
and samples were dried on speedvac. cDNA was resuspended in
the carbonate buffer (pH 9.029.3) and mixed with the Cy3- and
Cy5-NHS ethers (Amersham, Cat # PA23001 and PA25001,
respectively). After 1 hour incubation in the dark 20 mMol of
hydroxylamine were added to quench the reaction, and labeled
cDNA was purified using QIAquick PCR purification Kit.
Concentration of the labeled cDNA and labeling efficiency were
determined spectrophotometrically, and labeled cDNA were
hybridized to Agilent Whole Rat Genome Arrayfor 17 hours at
60uC according to manufacturer’s instructions. Two samples were
hybridized per chip. Therefore, the 40 samples were run on 20
Image Analysis and Data Processing
The microarrays were scanned at 5 micron resolution using a
GenePix4000B scanner (Axon Instruments at Molecular Devices)
and the resulting images were analyzed with the software package
GenePixPro 6.0 (Axon Instruments at Molecular Devices). Data
extracted from the images were transferred to the software
package Acuity 4.0 (AxonInstruments) for normalization and
statistical analysis. Each array was normalized for signal intensities
across the whole array and locally, using Lowess normalization.
Features for further analysis were selected according to the
following quality criteria: (1) at least 90% of the pixels in the spot
had intensity higher than background plus two standard
deviations; (2), there were less than 2% saturated pixels in the
spot; (3) signal to noise ratio (defined as ratio of the background
subtracted mean pixel intensity to standard deviation of back-
ground) was 3 or above for each channel; (4) the spot diameter was
between 110 and 150 micron; (5)the regression coefficient of ratios
of pixel intensity was 0.6 or above.
All data is MIAME compliant and all raw .gpr files from the 20
arrays are deposited in NCBI’s GEO database (GSE29255), a
MIAMI compliant database.
Gene Arrays: Global Transcription Analysis
All 20 raw gpr files (corresponding to the 40 samples of iliac
arteries) were imported into GeneSpring GX 11 software (Silicon
Genetics, Redwood City, CA). Each condition had 324
replicates/arrays. Normalized expression values were calculated
by the Robust Multi-array Average (RMA) method. The resultant
signal information was analyzed using one-way analysis of
variance (ANOVA) (p,0.05), assuming normality and equal
variances. No correction for multiple comparisons was done.
GeneSpring’s cross gene error model, which determines the
likelihood of observing a specific fold change to the likelihood of
observing a fold measurement by the 50.0 th percentile of all
measurements in that sample, then setting the average value of
expression level for each gene across the samples to 1.0, and
plotting the resulting normalized signal value for each sample
(values below 0.01 were set to 0.01). The list and the order of
various genes in which they appear in the heatmaps can be viewed
in tabular form in the supplemental files.
Analysis of Previous Aging Aortas Microarray Datasets
Similarly, we performed extensive analysis on a publicly
available microarray experiments on aging rat thoracic aortas:
(A) Sixteen chips from the rat thoracic aorta tissue from 3, 6, 18,
and 28 month old rats (n=4 per group)  (GEO Accession:
GSE7281). All 16 raw expression files were normalized using
RMA processor. All normalized expression data was analyzed
using GeneSpring software. Following normalization one-way
analysis of variance was performed for each gene to identify
statistically significant gene expression changes. Two criteria were
used to determine whether a gene was differentially expressed: fold
change of 62.0 and p value ,.05 using a two-tailed distribution.
No correction for multiple comparisons was done. Lists of
differentially expressed genes from different experiments were
compared within GeneSpring and displayed as Venn diagrams to
show overlapping and non-overlapping genes (Figure 3). As in our
previous work , the convergence of differentially expressed
genes (Venn diagrams) is what was used to replace the multiple
testing in further screening the genes that passed the ,.05
Cross sections were taken from different levels of the paraffin-
embedded arteries. After tissue rehydration, endogenous peroxi-
dase was blocked with 3% hydrogen peroxide. Epitope retrieval
was performed with citrate buffer (10 mM sodium citrate, pH 6.0)
in a Pascal chamber. Non-specific binding was blocked with 0.5%
blocking solution (DAKO, Carpinteria, CA). Slides with the Myl9
primary antibody (1:250, Abcamab64161)were incubated for
1 hour at room temperature (RT). Biotinylated secondary
antibodies (DAKO Universal link) were applied for 30 minutes,
followed by a washing step with PBS and 15 min incubation with
Vascular Myl9 with Injury and Aging
PLoS ONE | www.plosone.org5 October 2011 | Volume 6 | Issue 10 | e25855
HRP-streptavidin solution (DAKO) at RT. Color was developed Download full-text
with a DAB chromogenic solution (DAKO). Nuclei were
counterstained with Meyer’s hematoxylin and mounted as
described above. Images were taken with an Olympus 1X71
camera fitted to an Olympus BX 40 microscope (Olympus
America Inc, Center Valley, PA).
Injured Versus Young Control Iliac Arteries at 3 Days
Post-Injury. Listed are the 924 total transcripts differentially
expressed by 2 fold (p,.05 with no multiple correction) in old
Injured versus young control iliac arteries at 3 days post injury
(n=3 per group).
B: Differentially Expressed Genes in Old
Injured Versus Young Control Iliac Arteries at 30
Minutes Post-Injury. Listed are the 1751 total transcripts
A: Differentially Expressed Genes in Young
differentially expressed by 2 fold (p,.05 with no multiple
correction) in young Injured versus control iliac arteries at 30
minutes post injury (n=3 per group).
We would like to thank Dr. Lubov Nathanson for running the arrays at
Hussman Institute for Human Genomics at University of Miami, and Dr.
Nicholas Tsinoremas from the Center for Computational Sciences at
University of Miami for providing GeneSpring X Software used for
analysis of microarray data.
Conceived and designed the experiments: LAS RV-P. Performed the
experiments: LAS RV-P. Analyzed the data: LAS RV-P. Contributed
reagents/materials/analysis tools: LAS RV-P KAW JMH. Wrote the
paper: LAS RV-P.
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Vascular Myl9 with Injury and Aging
PLoS ONE | www.plosone.org6 October 2011 | Volume 6 | Issue 10 | e25855