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Association of COL1A1 polymorphism with high myopia: a Meta-analysis
Guang-Ming Jin1,
Xiao-Jing Zhao2, Ai-Ming Chen3, Yong-Xing Chen4,
Qin Li2
1State Key Laboratory of Ophthalmology,
Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou
510060, Guangdong Province, China
2Department of Ophthalmology, the
Fifth Affiliated Hospital of Sun
Yat-sen University, Zhuhai 519000, Guangdong Province, China
3Department of Pharmacy,
the Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai 519000,
Guangdong Province, China
4Department of
Otorhinolaryngology, Jiangmen Central
Hospital, Jiangmen 529030, Guangdong Province, China
Co-first authors: Guang-Ming Jin,
Xiao-Jing Zhao and
Ai-Ming Chen
Correspondence to: Qin
Li. Department of
Ophthalmology, the Fifth Affiliated Hospital of Sun Yat-sen University, No.52 meihua Road, Zhuhai 519000, Guangdong Province, China. qinli1960@163.com
Received: 2014-05-27 Accepted:
2015-07-20
Abstract
AIM: To
investigate the association between collagen type I alpha 1 (COL1A1)
gene and high myopia.
METHODS:
In this Meta-analysis, we examined 5 published case-control studies that
involved 1942
high myopia cases and 2929
healthy controls to assess the association between the COL1A1 rs2075555 polymorphism
and high myopia risk. We calculated the pooled odds ratios (ORs) of COL1A1
rs2075555 polymorphism in high myopia cases vs
healthy controls to evaluate the strength of the association.
RESULTS: Overall, there was no significant difference both in the genotype and allele distributions of COL1A1 rs2075555 polymorphism between high myopia cases and healthy controls: CC vs AA OR=1.10, 95% confidence interval (CI)=0.76-1.58; AC vs AA OR=0.98, 95%CI 0.80-1.20; CC/AC vs AA/OR=1.01, 95%CI 0.84-1.22; CC vs AC/AA OR=1.06, 95%CI=0.93-1.20; C vs A OR=1.06, 95%CI 0.91-1.23). In addition, in the stratified analyses by ethnicity, no significant associations were found in any genetic model both in European and Asia cohorts.
CONCLUSION:
Our results indicate that the COL1A1 rs2075555 polymorphism may not affect
susceptibility to high myopia.
KEYWORDS:
collagen type I alpha 1;
polymorphism; high myopia; Meta-analysis
DOI:10.18240/ijo.2016.04.22
Citation: Jin GM, Zhao XJ, Chen AM, Chen YX, Li Q.
Association of COL1A1 polymorphism with high myopia: a Meta-analysis. Int J Ophthalmol 2016;9(4):604-609
INTRODUCTION
Myopia is a common eye disorder that has been widely
studied in recent years[1-3], particularly because
of its increasing prevalence across populations worldwide[4]. According to epidemiological
evidence, the incidence of myopia is increasing, especially in East Asia[3,5-6]. Previous studies have
indicated that the greatest contributor to myopic refraction is the axial
length[7],
and when the elongation of the eyeball is excessive, high myopia occurs. High
myopia is an extreme form of myopia that is characterized by a spherical
equivalent of less than -6.00 diopters or an axial length greater than 26 mm.
Many serious complications are associated with high myopia, including retinal
detachment, glaucoma, cataracts, macular degeneration, and scleral staphyloma[8]. High myopia is one of
the major causes of blindness in many countries and is an important public
health problem worldwide[9].
Unfortunately, the pathogenesis of high myopia
remains unclear. Although environmental factors such as near work, higher
educational levels, and poor economic development levels have been implicated
in the occurrence of high myopia[10-11],
they cannot explain all cases. However, many studies suggest that genetic
factors may be responsible for high myopia[12-14].
Recent reports have demonstrated that interactions of multiple genetic and
environmental factors may contribute to the development of high myopia[15-16], and several genes
have been confirmed to have an association with susceptibility to high myopia[12,14,17-19]. However, other
studies have not been able to replicate the original findings for these genes[20-22]. In particular, the
collagen type I alpha 1 (COL1A1) gene has been studied.
The COL1A1 gene is located on chromosome 17 (17q21.23), which
contains the myopia 5 (MYP517q21-22) locus[23].
This gene encodes the major component (pro-α1 chains) of type I collagen.
Mutations or single nucleotide polymorphisms (SNPs) of the COL1A1
gene may affect the formation of COL1A1 products by altering COL1A1 gene
expression, which as a result contributes to the susceptibility to
collagen-related diseases such as osteoporosis, osteogenesis imperfecta,
Ehlers-Danlos syndrome, and Marfan syndrome, as well as scleral thinning[24]. The COL1A1 gene also
reportedly plays an important role in the development of animal myopia[25-26]. Recently, several
studies performed in different regions investigated a genetic mutation in the
COL1A1 sequence [rs2075555 (homosapiens), adenine to cytosine,
A>C], as a candidate biomarker associated with high myopia[19,21,27-29]. However, the
conclusions of these previous studies remain controversial and conflicting. To
further investigate the role of COL1A1 rs2075555 polymorphism in high myopia,
we performed a Meta-analysis involving all the relevant published studies
available.
Literature Search Strategy Potential
articles were identified by a systematic search on the ISI Web of Science,
PubMed, EMBASE, Wiley Online Library, and Science Direct
databases up to December 15,
2013, using a combination of search
terms: “collagen type I alpha 1” OR “COL1A1”, “polymorphism” OR “variation”
OR “mutation” AND ”myopia” without language or publication date restrictions.
All relevant publications and their reference were manually screened to
identify eligible studies.
Selection Criteria Papers
identified during the literature search had to meet the following inclusion
criteria in order to be included in our study: 1) case-control or cohort design
studies of humans; 2) evaluation of the association of COL1A1 rs2075555 polymorphism with high
myopia; 3) sufficient published data available for our team to estimate odds
ratios (ORs) of different genotype frequencies; 4) published original full-text
literature. We excluded studies based on the following criteria: 1)
insufficient reported data; 2) abstracts, review papers, and case-only studies;
3) duplication of previously published literature.
Data Extraction Three
investigators (Jin GM, Zhao XJ, and Chen YX) independently extracted the data.
Discrepancies between different investigators were adjudicated by another 2
investigators (Chen AM and Li Q), who reached consensus. The collected data
included: name of the first author, publication date, geographical location,
ethnicity, source of control, genotyping methods, genotype frequencies,
matching variables, and the numbers of cases and controls.
Quality Assessment We employed the Newcastle-Ottawa scale
(NOS), which has been described in detail in previous study[30]
to evaluate the quality of the included studies by 2 investigators (Jin GM and
Zhao XJ). A study scoring less than 3 stars was categorized as “low quality”,
while 4 to 6 stars and 7 to 9 stars were categorized as “moderate quality” and
“high quality”, respectively[31].
Discrepancies between investigators were resolved by discussion.
Statistical Analysis The
allelic frequency of COL1A1 rs2075555 was calculated, and Hardy-Weinberg
equilibrium (HWE) was assessed for the control group in each included study.
Pearson’s χ2 test was used,
and significant disequilibrium was defined as P<0.05. The strength of the association between COL1A1 rs2075555
polymorphism and high myopia susceptibility was assessed by ORs with 95%
confidence intervals (CIs). We used Z-test to judge the significance of the pooled ORs, and statistical
significance was considered when P<0.05.
The pooled ORs were calculated for 5 genetic models: allele model (C vs A); homozygote model (CC vs AA); heterozygote model (AC vs AA); dominant genetic model (AC/CC vs AA); and recessive genetic model (CC vs AC/AA). Stratified analysis in
different genetic models was performed by ethnicity. Heterogeneity among
included studies was evaluated by the χ2-based
Q test[32]
and the I2 index[33];
P<0.10 or I2>50% were considered statistically significant. The
random effects model was used to estimate the pooled ORs when obvious
heterogeneity was present[34],
otherwise the fixed-effects model was used[35].
The sources of the heterogeneity were identified by the Galbraith plot[36]. Sensitivity analyses
that deleted 1 study at a time to reflect the effects of the individual study
to the pooled ORs were used to estimate the stability of our results[37]. Publication bias of
articles was assessed using Begg’s funnel plots and Egger’s test[38]. Significant
publication bias was considered when P<0.05.
All statistical analyses were performed with STATA 12.0 software (StataCorp LP,
College Station, TX, USA).
RESULTS
Characteristics of Eligible Studies Overall,
151 published articles were retrieved by our literature search strategy. From
this group we ultimately analyzed 5 case-control studies that included four
Asian studies and one European study and in total involved 1942 cases and 2929 controls. Figure 1 shows the
literature selection process. Genotype frequencies in the controls of one study
showed significant deviation from the HWE, which required sensitivity analysis
and evaluation of possible selection bias. As evaluated by the NOS, two studies
were scored as “moderate quality” and three studies were scored as ‘‘high
quality’’, indicating that the quality of the included articles was acceptable
for the Meta-analysis. Individual characteristics of the studies, patients, and
the control groups are shown in Tables 1 and 2.
Figure 1 Flow chart for the selection
of studies according to the criteria of this Meta-analysis.
Table 1 Main
characteristics of eligible studies included in the Meta-analysis
|
First author |
Year |
Region |
Ethnicity |
Genotyping method |
Source |
Matching |
|
Inamori Y[19] |
2007 |
Japan |
Asia |
Probe method |
HB |
Age, sex and
ethnicity |
|
Liang CL[29] |
2007 |
Taiwan |
Asia |
TaqMan |
PB |
Age, sex and ethnicity |
|
Vatavuk Z[28] |
2009 |
Croatia |
European |
BeadChip assay |
PB |
NA |
|
Nakanishi H[21] |
2009 |
Japan |
Asia |
TaqMan |
PB |
NA |
|
Zhang D[27] |
2011 |
China |
Asia |
SNaPshot method |
HB |
Age and sex |
HB: Hospital-based study; PB: Population-based study; NA: Not available.
Table 2
Distribution of COL1A1 rs2075555 genotypes among high myopia cases and controls
included in the Meta-analysis
|
First author |
No. |
Case |
Control |
P for HWE |
|||||
|
Case |
Control |
|
AC |
CC |
AA |
AC |
CC |
||
|
Inamori Y[19] |
330 |
330 |
34 |
166 |
128 |
52 |
176 |
98 |
0.07 |
|
Liang CL[29] |
471 |
623 |
36 |
161 |
183 |
53 |
269 |
296 |
0.46 |
|
Vatavuk Z[28] |
17 |
794 |
0 |
5 |
12 |
19 |
210 |
565 |
0.92 |
|
Nakanishi H[21] |
427 |
420 |
65 |
194 |
167 |
72 |
189 |
158 |
0.23 |
|
Zhang D[27] |
697 |
762 |
91 |
333 |
273 |
79 |
374 |
309 |
0.03 |
COL1A1: Collagen type I alpha 1; HWE: Hardy-Weinberg equilibrium.
Results of Meta-analysis The
primary results of the Meta-analysis regarding rs2075555 polymorphism and high
myopia risk are shown in Table 3. Overall, no obvious associations between
rs2075555 polymorphism and high myopia susceptibility were found in any genetic
models (CC
vs AA: OR=1.10; 95%CI
0.76-1.58); (AC vs AA: OR=0.98, 95%CI
0.80-1.20); (CC/AC vs AA: OR=1.01,
95%CI 0.84-1.22); (CC vs AC/AA:
OR=1.06, 95%CI 0.93-1.20); (C vs A: OR=1.06, 95%CI
0.91-1.23). In the stratified analysis by ethnicity, we
found no significant associations between rs2075555 polymorphism and high
myopia for any genetic models (Figure 2).
Table 3
Meta-analysis of COL1A1 rs2075555 polymorphism and susceptibility to high
myopia
COL1A1: Collagen type I alpha 1; OR: Odds ratio; R: Random-effect model; F: Fixed-effect
model.
Figure 2 Forest plot of the association
between COL1A1 rs2075555 polymorphism and susceptibility to high myopia in the
heterozygote model (AC vs AA) in
different ethnicities.
Test of Heterogeneity In
our current Meta-analysis, significant heterogeneity was observed in 2 genetic
models (CC vs AA and C vs A) (Table 3). The sources of the
heterogeneity were assessed by the Galbraith plot of all included studies.
Inamori et al’s[19] study was identified
as the main source of heterogeneity for the association between rs2075555
polymorphism and high myopia susceptibility both in the CC vs AA and the C vs A
models. The pooled ORs in these 2 models were not significantly influenced when
this study was removed.
Sensitivity Analysis A
single study included in the current Meta-analysis was excluded at the time of
sensitivity analysis. Similar results were revealed, and pooled ORs were not
obviously altered in any of the genetic models (Figure 3) shows the sensitivity
analysis results in the CA vs AA
model), suggesting the reliability and stability of our results.
Figure 3 Sensitivity analysis performed to
evaluate the influence of a single study on the pooled ORs in the heterozygote
model (AC vs AA).
Publication Bias Publication
bias was evaluated using Begg’s funnel plot and Egger’s test. As Figure 4 shows, the funnel plot shape for the
heterozygote model (CA vs AA) seems
approximately symmetrical, which suggests that publication bias in this study
can be neglected. In addition, Egger’s test provides further statistical
evidence of the funnel plots’ symmetry (P=0.712).
Overall, neither Begg’s funnel plot nor Egger’s test suggested any
statistically significant publication bias in any genetic model. These results
indicate that there is no evidence of publication bias in our Meta-analysis.
Figure 4 Begg’s funnel plot of COL1A1
rs2075555 polymorphism and high myopia susceptibility in the heterozygote model
(AC vs AA).
DISCUSSION
Although
the association between COL1A1 rs2075555 polymorphism and high myopia has been
reported many times in several geographic locations, the results generally were
conflicting rather than consistent[18,20,27-29].
Different genetic backgrounds, sources of controls, and study designs may be
responsible for these inconsistencies among different studies. An individual
study with a small sample size may be underpowered to evaluate the relationship
between gene mutation and high myopia, but pooling all eligible data by
Meta-analysis can possibly provide more powerful and credible evidence. The current Meta-analysis evaluating the possible effect
of the COL1A1 rs2075555 polymorphism on high myopia susceptibility was based on
a substantial amount of data from 5 individual case-control studies that
included a total of 1942
high myopia cases and 2929
controls. Unfortunately, no valid association between COL1A1 rs2075555 polymorphism
and high myopia was detected according to the pooled ORs in the different
genetic contrast models. Population stratification is a factor that can lead to
false evidence about the association between gene markers and high myopia.
Previous studies have demonstrated that the prevalence of myopia varies
according to ethnicity[39] and is much higher in the Asian population[40-41], especially in China[42]. Because
of this, stratified analysis by ethnicity was performed but did not reveal a
significant relation between the COL1A1 rs2075555 polymorphism and high myopia
in either the Asian or European populations. The results of this study suggest
that ethnicity is not a factor that influences the relationship between COL1A1
rs2075555 polymorphism and high myopia susceptibility.
A previous Meta-analysis performed by Nakanishi et al[21] showed a limited significance between COL1A1 rs2075555
polymorphism and high myopia susceptibility (OR=1.19; 95%CI 1.03-1.38, P<0.05) which is a result that is inconsistent with our
findings. However, in their Meta-analysis, Nakanishi et al[21] combined data of their own with data from a previously
published Japanese study that was the first reported positive association. As
we know, the reported ORs in the first positive studies are usually higher than
ORs reported in subsequent replication studies[43],
so there was a possible correlation between COL1A1 rs2075555 polymorphism and
high myopia susceptibility[19]. In addition, it is possible that publication bias
affected the results in the first positive study, and the actual OR of the SNP
was overestimated in their analysis, which included only 2 studies. Lastly,
both of the studies included in their Meta-analysis were conducted in Japanese
patients, and the sample size was too small to provide a powerful and precise
estimate for COL1A1 rs2075555 polymorphism and high myopia risk. In contrast, our
current Meta-analysis
combined all the eligible published studies we could identify and used enhanced
statistical methods to provide more reliable evidence that COL1A1 rs2075555
polymorphism does not contribute to high myopia susceptibility, even when different
ethnicities are taken into consideration.
Several
potential limitations of our Meta-analysis should be considered. Firstly, although a
statistically significant publication bias was not found in all the genetic
models, publication bias could still have occurred among the published articles
meeting the inclusion criteria. Secondly, a lack of sufficient raw data such as
age distribution and the sex of the patients included in the identified
articles limited further exploration of potential interactions, and more
precise and convincing analysis should be performed. Thirdly, all of the
studies included in our study were conducted in Asians and Europeans cohorts,
and, thus, conclusions from our Meta-analysis may be restricted to these two populations. However,
some advantages of the current Meta-analysis can be highlighted. Firstly, based on the strict
criteria of inclusion and exclusion, all the included studies were of
acceptable quality, which significantly enhances the statistical power of our
Meta-analysis. Secondly, we attempted to obtain adjusted estimates in different
populations by performing a subgroup analysis between different ethnicities.
Thirdly, no evidence of obvious publication bias was detected for any of the
genetic models, which suggests that our results are unbiased and statistically
reliable.
In summary, our Meta-analysis suggests that the
COL1A1 rs2075555 polymorphism is not a risk factor for susceptibility to high
myopia. Nevertheless, high myopia is a complex multifactorial eye disease that
is influenced by both genetic and environmental factors as well as their
interactions. Unfortunately, due to a lack of sufficient raw data from the
included studies, interactions such as gene-gene, SNP-SNP, and gene-environment
could not be evaluated. Further related research with larger sample sizes and
enhanced designs are needed.
ACKNOWLEDGEMENTS
Conflicts
of Interest: Jin GM, None;
Zhao XJ,
None; Chen AM, None;
Chen YX,
None; Li Q, None.
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