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Article
Peer-Review Record

The Role of WNT3A Protein and Gene Variants in Allergic Rhinitis: A Case-Control Study

Curr. Issues Mol. Biol. 2024, 46(9), 9523-9533; https://doi.org/10.3390/cimb46090565 (registering DOI)
by Durkadin Demir Eksi 1,* and Huseyin Gunizi 2
Reviewer 1: Anonymous
Reviewer 2:
Curr. Issues Mol. Biol. 2024, 46(9), 9523-9533; https://doi.org/10.3390/cimb46090565 (registering DOI)
Submission received: 28 July 2024 / Revised: 22 August 2024 / Accepted: 27 August 2024 / Published: 29 August 2024

Round 1

Reviewer 1 Report

Comments and Suggestions for Authors

The article presents a study investigating the relationship between serum WNT3A protein levels, WNT3A polymorphisms, and allergic rhinitis (AR).

The study is well-structured and addresses a relevant topic. It provides valuable insights into the potential role of WNT3A in the pathogenesis of AR, adding novelty and value to the existing literature.

The research design is good, with a well-defined patient population and control group. However, the exclusion criteria listed in the study do not account for the smoking status of the participants, which is a significant oversight given the nature of the research on allergic rhinitis (AR). This can potentially confound the results. I recommend controlling for smoking status in the statistical analyses or, ideally, including smoking status in the exclusion criteria to eliminate this confounder. If this is not possible, I suggest acknowledging this limitation and its potential impact on the findings.

The conclusion section is lacking. Even if the conclusions result indirectly from the discussion section, I suggest adding a separate section to summarize your findings and make it easier to see.

The references are appropriate and recently published. 

Author Response

Please see the attachment.

Author Response File: Author Response.pdf

Reviewer 2 Report

Comments and Suggestions for Authors

Eksi and Gunizi studied the association of WNT3A with Allergic Rhinitis (AR) and evaluated it for the potential biomarker of AR. They employed ELISA for biomarker assay and PCR-RFLP for genotyping two SNPs. The suggested that WNT3A protein could be a potential biomarker for AR whereas the association of a SNP is not conclusive. Here are the comments that could be followed further to modify the manuscript.

1.      In materials and methods, ELISA should be described in more detail e.g. which plate reader (manufacturer, etc) was used. Procedure in brief should be written. How many times each sample are measured? Etc.

2.      Line 93, NEB is US company, unless a branch is in UK.

3.      In Table 3, authors obtained a higher (4.8ng/ml) WNT3A protein value in mild AR than in moderate/severe (3.1 ng/ml)? How can they explain it is elevated in AR than control? need explanation?

4.      In Figure 3, for rs3121310, the last lane (GA) of the gel blot could be omitted.

5.      rs3121310 is not associated with elevated levels of WNT3A plasma protein. Is there any expectation that rs3121310 changes the expression of WNT3A which means whether it is in cis-eQTL with WNT3A. This information could be obtained from gTEX portal. (https://www.gtexportal.org). If it is in cis-eQTL, then  authors expect the SNP to regulate the expression of its own gene. Based on the findings, they should incorporate the results in the discussion.

Comments for author File: Comments.pdf

Author Response

Please see the attachment.

Author Response File: Author Response.pdf

Round 2

Reviewer 2 Report

Comments and Suggestions for Authors

The paper is now improved

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