Human C15orf39 Inhibits Inflammatory Response via PRMT2 in Human Microglial HMC3 Cell Line

Round 1

Reviewer 1 Report

Comments and Suggestions for Authors

Human C15orf39 Inhibits Inflammatory Response via PRMT2 2 in Human Microglial HMC3 Cell Line

In this work the authors examined the inhibitory effects of human C15orf39 on inflammatory response in human microglial cells.

General revision: I suggest to check the English and the formatting of the figures.

Introduction: I suggest to highlight the importance of understanding the molecular mechanisms that regulate microglial inflammatory responses in the context of neurological disorders.

Matherials and methods: I suggest to add references for established methods or protocols used in the study.

Others: Have you tried to evaluate other pathways as NLRP3 or TLR? Have you evaluated other interleukins as IL-1?

Comments on the Quality of English Language

Moderate editing of English language required

Author Response

Please see the attachment

Author Response File: Author Response.pdf

Reviewer 2 Report

Comments and Suggestions for Authors

The manuscript " Human C15orf39 Inhibits Inflammatory Response via PRMT2 2 in Human Microglial HMC3 Cell Line” - is a search for the cause of the development of diseases related to microglia activation.

 

My comments:

1.       Introduction –

“Once inflammation response is excessive and uncontrolled, detrimental harm may appear in the host tissue [5, 7]” - in response to infectious and other factors, it creates pathological beta amyloid proteins.

“Thus, microglia may be regarded as a promising therapeutic target in nervous system diseases [11, 12, 13].” – on what basis?

A more complex process.

“C15orf39 is expressed in various tissues including the brain in the NCBI database.” –add Ref.

“suggesting that C15orf39 may be a potential therapeutic target in many central nervous system diseases.” - what neurological diseases”?

what was the purpose of the research?

2.       Methods –

Has consent been obtained for the research?

3.       Discussion –

“Thus, our study provides some valuable evidence for controlling the

detrimental role of NF-κB signaling in brain injury diseases by overexpressing C15orf39.” - the studies were conducted in vitro, they would need to be confirmed in vivo to suggest such a role.

4.       Conclusion -

“Our study provides new information on the molecular biological function of C15orf39. It also provides some valuable hints for the treatment of the central nervous system diseases by overexpressing C15orf39.” - such studies have not been conducted. Too forward-looking conclusions.

Author Response

Please see the attachment.

Author Response File: Author Response.pdf