See the published version of this preprint at Archives of Gynecology and Obstetrics.
This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Learn more about In Review
A new preprint design is coming!
We have improved readability, clarity, accessibility, and opportunities for engagement.
Research Article
Yazhen Xie
Nanjing University of Chinese Medicine
Corresponding Author
ORCiD: https://orcid.org/0000-0001-8198-2349
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Purpose The aim of this study was to investigate differentially expressed proteins (DEPs) and their functions in the uteruses of primary dysmenorrhea (PD) rats by using label-free quantitative proteomics analysis.
Methods The PD rat model was induced by injecting both estradiol benzoate and oxytocin. Twenty rats were equally divided into two groups: a control group (normal rats), a PD model group (PD rats). Writhing scores and serum levels of Prostaglandin E2 (PGE2) and Prostaglandin F2α (PGF2α) were used to evaluate the success of the rat PD model. The DEPs were identified and analyzed by label-free quantitative proteomics and bioinformatics analyses.
Results A total of 276 DEPs were identified, including 119 up-regulated DEPs and 157 down-regulated DEPs. Bioinformatics revealed that the DEPs were mainly associated with ‘protein binding’, ‘metabolism’, ‘signal conduction’ and ‘focal adhesion’. The proteomic findings were verified by western blot analysis, which confirmed that myosin light chain kinase (MLCK), heat shock protein 90 AB1 (HSP90AB1), apolipoprotein A1 (Apoa1), p38 MAP kinase, c-Jun N-terminal kinase (JNK), and extracellular signal-related kinase 1/2 (ERK1/2) were significantly differentially expressed in between the control and PD samples.
Conclusions These results provide a deeper understanding the molecular pathogenesis of PD. The DEPs found in the present study may provide new ideas for further study of the mechanism of PD and aid the search for biomarkers for early diagnosis and treatment.
Keywords
Primary dysmenorrhea, Proteomics, Differentially expressed proteins
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Figure 6
Loading...
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
Peer Review Timeline
CURRENT STATUS: Published
View the published article at Archives of Gynecology and Obstetrics.
Version 1
Posted 29 Apr, 2021
No community comments so far
Editorial decision: Minor revisions
On 17 Jun, 2021
Reviews received
Received 25 Apr, 2021
Editor assigned
On 30 Mar, 2021
First submitted
On 30 Mar, 2021
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Obstetrics & Gynecology
Learn more about our company.
A new preprint design is coming!
We have improved readability, clarity, accessibility, and opportunities for engagement.
See the published version of this preprint at Archives of Gynecology and Obstetrics.
This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Learn more about In Review
Research Article
Yazhen Xie
Nanjing University of Chinese Medicine
Corresponding Author
ORCiD: https://orcid.org/0000-0001-8198-2349
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
Peer Review Timeline
CURRENT STATUS: Published
View the published article at Archives of Gynecology and Obstetrics.
Version 1
Posted 29 Apr, 2021
No community comments so far
Editorial decision: Minor revisions
On 17 Jun, 2021
Reviews received
Received 25 Apr, 2021
Editor assigned
On 30 Mar, 2021
First submitted
On 30 Mar, 2021
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Obstetrics & Gynecology
License:
This work is licensed under a CC BY 4.0 License. Read Full License
View the published article at Archives of Gynecology and Obstetrics.
Purpose The aim of this study was to investigate differentially expressed proteins (DEPs) and their functions in the uteruses of primary dysmenorrhea (PD) rats by using label-free quantitative proteomics analysis.
Methods The PD rat model was induced by injecting both estradiol benzoate and oxytocin. Twenty rats were equally divided into two groups: a control group (normal rats), a PD model group (PD rats). Writhing scores and serum levels of Prostaglandin E2 (PGE2) and Prostaglandin F2α (PGF2α) were used to evaluate the success of the rat PD model. The DEPs were identified and analyzed by label-free quantitative proteomics and bioinformatics analyses.
Results A total of 276 DEPs were identified, including 119 up-regulated DEPs and 157 down-regulated DEPs. Bioinformatics revealed that the DEPs were mainly associated with ‘protein binding’, ‘metabolism’, ‘signal conduction’ and ‘focal adhesion’. The proteomic findings were verified by western blot analysis, which confirmed that myosin light chain kinase (MLCK), heat shock protein 90 AB1 (HSP90AB1), apolipoprotein A1 (Apoa1), p38 MAP kinase, c-Jun N-terminal kinase (JNK), and extracellular signal-related kinase 1/2 (ERK1/2) were significantly differentially expressed in between the control and PD samples.
Conclusions These results provide a deeper understanding the molecular pathogenesis of PD. The DEPs found in the present study may provide new ideas for further study of the mechanism of PD and aid the search for biomarkers for early diagnosis and treatment.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Figure 6
Loading...