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The molecular pathogenesis of achalasia: a paired lower esophageal sphincter muscle and serum 4D label-free proteomic study

BACKGROUND: Achalasia is a primary esophageal motility disorder with potential molecular pathogenesis remaining uncertain. This study aimed to identify the differentially expressed proteins and potential pathways among achalasia subtypes and controls to further reveal the molecular pathogenesis of a...

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Autores principales: Chen, Songfeng, Xing, Xiangbin, Hou, Xun, Zhuang, Qianjun, Tan, Niandi, Cui, Yi, Wang, Jinhui, Zhang, Mengyu, Hu, Shixian, Xiao, Yinglian
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Oxford University Press 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10260389/
https://www.ncbi.nlm.nih.gov/pubmed/37324545
http://dx.doi.org/10.1093/gastro/goad031
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author Chen, Songfeng
Xing, Xiangbin
Hou, Xun
Zhuang, Qianjun
Tan, Niandi
Cui, Yi
Wang, Jinhui
Zhang, Mengyu
Hu, Shixian
Xiao, Yinglian
author_facet Chen, Songfeng
Xing, Xiangbin
Hou, Xun
Zhuang, Qianjun
Tan, Niandi
Cui, Yi
Wang, Jinhui
Zhang, Mengyu
Hu, Shixian
Xiao, Yinglian
author_sort Chen, Songfeng
collection PubMed
description BACKGROUND: Achalasia is a primary esophageal motility disorder with potential molecular pathogenesis remaining uncertain. This study aimed to identify the differentially expressed proteins and potential pathways among achalasia subtypes and controls to further reveal the molecular pathogenesis of achalasia. METHODS: Paired lower esophageal sphincter (LES) muscle and serum samples from 24 achalasia patients were collected. We also collected 10 normal serum samples from healthy controls and 10 normal LES muscle samples from esophageal cancer patients. The 4D label-free proteomic analysis was performed to identify the potential proteins and pathways involved in achalasia. RESULTS: Analysis of Similarities showed distinct proteomic patterns of serum and muscle samples between achalasia patients and controls (both P < 0.05). Functional enrichment analysis suggested that these differentially expressed proteins were immunity-, infection-, inflammation-, and neurodegeneration-associated. The mfuzz analysis in LES specimens showed that proteins involved in the extracellular matrix–receptor interaction increased sequentially between the control group, type III, type II, and type I achalasia. Only 26 proteins altered in the same directions in serum and muscle samples. CONCLUSIONS: This first 4D label-free proteomic study of achalasia indicated that there were specific protein alterations in both the serum and muscle of achalasia, involving immunity, inflammation, infection, and neurodegeneration pathways. Distinct protein clusters between types I, II, and III revealed the potential molecular pathways associated with different disease stages. Analysis of proteins changed in both muscle and serum samples highlighted the importance of further studies on LES muscle and revealed potential autoantibodies.
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spelling pubmed-102603892023-06-15 The molecular pathogenesis of achalasia: a paired lower esophageal sphincter muscle and serum 4D label-free proteomic study Chen, Songfeng Xing, Xiangbin Hou, Xun Zhuang, Qianjun Tan, Niandi Cui, Yi Wang, Jinhui Zhang, Mengyu Hu, Shixian Xiao, Yinglian Gastroenterol Rep (Oxf) Original Article BACKGROUND: Achalasia is a primary esophageal motility disorder with potential molecular pathogenesis remaining uncertain. This study aimed to identify the differentially expressed proteins and potential pathways among achalasia subtypes and controls to further reveal the molecular pathogenesis of achalasia. METHODS: Paired lower esophageal sphincter (LES) muscle and serum samples from 24 achalasia patients were collected. We also collected 10 normal serum samples from healthy controls and 10 normal LES muscle samples from esophageal cancer patients. The 4D label-free proteomic analysis was performed to identify the potential proteins and pathways involved in achalasia. RESULTS: Analysis of Similarities showed distinct proteomic patterns of serum and muscle samples between achalasia patients and controls (both P < 0.05). Functional enrichment analysis suggested that these differentially expressed proteins were immunity-, infection-, inflammation-, and neurodegeneration-associated. The mfuzz analysis in LES specimens showed that proteins involved in the extracellular matrix–receptor interaction increased sequentially between the control group, type III, type II, and type I achalasia. Only 26 proteins altered in the same directions in serum and muscle samples. CONCLUSIONS: This first 4D label-free proteomic study of achalasia indicated that there were specific protein alterations in both the serum and muscle of achalasia, involving immunity, inflammation, infection, and neurodegeneration pathways. Distinct protein clusters between types I, II, and III revealed the potential molecular pathways associated with different disease stages. Analysis of proteins changed in both muscle and serum samples highlighted the importance of further studies on LES muscle and revealed potential autoantibodies. Oxford University Press 2023-06-12 /pmc/articles/PMC10260389/ /pubmed/37324545 http://dx.doi.org/10.1093/gastro/goad031 Text en © The Author(s) 2023. Published by Oxford University Press and Sixth Affiliated Hospital of Sun Yat-sen University https://creativecommons.org/licenses/by/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Article
Chen, Songfeng
Xing, Xiangbin
Hou, Xun
Zhuang, Qianjun
Tan, Niandi
Cui, Yi
Wang, Jinhui
Zhang, Mengyu
Hu, Shixian
Xiao, Yinglian
The molecular pathogenesis of achalasia: a paired lower esophageal sphincter muscle and serum 4D label-free proteomic study
title The molecular pathogenesis of achalasia: a paired lower esophageal sphincter muscle and serum 4D label-free proteomic study
title_full The molecular pathogenesis of achalasia: a paired lower esophageal sphincter muscle and serum 4D label-free proteomic study
title_fullStr The molecular pathogenesis of achalasia: a paired lower esophageal sphincter muscle and serum 4D label-free proteomic study
title_full_unstemmed The molecular pathogenesis of achalasia: a paired lower esophageal sphincter muscle and serum 4D label-free proteomic study
title_short The molecular pathogenesis of achalasia: a paired lower esophageal sphincter muscle and serum 4D label-free proteomic study
title_sort molecular pathogenesis of achalasia: a paired lower esophageal sphincter muscle and serum 4d label-free proteomic study
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10260389/
https://www.ncbi.nlm.nih.gov/pubmed/37324545
http://dx.doi.org/10.1093/gastro/goad031
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