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Abnormal expressions of AGEs, TGF-β1, BDNF and their receptors in diabetic rat colon–Associations with colonic morphometric and biomechanical remodeling

Present study aims to investigate the role of AGEs, TGF-β1, BDNF and their receptors on diabetes-induced colon remodeling. Diabetes was induced by a single tail vein injection 40 mg/kg of STZ. The parameters of morphometric and biomechanical properties of colonic segments were obtained from diabetic...

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Autores principales: Sha, Hong, Tong, Xiaolin, Zhao, Jingbo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6013484/
https://www.ncbi.nlm.nih.gov/pubmed/29930382
http://dx.doi.org/10.1038/s41598-018-27787-2
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author Sha, Hong
Tong, Xiaolin
Zhao, Jingbo
author_facet Sha, Hong
Tong, Xiaolin
Zhao, Jingbo
author_sort Sha, Hong
collection PubMed
description Present study aims to investigate the role of AGEs, TGF-β1, BDNF and their receptors on diabetes-induced colon remodeling. Diabetes was induced by a single tail vein injection 40 mg/kg of STZ. The parameters of morphometric and biomechanical properties of colonic segments were obtained from diabetic and normal rats. The expressions of AGE, RAGE, TGF- β1, TGF- β1 receptor, BDNF and TrkB were immunohistochemically detected in different layers of the colon. The expressions of AGE, RAGE, TGF-β1 and TGF- β1 receptor were increased whereas BDNF and TrkB were decreased in the diabetic colon (P < 0.05, P < 0.01). AGE, RAGE and TGF-β1 receptor expressions were positively correlated whereas the BDNF expression was negatively correlated with most of the morphometry and biomechanical parameters (P < 0.05, P < 0.01, P < 0.001). AGE, TGF- β1 and BDNF in different layers correlated with their receptors RAGE, TGF- β1 receptor and TrkB respectively. STZ-induced diabetes up-regulated the expression of AGE, RAGE, TGF- β1 and TGF- β1 receptors and down-regulated BDNF and TrkB in different layers of diabetic colon mainly due to hyperglycemia. Such changes maybe important for diabetes-induced colon remodeling, however it is needed to further perform mechanistic experiments in order to study causality or approaches that explain the relevance of the molecular pathways.
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spelling pubmed-60134842018-06-27 Abnormal expressions of AGEs, TGF-β1, BDNF and their receptors in diabetic rat colon–Associations with colonic morphometric and biomechanical remodeling Sha, Hong Tong, Xiaolin Zhao, Jingbo Sci Rep Article Present study aims to investigate the role of AGEs, TGF-β1, BDNF and their receptors on diabetes-induced colon remodeling. Diabetes was induced by a single tail vein injection 40 mg/kg of STZ. The parameters of morphometric and biomechanical properties of colonic segments were obtained from diabetic and normal rats. The expressions of AGE, RAGE, TGF- β1, TGF- β1 receptor, BDNF and TrkB were immunohistochemically detected in different layers of the colon. The expressions of AGE, RAGE, TGF-β1 and TGF- β1 receptor were increased whereas BDNF and TrkB were decreased in the diabetic colon (P < 0.05, P < 0.01). AGE, RAGE and TGF-β1 receptor expressions were positively correlated whereas the BDNF expression was negatively correlated with most of the morphometry and biomechanical parameters (P < 0.05, P < 0.01, P < 0.001). AGE, TGF- β1 and BDNF in different layers correlated with their receptors RAGE, TGF- β1 receptor and TrkB respectively. STZ-induced diabetes up-regulated the expression of AGE, RAGE, TGF- β1 and TGF- β1 receptors and down-regulated BDNF and TrkB in different layers of diabetic colon mainly due to hyperglycemia. Such changes maybe important for diabetes-induced colon remodeling, however it is needed to further perform mechanistic experiments in order to study causality or approaches that explain the relevance of the molecular pathways. Nature Publishing Group UK 2018-06-21 /pmc/articles/PMC6013484/ /pubmed/29930382 http://dx.doi.org/10.1038/s41598-018-27787-2 Text en © The Author(s) 2018 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
spellingShingle Article
Sha, Hong
Tong, Xiaolin
Zhao, Jingbo
Abnormal expressions of AGEs, TGF-β1, BDNF and their receptors in diabetic rat colon–Associations with colonic morphometric and biomechanical remodeling
title Abnormal expressions of AGEs, TGF-β1, BDNF and their receptors in diabetic rat colon–Associations with colonic morphometric and biomechanical remodeling
title_full Abnormal expressions of AGEs, TGF-β1, BDNF and their receptors in diabetic rat colon–Associations with colonic morphometric and biomechanical remodeling
title_fullStr Abnormal expressions of AGEs, TGF-β1, BDNF and their receptors in diabetic rat colon–Associations with colonic morphometric and biomechanical remodeling
title_full_unstemmed Abnormal expressions of AGEs, TGF-β1, BDNF and their receptors in diabetic rat colon–Associations with colonic morphometric and biomechanical remodeling
title_short Abnormal expressions of AGEs, TGF-β1, BDNF and their receptors in diabetic rat colon–Associations with colonic morphometric and biomechanical remodeling
title_sort abnormal expressions of ages, tgf-β1, bdnf and their receptors in diabetic rat colon–associations with colonic morphometric and biomechanical remodeling
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6013484/
https://www.ncbi.nlm.nih.gov/pubmed/29930382
http://dx.doi.org/10.1038/s41598-018-27787-2
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