Preliminary investigation on the establishment of a new meibomian gland obstruction model and gene expression

Abstract Meibomian gland dysfunction is a chronic ocular surface disease with a complex pathogenesis, whose main clinical manifestations are meibomian gland obstruction or/and lipid abnormalities. To explore the mechanism of MGD due to meibomian gland obstruction (MGO), we established a rat model of...

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Main Authors: Ming Sun, Huanmin Cheng, Zheng Yang, Jiangqin Tang, Shengshu Sun, Zhanglin Liu, Shaozhen Zhao, Lijie Dong, Yue Huang
Format: Article
Language:English
Published: Nature Portfolio 2024-10-01
Series:Scientific Reports
Online Access:https://doi.org/10.1038/s41598-024-73682-4
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author Ming Sun
Huanmin Cheng
Zheng Yang
Jiangqin Tang
Shengshu Sun
Zhanglin Liu
Shaozhen Zhao
Lijie Dong
Yue Huang
author_facet Ming Sun
Huanmin Cheng
Zheng Yang
Jiangqin Tang
Shengshu Sun
Zhanglin Liu
Shaozhen Zhao
Lijie Dong
Yue Huang
author_sort Ming Sun
collection DOAJ
description Abstract Meibomian gland dysfunction is a chronic ocular surface disease with a complex pathogenesis, whose main clinical manifestations are meibomian gland obstruction or/and lipid abnormalities. To explore the mechanism of MGD due to meibomian gland obstruction (MGO), we established a rat model of MGO by cauterizing the meibomian gland orifice. The morphology of the lid margins and meibomian gland orifices were visualized by slit lamp. The tear production of rats was measured by phenol red cotton thread, the tear film breakup time and corneal fluorescein staining scores of rats were detected under cobalt blue light of slit lamp. Changes in the histological structure of the meibomian gland (MG) were observed by HE staining, Oil Red O staining and immunofluorescence staining (collagen IV). RNA sequencing was used to detect differentially expressed genes in MGO and normal rats, which were validated by qPCR. In the MGO group after 4, 8, and 16 weeks, the meibomian gland orifices were closed, tear film break-up time decreased and corneal fluorescein staining score increased (p < 0.05). MG acini was smaller at 8-week and 16-week MGO rats in HE staining. Oil Red O staining showed less condensed staining in the 8- and 16-week MGO groups, while more condensed staining in the 4-week MGO group. Additionally, the basement membrane was destroyed in 16-week MGO group by immunofluorescence staining of collagen IV. Meanwhile, RNA sequencing and qPCR showed that lipid peroxidation (LPO), transient receptor potential vanilloid-3 (TRPV3) and genes in PPAR signaling pathway were differentially expressed in 16-week meibomian gland obstructive rats (p < 0.05). Consequently, meibomian gland obstruction model rats were established successfully with corneal damage and lower tear film stability. Meibomian gland obstruction is a causative factor of MGD, which led to abnormal histological structure in MG, differential expression of PPAR signaling pathway and TRPV3.
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spelling doaj-art-00fbcafa57d64e32aaa95c6334a04fd52025-01-19T12:24:50ZengNature PortfolioScientific Reports2045-23222024-10-0114111410.1038/s41598-024-73682-4Preliminary investigation on the establishment of a new meibomian gland obstruction model and gene expressionMing Sun0Huanmin Cheng1Zheng Yang2Jiangqin Tang3Shengshu Sun4Zhanglin Liu5Shaozhen Zhao6Lijie Dong7Yue Huang8Tianjin Key Laboratory of Retinal Functions and Diseases, Tianjin Branch of National Clinical Research Center for Ocular Disease, Eye Institute and School of Optometry, Tianjin Medical University Eye HospitalTianjin Key Laboratory of Retinal Functions and Diseases, Tianjin Branch of National Clinical Research Center for Ocular Disease, Eye Institute and School of Optometry, Tianjin Medical University Eye HospitalTianjin Key Laboratory of Retinal Functions and Diseases, Tianjin Branch of National Clinical Research Center for Ocular Disease, Eye Institute and School of Optometry, Tianjin Medical University Eye HospitalTianjin Key Laboratory of Retinal Functions and Diseases, Tianjin Branch of National Clinical Research Center for Ocular Disease, Eye Institute and School of Optometry, Tianjin Medical University Eye HospitalTianjin Key Laboratory of Retinal Functions and Diseases, Tianjin Branch of National Clinical Research Center for Ocular Disease, Eye Institute and School of Optometry, Tianjin Medical University Eye HospitalTianjin Key Laboratory of Retinal Functions and Diseases, Tianjin Branch of National Clinical Research Center for Ocular Disease, Eye Institute and School of Optometry, Tianjin Medical University Eye HospitalTianjin Key Laboratory of Retinal Functions and Diseases, Tianjin Branch of National Clinical Research Center for Ocular Disease, Eye Institute and School of Optometry, Tianjin Medical University Eye HospitalTianjin Key Laboratory of Retinal Functions and Diseases, Tianjin Branch of National Clinical Research Center for Ocular Disease, Eye Institute and School of Optometry, Tianjin Medical University Eye HospitalTianjin Key Laboratory of Retinal Functions and Diseases, Tianjin Branch of National Clinical Research Center for Ocular Disease, Eye Institute and School of Optometry, Tianjin Medical University Eye HospitalAbstract Meibomian gland dysfunction is a chronic ocular surface disease with a complex pathogenesis, whose main clinical manifestations are meibomian gland obstruction or/and lipid abnormalities. To explore the mechanism of MGD due to meibomian gland obstruction (MGO), we established a rat model of MGO by cauterizing the meibomian gland orifice. The morphology of the lid margins and meibomian gland orifices were visualized by slit lamp. The tear production of rats was measured by phenol red cotton thread, the tear film breakup time and corneal fluorescein staining scores of rats were detected under cobalt blue light of slit lamp. Changes in the histological structure of the meibomian gland (MG) were observed by HE staining, Oil Red O staining and immunofluorescence staining (collagen IV). RNA sequencing was used to detect differentially expressed genes in MGO and normal rats, which were validated by qPCR. In the MGO group after 4, 8, and 16 weeks, the meibomian gland orifices were closed, tear film break-up time decreased and corneal fluorescein staining score increased (p < 0.05). MG acini was smaller at 8-week and 16-week MGO rats in HE staining. Oil Red O staining showed less condensed staining in the 8- and 16-week MGO groups, while more condensed staining in the 4-week MGO group. Additionally, the basement membrane was destroyed in 16-week MGO group by immunofluorescence staining of collagen IV. Meanwhile, RNA sequencing and qPCR showed that lipid peroxidation (LPO), transient receptor potential vanilloid-3 (TRPV3) and genes in PPAR signaling pathway were differentially expressed in 16-week meibomian gland obstructive rats (p < 0.05). Consequently, meibomian gland obstruction model rats were established successfully with corneal damage and lower tear film stability. Meibomian gland obstruction is a causative factor of MGD, which led to abnormal histological structure in MG, differential expression of PPAR signaling pathway and TRPV3.https://doi.org/10.1038/s41598-024-73682-4
spellingShingle Ming Sun
Huanmin Cheng
Zheng Yang
Jiangqin Tang
Shengshu Sun
Zhanglin Liu
Shaozhen Zhao
Lijie Dong
Yue Huang
Preliminary investigation on the establishment of a new meibomian gland obstruction model and gene expression
Scientific Reports
title Preliminary investigation on the establishment of a new meibomian gland obstruction model and gene expression
title_full Preliminary investigation on the establishment of a new meibomian gland obstruction model and gene expression
title_fullStr Preliminary investigation on the establishment of a new meibomian gland obstruction model and gene expression
title_full_unstemmed Preliminary investigation on the establishment of a new meibomian gland obstruction model and gene expression
title_short Preliminary investigation on the establishment of a new meibomian gland obstruction model and gene expression
title_sort preliminary investigation on the establishment of a new meibomian gland obstruction model and gene expression
url https://doi.org/10.1038/s41598-024-73682-4
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