Particulate matter 2.5 exposure induces epithelial-mesenchymal transition via PI3K/AKT/mTOR pathway in human retinal pigment epithelial ARPE-19 cells

Hui Wen Lin; Ting Jing Shen; Peng Yu Chen; Tzu Chun Chen; Jui Hsuan Yeh; Shang Chun Tsou; Chane Yu Lai; Chang Han Chen; Yuan Yen Chang

doi:10.1016/j.bbrc.2022.05.072

Particulate matter 2.5 exposure induces epithelial-mesenchymal transition via PI3K/AKT/mTOR pathway in human retinal pigment epithelial ARPE-19 cells

Hui Wen Lin, Ting Jing Shen, Peng Yu Chen, Tzu Chun Chen, Jui Hsuan Yeh, Shang Chun Tsou, Chane Yu Lai, Chang Han Chen, Yuan Yen Chang

Research output: Contribution to journal › Article › peer-review

13 Citations (Scopus)

Abstract

Exposure to particulate matter 2.5 (PM2.5) has been linked to ocular surface diseases, yet knowledge of the molecular mechanism impacted on retina pathogenesis is limited. Therefore, the purpose of this study was to explore the effects and involved factors of PM2.5 exposure in human retinal pigment epithelial APRE-19 cells. Our data revealed a decreased cell viability and an increased migratory ability in APRE-19 cells after PM2.5 stimulation. The MMP-2 and MMP-9 protein levels were markedly increased while the MMPs regulators TIMP-1 and TIMP-2 were significantly reduced in PM2.5-exposed APRE-19 cells. PM2.5 also increased pro-MMP-2 expression in the cell culture supernatants. Additionally, PM2.5 promoted the EMT markers through the activation of PI3K/AKT/mTOR pathway. Moreover, the ICAM-1 production was also remarkably increased by PM2.5 but reduced by PI3K/AKT inhibitor LY294002 in APRE-19 cells. Taken together, these results suggest that PM2.5 promotes EMT in a PI3K/AKT/mTOR-dependent manner in the retinal pigment epithelium.

Original language	English
Pages (from-to)	11-17
Number of pages	7
Journal	Biochemical and Biophysical Research Communications
Volume	617
DOIs	https://doi.org/10.1016/j.bbrc.2022.05.072
Publication status	Published - Aug 30 2022
Externally published	Yes

Keywords

Epithelial-mesenchymal transition
Ocular surface diseases
PI3K/AKT/mTOR signaling
PM2.5

ASJC Scopus subject areas

Biophysics
Biochemistry
Molecular Biology
Cell Biology

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/j.bbrc.2022.05.072

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Lin, H. W., Shen, T. J., Chen, P. Y., Chen, T. C., Yeh, J. H., Tsou, S. C., Lai, C. Y., Chen, C. H., & Chang, Y. Y. (2022). Particulate matter 2.5 exposure induces epithelial-mesenchymal transition via PI3K/AKT/mTOR pathway in human retinal pigment epithelial ARPE-19 cells. Biochemical and Biophysical Research Communications, 617, 11-17. https://doi.org/10.1016/j.bbrc.2022.05.072

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title = "Particulate matter 2.5 exposure induces epithelial-mesenchymal transition via PI3K/AKT/mTOR pathway in human retinal pigment epithelial ARPE-19 cells",

abstract = "Exposure to particulate matter 2.5 (PM2.5) has been linked to ocular surface diseases, yet knowledge of the molecular mechanism impacted on retina pathogenesis is limited. Therefore, the purpose of this study was to explore the effects and involved factors of PM2.5 exposure in human retinal pigment epithelial APRE-19 cells. Our data revealed a decreased cell viability and an increased migratory ability in APRE-19 cells after PM2.5 stimulation. The MMP-2 and MMP-9 protein levels were markedly increased while the MMPs regulators TIMP-1 and TIMP-2 were significantly reduced in PM2.5-exposed APRE-19 cells. PM2.5 also increased pro-MMP-2 expression in the cell culture supernatants. Additionally, PM2.5 promoted the EMT markers through the activation of PI3K/AKT/mTOR pathway. Moreover, the ICAM-1 production was also remarkably increased by PM2.5 but reduced by PI3K/AKT inhibitor LY294002 in APRE-19 cells. Taken together, these results suggest that PM2.5 promotes EMT in a PI3K/AKT/mTOR-dependent manner in the retinal pigment epithelium.",

keywords = "Epithelial-mesenchymal transition, Ocular surface diseases, PI3K/AKT/mTOR signaling, PM2.5, Epithelial-mesenchymal transition, Ocular surface diseases, PI3K/AKT/mTOR signaling, PM2.5",

author = "Lin, \{Hui Wen\} and Shen, \{Ting Jing\} and Chen, \{Peng Yu\} and Chen, \{Tzu Chun\} and Yeh, \{Jui Hsuan\} and Tsou, \{Shang Chun\} and Lai, \{Chane Yu\} and Chen, \{Chang Han\} and Chang, \{Yuan Yen\}",

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year = "2022",

month = aug,

day = "30",

doi = "10.1016/j.bbrc.2022.05.072",

language = "English",

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T1 - Particulate matter 2.5 exposure induces epithelial-mesenchymal transition via PI3K/AKT/mTOR pathway in human retinal pigment epithelial ARPE-19 cells

AU - Lin, Hui Wen

AU - Shen, Ting Jing

AU - Chen, Peng Yu

AU - Chen, Tzu Chun

AU - Yeh, Jui Hsuan

AU - Tsou, Shang Chun

AU - Lai, Chane Yu

AU - Chen, Chang Han

AU - Chang, Yuan Yen

PY - 2022/8/30

Y1 - 2022/8/30

N2 - Exposure to particulate matter 2.5 (PM2.5) has been linked to ocular surface diseases, yet knowledge of the molecular mechanism impacted on retina pathogenesis is limited. Therefore, the purpose of this study was to explore the effects and involved factors of PM2.5 exposure in human retinal pigment epithelial APRE-19 cells. Our data revealed a decreased cell viability and an increased migratory ability in APRE-19 cells after PM2.5 stimulation. The MMP-2 and MMP-9 protein levels were markedly increased while the MMPs regulators TIMP-1 and TIMP-2 were significantly reduced in PM2.5-exposed APRE-19 cells. PM2.5 also increased pro-MMP-2 expression in the cell culture supernatants. Additionally, PM2.5 promoted the EMT markers through the activation of PI3K/AKT/mTOR pathway. Moreover, the ICAM-1 production was also remarkably increased by PM2.5 but reduced by PI3K/AKT inhibitor LY294002 in APRE-19 cells. Taken together, these results suggest that PM2.5 promotes EMT in a PI3K/AKT/mTOR-dependent manner in the retinal pigment epithelium.

AB - Exposure to particulate matter 2.5 (PM2.5) has been linked to ocular surface diseases, yet knowledge of the molecular mechanism impacted on retina pathogenesis is limited. Therefore, the purpose of this study was to explore the effects and involved factors of PM2.5 exposure in human retinal pigment epithelial APRE-19 cells. Our data revealed a decreased cell viability and an increased migratory ability in APRE-19 cells after PM2.5 stimulation. The MMP-2 and MMP-9 protein levels were markedly increased while the MMPs regulators TIMP-1 and TIMP-2 were significantly reduced in PM2.5-exposed APRE-19 cells. PM2.5 also increased pro-MMP-2 expression in the cell culture supernatants. Additionally, PM2.5 promoted the EMT markers through the activation of PI3K/AKT/mTOR pathway. Moreover, the ICAM-1 production was also remarkably increased by PM2.5 but reduced by PI3K/AKT inhibitor LY294002 in APRE-19 cells. Taken together, these results suggest that PM2.5 promotes EMT in a PI3K/AKT/mTOR-dependent manner in the retinal pigment epithelium.

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KW - Ocular surface diseases

KW - PI3K/AKT/mTOR signaling

KW - PM2.5

KW - Epithelial-mesenchymal transition

KW - Ocular surface diseases

KW - PI3K/AKT/mTOR signaling

KW - PM2.5

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ER -

Particulate matter 2.5 exposure induces epithelial-mesenchymal transition via PI3K/AKT/mTOR pathway in human retinal pigment epithelial ARPE-19 cells

Abstract

Keywords

ASJC Scopus subject areas

UN SDGs

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