Apolipoprotein A1 Inhibits TGF-β1–Induced Epithelial-to-Mesenchymal Transition of Alveolar Epithelial Cells

Baek, Ae-Rin; Lee, Ji Min; Seo, Hye Sun; Park, Jong Suk; Lee, June Hyuk; Park, Sung Woo; Kim, Dojin; Koh, Eun Suk; Uh, Soo Taek; Kim, Yong Hoon; Park, Choon-Sik

doi:10.4046/trd.2016.79.3.143

Cited by 18 publications

(18 citation statements)

References 36 publications

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“…15 TGF-β1 induced nonSmad responses, including extracellular signal-regulated kinase (ERK) and p38 mitogen-activated protein kinase (p38 MAPK) mediated signaling. 16 The present study mainly explores the nonSmad signaling pathway.…”

Section: Introductionmentioning

confidence: 99%

“…18 For mammals, members of the MAPKs superfamily mainly include the ERK, p38 MAPK, and c-JUN, NH2-terminal protein kinase (JNK). 19 Although study has shown that MAPK signaling pathway could be activated in the signal transduction of the TGF-β1-induced pulmonary fibrosis, 16 it still have differences between species and cell types. 20,21 ECM deposition is one of the mechanisms in pulmonary fibrosis.…”

Section: Introductionmentioning

confidence: 99%

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TGF‐β1 mediated MAPK signaling pathway promotes collagen formation induced by Nano NiO in A549 cells

Tian

Chang

Zhang

et al. 2019

Environmental Toxicology

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Nickel oxide nanoparticles (Nano NiO) could induce pulmonary fibrosis, however, the mechanisms are still unknown. The aim of the present study was to explore the roles of transforming growth factor‐β1 (TGF‐β1), mitogen‐activated protein kinase (MAPK) pathway and MMPs/TIMPs balance in Nano NiO‐induced pulmonary fibrosis. For that purpose, we first established Nano NiO‐induced human lung adenocarcinoma epithelial cells (A549 cells) model of collagen excessive formation through detecting the levels of hydroxyproline (Hyp) and type I collagen (Col‐I). Then the protein levels of TGF‐β1, MAPKs, and MMPs/TIMPs were assessed by Western blot. The results showed that Nano NiO resulted in the increased contents of Hyp, Col‐I, and TGF‐β1, the MAPK pathway activation and MMPs/TIMPs imbalance with a dose‐dependent manner. In addition, to investigate whether TGF‐β1 mediated MAPK signaling pathway, A549 cells were treated by 100 μg/mL Nano NiO combined with TGF‐β1, p38 MAPK, and ERK1/2 inhibitors (10 μM SB431542, 10 μM SB203580, and 10 μM U0126), respectively. We found that MAPK signal pathway was suppressed by TGF‐β1 inhibitor. Meanwhile, the increased contents of Hyp and Col‐I, and MMPs/TIMPs imbalance were alleviated by the p38 MAPK and ERK1/2 inhibitors, respectively. These findings indicated that the MAPK pathway and MMPs/TIMPs imbalance were involved in collagen excessive formation induced by Nano NiO.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

TGF‐β1 mediated MAPK signaling pathway promotes collagen formation induced by Nano NiO in A549 cells

Tian

Chang

Zhang

et al. 2019

Environmental Toxicology

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“…Epithelial-to-mesenchymal transition (EMT) plays a critical role in driving cancer cell metastasis 8 , 9 . Transforming growth factor β (TGF-β1) is the driver of EMT, and many influencing factors promote EMT through this signaling pathway 10 , 11 . Recently, several reports revealed that lncRNA Metastasis-Associated Lung Adenocarcinoma Transcript 1 (MALAT1) has crucial functions in malignant cancer progression 12 .…”

Section: Introductionmentioning

confidence: 99%

TGF-β1-Induced Upregulation of MALAT1 Promotes Kazakh's Esophageal Squamous Cell Carcinoma Invasion by EMT

Liu¹,

Chen²,

Liu³

et al. 2020

J. Cancer

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Transforming growth factor β1 (TGF-β1) plays an important role in tumor initiation and development by inducing epithelial-mesenchymal Transition (EMT). Metastasis-Associated Lung Adenocarcinoma Transcript 1 (MALAT1) is a long noncoding RNA (lncRNA) that contributes to the invasion and metastasis of tumors, including esophageal squamous cell carcinoma (ESCC). The aim of the present study was to explore the underlying mechanisms implicated in EMT and to clarify whether TGF-β1 regulates MALAT1 expression, thereby promoting the invasion of ESCC. Expression of TGF-β1, MALAT1 and EMT-related markers, including E-cadherin and Vimentin, was detected in clinical samples of Kazakh's ESCC. The role of TGF-β1 in the regulation of MALAT1 in ESCC invasion was evaluated at the ESCC cell line level. High TGF-β1 expression was significantly associated with poor survival among patients with Kazakh's ESCC. Additionally, the expression of Vimentin was upregulated, and the expression of E-cadherin was downregulated and varied. The expression of MALAT1 positively correlated with the expression of TGF-β1 both in vivo and in vitro . Furthermore, knockdown of MALAT1 inhibited TGF-β1-induced EMT. Our data indicate that MALAT1 is heavily involved in EMT induced by TGF-β1. MALAT1 may be a therapeutic target in the suppression of metastasis and invasion of ESCC.

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“…To induce EndMT, the cells were stimulated for 48 h in serum-free medium (SFM) with 0.1% bovine serum albumin (BSA) and TGF-β1 (10 ng/mL, R&D Systems, Minneapolis, MN, USA). To evaluate the effect of ApoA-I on the TGF-β1-induced EndMT, the culture medium was replaced with SFM supplemented with 0.1% BSA, TGF-β1 (10 ng/mL) and recombinant human ApoA-I (50 ng/mL, Calbiochem, San Diego, CA, USA), and the cells were incubated for 48 h. Control cells were maintained in SFM with 0.1% BSA for 48 h [16]. Cells were cultured in a humidified 5% CO 2 incubator at 37°C and used between the fourth and sixth passages.…”

Section: Methodsmentioning

confidence: 99%

“…Moreover, studies have demonstrated that ApoA-I can inhibit the oxidation of low-density lipoprotein (LDL), damage to the endothelium, and the transformation of macrophages to foam cells [11,12,13,14,15]. Recently, ApoA-I has been found to have an inhibitory effect on the TGF-β1-induced epithelial-to-mesenchymal transition of alveolar epithelial cells [16]. In addition, it has recently been reported that HDL reduces TGF-β1-induced EndMT in human aortic ECs [17].…”

Section: Introductionmentioning

confidence: 99%

Apolipoprotein A1 Inhibits the TGF-β1-Induced Endothelial-to-Mesenchymal Transition of Human Coronary Artery Endothelial Cells

Feng

Zhang²,

Jackson³

et al. 2017

Cardiology

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Objective: Transforming growth factor β1 (TGF-β1) is the major cytokine for stimulating endothelial cells (ECs) to transdifferentiate to mesenchymal cells (MCs) in the process known as endothelial-to-mesenchymal transition (EndMT). Recently, TGF-β1-induced EndMT has been implicated in the pathogenesis of atherosclerosis (AS). It has been identified that apolipoprotein A1 (ApoA-I) obstructs TGF-β1-induced endothelial dysfunction, providing a protective effect for ECs and also anti-AS activity. However, the exact role of ApoA-I in TGF-β1-induced EndMT is not clear. In this study, we aimed to investigate whether ApoA-I can modulate TGF-β1-induced EndMT in human coronary artery ECs (HCAECs). Methods and Results: The HCAECs were treated with TGF-β1 with or without ApoA-I. Morphological changes in HCAECs and the expression of EndMT-related markers were evaluated. HCAECs treated with TGF-β1 were found to transform to MC morphology, with inconspicuous expression of EC markers such as vascular endothelial cadherin and CD31, and conspicuous expression of fibroblast-specific protein 1 (FSP-1) and α-smooth muscle actin. The treatment of HCAECs with ApoA-I inhibited the TGF-β1-induced EndMT, and elevated expression of EC markers was observed but reduced expression of MC markers. Moreover, ApoA-I impeded the expression level of Slug and Snail, crucial transcriptional factors of EndMT, and it inhibited the TGF-β1-induced phosphorylation of Smad2 and Smad3 which affected the EC morphology. In addition, the knockdown of ABCA1 by RNA interference eliminated the inhibition effect of ApoA-I on TGF-β1-induced EndMT. Conclusions: Our findings revealed a novel mechanism for the ApoA-I protective effect on endothelium function via the inhibition of TGF-β1-induced EndMT. This might provide new insights for developing strategies for modulating AS and vascular remodeling.

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Apolipoprotein A1 Inhibits TGF-β1–Induced Epithelial-to-Mesenchymal Transition of Alveolar Epithelial Cells

Cited by 18 publications

References 36 publications

TGF‐β1 mediated MAPK signaling pathway promotes collagen formation induced by Nano NiO in A549 cells

TGF‐β1 mediated MAPK signaling pathway promotes collagen formation induced by Nano NiO in A549 cells

TGF-β1-Induced Upregulation of MALAT1 Promotes Kazakh's Esophageal Squamous Cell Carcinoma Invasion by EMT

Apolipoprotein A1 Inhibits the TGF-β1-Induced Endothelial-to-Mesenchymal Transition of Human Coronary Artery Endothelial Cells

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