Myofibroblast transdifferentiation: The dark force in ocular wound healing and fibrosis

Shu, Daisy Y.; Lovicu, Frank J.

doi:10.1016/j.preteyeres.2017.08.001

Cited by 272 publications

(259 citation statements)

References 279 publications

(423 reference statements)

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“…In the process of EMT, epithelial cells can lose tight junction and get mesenchymal markers in EMT process. 47,48 Study reported that CCl 4 (0.1 mL/100 g body weight) induced EMT occurrence by upregulating the contents of α-SMA, vimentin, fibronectin, and Ncadherin, and down-regulating the level of E-cadherin in the rat model of liver fibrosis. 49 Our results showed that the protein level of α-SMA increased and that E-cadherin content declined, which implied that Nano NiO led to EMT occurrence in rat liver.…”

Section: Effects Of Nano Nio On Tgf-β1 Smad and Mapk Pathways Emtmentioning

confidence: 99%

TGF‐β1 mediated Smad signaling pathway and EMT in hepatic fibrosis induced by Nano NiO in vivo and in vitro

Zhang

Chang

Wang

et al. 2019

Environmental Toxicology

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Nickel oxide nanoparticles (Nano NiO) bears hepatotoxicity, while whether it leads to liver fibrosis remains unclear. The aim of this study was to establish the Nano NiO‐induced hepatic fibrosis model in vivo and investigate the roles of transforming growth factor β1 (TGF‐β1) in Smad pathway activation, epithelial‐mesenchymal transition (EMT) occurrence, and extracellular matrix (ECM) deposition in vitro. Male Wistar rats were exposed to 0.015, 0.06, and 0.24 mg/kg Nano NiO by intratracheal instilling twice a week for 9 weeks. HepG2 cells were treated with 100 μg/mL Nano NiO and TGF‐β1 inhibitor (SB431542) to explore the mechanism of collagen formation. Results of Masson staining as well as the elevated levels of type I collagen (Col‐I) and Col‐III suggested that Nano NiO resulted in hepatic fibrosis in rats. Furthermore, Nano NiO increased the protein expression of TGF‐β1, p‐Smad2, p‐Smad3, alpha‐smooth muscle actin (α‐SMA), matrix metalloproteinase9 (MMP9), and tissue inhibitors of metalloproteinase1 (TIMP1), while decreased the protein content of E‐cadherin and Smad7 in rat liver and HepG2 cells. Most importantly, Nano NiO‐triggered the abnormal expression of the abovementioned proteins were all alleviated by co‐treatment with SB431542, implying that TGF‐β1‐mediated Smad pathway, EMT and MMP9/TIMP1 imbalance were involved in overproduction of collagen in HepG2 cells. In conclusion, these findings indicated that Nano NiO induced hepatic fibrosis via TGF‐β1‐mediated Smad pathway activation, EMT occurrence, and ECM deposition.

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Section: Effects Of Nano Nio On Tgf-β1 Smad and Mapk Pathways Emtmentioning

confidence: 99%

TGF‐β1 mediated Smad signaling pathway and EMT in hepatic fibrosis induced by Nano NiO in vivo and in vitro

Zhang

Chang

Wang

et al. 2019

Environmental Toxicology

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“…In view of the complexity and importance of corneal wound healing, a large number of related experiments have been carried out . Despite great progress been made in recent years, there are still limited therapeutic drugs that can promote corneal healing .…”

Section: Introductionmentioning

confidence: 99%

Tetrahedral Framework Nucleic Acids Promote Corneal Epithelial Wound Healing in Vitro and in Vivo

Liu

Zhang

et al. 2019

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Poor post‐traumatic wound healing can affect the normal function of damaged tissues and organs. For example, poor healing of corneal epithelial injuries may lead to permanent visual impairment. It is of great importance to find a therapeutic way to promote wound closure. Tetrahedral framework nucleic acids (tFNAs) are new promising nanomaterials, which can affect the biological behavior of cells. In the experiment, corneal wound healing is used as an example to explore the effect of tFNAs on wound healing. Results show that the proliferation and migration of human corneal epithelial cells are enhanced by exposure to tFNAs in vitro, possibly relevant to the activation of P38 and ERK1/2 signaling pathway. An animal model of corneal alkali burn is established to further identify the facilitation effect of tFNAs on corneal wound healing in vivo. Clinical evaluations and histological analyses show that tFNAs can improve the corneal transparency and accelerate the re‐epithelialization of wounds. Both in vitro and in vivo experiments show that tFNAs can play a positive role in corneal epithelial wound healing.

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“…Previous studies have shown that EMT is a vital source of myobroblasts. [30][31][32] Tanjore H. et al 33 found that in lung brosis, approximately 33% of myobroblasts were transformed from epithelial cells through EMT. Therefore, further study on the mechanism of EMT is helpful to understand the pathogenesis of silicosis.…”

Section: Discussionmentioning

confidence: 99%

miR-let-7d attenuates EMT by targeting HMGA2 in silica-induced pulmonary fibrosis

Zhai

Bai

et al. 2019

RSC Adv.

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Silicosis is a serious occupational disease characterized by pulmonary chronic inflammation and progressive fibrosis. Epithelial-mesenchymal transition (EMT) of alveolar epithelial cells plays a vital role in silicosis. Recent studies discovered a variety of microRNAs (miRNAs) participating in fibrotic diseases.Here, we aimed to explore the function and mechanism of miRNA let-7d in the EMT process in silicainduced alveolar epithelial cells. To detect whether let-7d and its target HMGA2 were involved in silicainduced EMT, we established a silicosis mouse model and found that let-7d was down-regulated and HMGA2 was up-regulated in the silica-treated group. Then we applied an in vitro co-culture system to imitate the EMT process in A549 cells after silica treatment. The down-regulation of let-7d and upregulation of HMGA2 were also observed in vitro. The knockdown of HMGA2 significantly inhibited the silica-induced EMT. Furthermore, we found that overexpression of let-7d could reduce the expression of HMGA2 and consequently inhibited the silica-induced EMT, whereas inhibition of let-7d increased the expression of HMGA2 and promoted the silica-induced EMT. In conclusion, let-7d negatively regulated silica-induced EMT and inhibited silica-induced pulmonary fibrosis, which might be partially realized by directly binding to HMGA2. Our data suggested that miRNA let-7d might have a potential protective effect in the fibrotic process and become a new therapeutic target for silicosis or other fibrotic diseases. Fig. 7 Let-7d modulates the EMT by regulating the expression of HMGA2. A549 cells were transfected with 50 nM siR-HMGA2 alone, 100 nM let-7d inhibitor alone, or both co-transfected. The EMT-related genes were detected by qRT-PCR (A). The protein levels was detected by Western blot and quantification analysis was conducted and shown as a graph (B). Means AE SEM (n ¼ 3), *P < 0.05 versus siR-NC group, # P < 0.05 versus siR-HMGA2 group.19362 | RSC Adv., 2019,9,[19355][19356][19357][19358][19359][19360][19361][19362][19363][19364] This journal is

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Myofibroblast transdifferentiation: The dark force in ocular wound healing and fibrosis

Cited by 272 publications

References 279 publications

TGF‐β1 mediated Smad signaling pathway and EMT in hepatic fibrosis induced by Nano NiO in vivo and in vitro

TGF‐β1 mediated Smad signaling pathway and EMT in hepatic fibrosis induced by Nano NiO in vivo and in vitro

Tetrahedral Framework Nucleic Acids Promote Corneal Epithelial Wound Healing in Vitro and in Vivo

miR-let-7d attenuates EMT by targeting HMGA2 in silica-induced pulmonary fibrosis

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