Arsenic Trioxide Inhibits Proliferation of Rabbit Tenon's Capsule Fibroblasts After Trabeculectomy by Downregulating Expression of Extracellular Matrix Proteins

Su, Ying; Jiang, Chuanhai; Zhang, Ling; Wang, Feng

doi:10.1167/iovs.15-17289

Cited by 6 publications

(7 citation statements)

References 29 publications

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“…These findings suggest that ATO does not alter DNA synthesis but rather prevents the entry of HLFs into mitosis. ATO is known to disturb the cell cycle by modulating the expression of cyclin and CDK (Liu et al, 2015;Park et al, 2001;Su et al, 2015;Zhao et al, 2002). In HLF ATO did not alter the concentration of cyclin-D1, which controls the G0 to G1 progression, but it decreased the concentrations of cyclin-A, cyclin-B and CDK2, all key regulators of the G2/M phase transition, so retarding mitosis.…”

Section: Discussionmentioning

confidence: 92%

“…Interestingly, experimental studies have demonstrated that these concentrations of ATO measured in the plasma of patients suffering from APL exhibit, in vitro, strong antifibrotic actions. ATO decreases the myofibroblast differentiation induced by TGF-β1 in both dermal and non-IPF HLFs in vitro (Luo et al, 2014;Zhong et al, 2019) and decreased the proliferation of ocular fibroblasts in vitro (Su et al, 2015). It attenuates both cisplatin-induced renal fibrosis in rats (Maghmomeh et al, 2020) and lung fibrosis in a murine model of systemic sclerosis in vivo (Kavian et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

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Arsenic trioxide inhibits the functions of lung fibroblasts derived from patients with idiopathic pulmonary fibrosis

Joannes

Morzadec

Gutierrez

et al. 2022

Revue des Maladies Respiratoires

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Section: Discussionmentioning

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Arsenic trioxide inhibits the functions of lung fibroblasts derived from patients with idiopathic pulmonary fibrosis

Joannes

Morzadec

Gutierrez

et al. 2022

Revue des Maladies Respiratoires

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“…From the previous studies, it can be understood that ATO exerts anti‐proliferative activity in various pathological processes. F. P. Wang et al (2016) stated that ATO could inhibit the proliferation of K562 cells in a dose‐ and time‐ dependent manner by reducing the expression of CyclinD1, finally leading to the suppression of myelogenous leukemia progression; Su et al (2015) reported that ATO could inhibit proliferation of rabbit Tenon's capsule fibroblasts after trabeculectomy, as well as reducing the expression of PCNA. In addition, recombinant canstatin also had anti‐proliferative function in human umbilical vein endothelial cells, oral SCC cells, and so on (Hou et al, 2004; Hwang‐Bo et al, 2010).…”

Section: Discussionmentioning

confidence: 99%

Combination of canstatin and arsenic trioxide suppresses the development of hepatocellular carcinoma

Zhang

Duan

Song

et al. 2020

Drug Development Research

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Complication of arsenic trioxide (ATO) and other drugs in cancer treatment has attracted much focus, but is limitedly investigated in hepatocellular carcinoma (HCC). This study aimed to explore the role of ATO combined with canstatin in HCC. HepG2 cells were treated with different concentrations of ATO with or without canstatin, CCK‐8, flow cytometry, Transwell assays were conducted to determine cell proliferation, apoptosis, adhesion, migration, and invasion abilities. Besides, the protein expression or mRNA level of caspase‐3, PCNA, and MMP‐2 was measured using western blotting or qRT‐PCR. BALB/c‐nu/nu mice were used to establish nude mouse transplantation tumor model, and received ATO or canstatin treatment for 3 weeks. The results showed that ATO inhibited cell proliferation, adhesion, migration and invasion, and promoted cell apoptosis with a concentration‐dependent way. Canstatin had a significantly inhibitory effect on cell proliferation, but had limited effects on the other cellular behaviors. Besides, combination with ATO and canstatin strengthened the effects of ATO alone on cell proliferation inhibition and cell apoptosis promotion. Moreover, both of ATO and canstatin increased the protein expression of caspase‐3, while decreased PCNA and MMP‐2, which was further strengthened upon their combination. Furthermore, both of ATO and canstatin inhibited tumor growth in vivo, which was also strengthened upon their combination. Collectively, we found that combined canstatin and ATO significantly inhibited cell proliferation, migration and adhesion abilities, and promoted cell apoptosis, and inhibited tumor growth, thus suppressed the progression of HCC.

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“…Tenon's capsule fibroblasts were isolated from subconjunctival tissue and the tissues were from the elderly cataract patients as previously described [18]. In general, tissue explant method was used in the primary culture.…”

Section: Cell Culturementioning

confidence: 99%

A key role of microRNA-26a in the scar formation after glaucoma filtration surgery

Wang

Deng

2017

Artificial Cells, Nanomedicine, and Biotechnology

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Glaucoma is one of the leading causes of blind worldwide. Post-operative scar formation of filtering tract was one of the main reasons for failure of glaucoma filtration surgery. In this study, we conducted several experiments to detect the expression of miR-26a in the scar tissue in filtering tract and then detect its potential biological effects as well as its target gene. In our present study, it was found that miR-26a was significantly down-regulated in filtering tract scar. Advanced study on the association between the miR-26a and connective tissue growth factor (CTGF) micro RNA (mRNA) showed that miR-26a was inversely correlated with CTGF mRNA level. Advanced biological studies showed that overexpression of miR-26a could decrease the cell viability and migration ability of human Tenon's fibroblasts (HTFs) fibrosis in vitro model. It was also found that miR-26a might up-regulate the apoptotic level of HTFs. Through protein expression detection and luciferase reporter assay, it was found that miR-26a could produce functions that directly target the CTGF. In conclusion, the key finding of the current study is that miR-26a can suppress the activation of HTFs by transforming growth factor (TGF)-β by targeting CTGF. This data indicates that miR-26a plays an essential role in the formation of filtering tract scar and function as a potential drug target.

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Arsenic Trioxide Inhibits Proliferation of Rabbit Tenon's Capsule Fibroblasts After Trabeculectomy by Downregulating Expression of Extracellular Matrix Proteins

Cited by 6 publications

References 29 publications

Arsenic trioxide inhibits the functions of lung fibroblasts derived from patients with idiopathic pulmonary fibrosis

Arsenic trioxide inhibits the functions of lung fibroblasts derived from patients with idiopathic pulmonary fibrosis

Combination of canstatin and arsenic trioxide suppresses the development of hepatocellular carcinoma

A key role of microRNA-26a in the scar formation after glaucoma filtration surgery

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