Inhibition of Interleukin-1β-Induced Matrix Metalloproteinase Expression in Human Corneal Fibroblasts by Tranilast

Liu, Ye; Xu, Dan; Li, Jing; Liu, Yang

doi:10.3109/02713683.2014.884598

Cited by 6 publications

(4 citation statements)

References 49 publications

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“… 24 Moreover, a previous study found that IL-1β stimulated the expression of MMP2 and MMP9. 25 VCAM-1 is an inflammatory mediator secreted from endothelial cells and has been identified as a marker of endothelial dysfunction in the inflammatory response, 26 whereas endothelial injury and dysfunction are compulsory conditions for the development of thrombosis. 27 In addition, IL-1β increases the expression of VCAM-1 to improve cardiac function following an ischemic attack.…”

Section: Discussionmentioning

confidence: 99%

RETRACTED: Overexpression of MicroRNA-340-5p Inhibits Pulmonary Arterial Hypertension Induced by APE by Downregulating IL-1β and IL-6

Ou¹,

Zhang²,

Chen³

et al. 2020

Molecular Therapy - Nucleic Acids

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Pulmonary arterial hypertension (PAH) is a fatal cardiovascular disease that could eventually result in right ventricular failure. Recently, the roles of microRNAs (miRNAs) in PAH have been highlighted. The present study aims to investigate the effects of miRNA (miR)-340-5p on PAH induced by acute pulmonary embolism (APE) and the underlying mechanisms. miR-340-5p was lowly expressed, whereas interleukin 1β (IL-1β) and IL-6 were highly expressed in plasma of APE-PAH patients as compared to normal human plasma. Subsequently, IL-1β and IL-6 were confirmed to be two target genes of miR-340-5p using a dual-luciferase reporter gene assay. By conducting overexpression and rescue experiments, overexpression of miR-340-5p was evidenced to inhibit proliferation and migration of pulmonary artery smooth muscle cells (PASMCs) and inflammation via reducing IL-1β and IL-6 levels. Meanwhile, miR-340-5p led to the blocked nuclear factor κB (NF-κB) pathway with reduced NF-κB p65, matrix metalloproteinase 2 (MMP2), and MMP9 expression in PASMCs. Finally, the ameliorative effect of miR-340-5p on pathological lesions was further verified in rat models of APE-PAH. Altogether, overexpressed miR-340-5p inhibited the inflammatory response, proliferation, and migration of PASMCs by downregulating IL-1β and IL-6, thereby suppressing the progression of APE-PAH. miR-340-5p therefore holds promise as an anti-inflammatory therapeutic target.

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Section: Discussionmentioning

confidence: 99%

RETRACTED: Overexpression of MicroRNA-340-5p Inhibits Pulmonary Arterial Hypertension Induced by APE by Downregulating IL-1β and IL-6

Ou¹,

Zhang²,

Chen³

et al. 2020

Molecular Therapy - Nucleic Acids

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“…PPAR-α activation has been also reported to cause neuroprotection in neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease, and multiple sclerosis (MS) [ 93 , 94 ]. In another study, Tranilast had inhibited the production of MMP-1, 2, 3 induced by IL-1 in human corneal fibroblasts by the inhibition of some signaling pathways such as mitogen-activated protein kinase (MAPK) and NF-κB, as the main pathways for inflammatory responses [ 95 ]. This drug had appeared to inhibit MCP-1 production by impairing NF-κB and c-Jun N-terminal kinase (JNK) signaling pathways [ 81 ].…”

Section: A Body Of Literaturementioning

confidence: 99%

Tranilast: a potential anti-Inflammatory and NLRP3 inflammasome inhibitor drug for COVID-19

Saeedi-Boroujeni

Mahmoudian-Sani

Nashibi

et al. 2021

Immunopharmacology and Immunotoxicology

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SARS-CoV-2 is a type of beta-CoV that develops acute pneumonia, which is an inflammatory condition. A cytokine storm has been recognized as one of the leading causes of death in patients with COVID-19. ALI and ARDS along with multiple organ failure have also been presented as the consequences of acute inflammation and cytokine storm. It has been previously confirmed that SARS-CoV, as another member of the beta-CoV family, activates NLRP3 inflammasome and consequently develops acute inflammation in a variety of ways through having complex interactions with the host immune system using structural and nonstructural proteins. Numerous studies conducted on Tranilast have further demonstrated that the given drug can act as an effective anti-chemotactic factor on controlling inflammation, and thus, it can possibly help the improvement of the acute form of COVID-19 by inhibiting some key inflammation-associated transcription factors such as NF-κB and impeding NLRP3 inflammasome. Several studies have comparably revealed the direct effect of this drug on the prevention of inappropriate tissue’s remodeling; inhibition of neutrophils, IL-5, and eosinophils; repression of inflammatory cell infiltration into inflammation site; restriction of factors involved in acute airway inflammation like IL-33; and suppression of cytokine IL-13, which increase mucosal secretions. Therefore, Tranilast may be considered as a potential treatment for patients with the acute form of COVID-19 along with other drugs.

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“…Several studies have confirmed that IL-1␤ had the function of stimulating the production of MMPs in corneal fibroblasts (37,49), and, taking into account our previous studies, senescent corneal fibroblasts promoted CNV by enhancing the expression of MMPs and other genes related to the generation of neovascularization (53). Therefore, we compared the different expression levels of angiogenesis-related genes in normal or senescent fibroblasts pretreated with or without IL-1␤.…”

Section: C739mentioning

confidence: 72%

“…As a major secretory factor in SASP, IL-1␤ reportedly plays an important physiological role in the tissue microenvironment regulated by senescent cells. Moreover, IL-1␤ has already been confirmed to induce the upregulation of MMP expression in cornea (15,26,37,45,49).…”

Section: Introductionmentioning

confidence: 89%

Autocrine IL-1β mediates the promotion of corneal neovascularization by senescent fibroblasts

Dong

Yang

et al. 2018

American Journal of Physiology-Cell Physiology

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Our previous study has confirmed that senescent fibroblasts promote corneal neovascularization (CNV) partially via the enhanced secretion of matrix metalloproteases (MMPs). However, the regulation of MMPs expression in senescent fibroblasts remained unclear. In this study, we identified that the expression and secretion levels of interleukin-1β (IL-1β) were significantly up-regulated in senescent human corneal fibroblasts than that in normal fibroblasts. Moreover, compared with vehicle-pretreated senescent fibroblasts, IL-1β pretreatment enhanced the expression of angiogenic factors, while reduced the expression of angiostatic factors in senescent fibroblasts. When co-cultured with human umbilical vein endothelial cells, IL-1β-pretreated senescent fibroblasts more strongly promoted their proliferation, migration, and tube-formation capacities than the vehicle-controlled senescent fibroblasts. In addition, either interleukin-1 receptor antagonist (IL-1ra) or anti-IL-1β neutralization completely inhibited the promotion of senescent fibroblasts in vascular tube formation in vitro and CNV in vivo. Therefore, we concluded that autocrine IL-1β mediated the promotion of senescent fibroblasts on corneal neovascularization.

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Inhibition of Interleukin-1β-Induced Matrix Metalloproteinase Expression in Human Corneal Fibroblasts by Tranilast

Cited by 6 publications

References 49 publications

RETRACTED: Overexpression of MicroRNA-340-5p Inhibits Pulmonary Arterial Hypertension Induced by APE by Downregulating IL-1β and IL-6

RETRACTED: Overexpression of MicroRNA-340-5p Inhibits Pulmonary Arterial Hypertension Induced by APE by Downregulating IL-1β and IL-6

Tranilast: a potential anti-Inflammatory and NLRP3 inflammasome inhibitor drug for COVID-19

Autocrine IL-1β mediates the promotion of corneal neovascularization by senescent fibroblasts

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