Silencing Matrix Metalloproteinases 9 and 2 Inhibits Human Retinal Microvascular Endothelial Cell Invasion and Migration

Gu, Yonghao; Ke, Genjie; Wang, Lin; Gu, Q; Zhou, Enliang; He, Qin; Wang, Shiying

doi:10.1159/000441501

Cited by 9 publications

(9 citation statements)

References 19 publications

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“…Most of such studies focused on cancer cells in which silencing of selected MMP expression resulted in the inhibition of the cell migration and invasion to other tissues (Sun et al, 2008;Tsung et al, 2008;Shen et al, 2012;Tang et al, 2013;Li et al, 2014). Also in other cell types, such as human retinal microvascular endothelial cells (HRMECs), decrease of MMPs expression, for example, MMP-2 and MMP-9, resulted in the inhibition of cell invasion and migration (Gu et al, 2015).…”

Section: Discussionmentioning

confidence: 99%

Silencing of gelatinase expression delays myoblast differentiation in vitro

Nowak

Gawor

Ciemerych

et al. 2017

Cell Biology International

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Skeletal muscle growth and regeneration relies on the activation of muscle specific stem cells, that is, satellite cells. The activation and differentiation of satellite cells into myoblasts, as well as their migration, proliferation, and fusion of mononuclear myoblasts into a functional multi-nucleated muscle fiber, are associated with extracellular matrix (ECM) protein synthesis and degradation. The extracellular environment is dynamically adapting to the changes accompanying skeletal muscle growth or repair. Enzymes engaged in many biological processes that involve ECM remodeling are matrix metalloproteinases (MMPs). Among metalloproteinases crucial for skeletal muscles are two gelatinases-MMP-9 and MMP-2. In the current study we test the effect of silencing the MMP-9 and MMP-2 expression on the proliferation and differentiation of in vitro cultured skeletal muscle myoblasts. We show that downregulating gelatinase MMP-9 expression results in a delayed myoblast differentiation.

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Section: Discussionmentioning

confidence: 99%

Silencing of gelatinase expression delays myoblast differentiation in vitro

Nowak

Gawor

Ciemerych

et al. 2017

Cell Biology International

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“…The best-described proteins related to these processes are metalloproteinases 2 and 9 (MMP-2 and MMP-9). These proteins have acidic properties, are rich in cysteine, and promote angiogenesis as they act to degrade the extracellular matrix, increasing the filtering of molecules that modify the microenvironment finally promoting the formation of new blood vessels [ 11 ] ( Figure 2(b) ).…”

Section: Molecular Mechanismsmentioning

confidence: 99%

Age‐Related Macular Degeneration: New Paradigms for Treatment and Management of AMD

Hernández-Zimbrón

Zamora-Alvarado

Paz

et al. 2018

Oxidative Medicine and Cellular Longevity

186

150

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Age-related macular degeneration (AMD) is a well-characterized and extensively studied disease. It is currently considered the leading cause of visual disability among patients over 60 years. The hallmark of early AMD is the formation of drusen, pigmentary changes at the macula, and mild to moderate vision loss. There are two forms of AMD: the “dry” and the “wet” form that is less frequent but is responsible for 90% of acute blindness due to AMD. Risk factors have been associated with AMD progression, and they are taking relevance to understand how AMD develops: (1) advanced age and the exposition to environmental factors inducing high levels of oxidative stress damaging the macula and (2) this damage, which causes inflammation inducing a vicious cycle, altogether causing central vision loss. There is neither a cure nor treatment to prevent AMD. However, there are some treatments available for the wet form of AMD. This article will review some molecular and cellular mechanisms associated with the onset of AMD focusing on feasible treatments for each related factor in the development of this pathology such as vascular endothelial growth factor, oxidative stress, failure of the clearance of proteins and organelles, and glial cell dysfunction in AMD.

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“…MMP-2 can degrade components such as type IV collagen, fibronectin, elastin and denatured interstitial collagen (15). Mason found that MMP-2 can promote the migration of SMC, inhibit the invasion and migration of human retinal microvascular endothelial cells, and change vascular remodeling (16,17). MMP-2, which is localized in cardiomyocytes, can degrade type-IV collagen and other bioactive molecules, and is overexpressed in head and neck squamous cell carcinomas during cancer invasion and metastasis (18).…”

Section: Discussionmentioning

confidence: 99%

“…MMP-2, which is localized in cardiomyocytes, can degrade type-IV collagen and other bioactive molecules, and is overexpressed in head and neck squamous cell carcinomas during cancer invasion and metastasis (18). A survey of available literature shows that MMP-2 expression was suppressed with RNA interference (RNAi), and its inhibitory effects were observed on the invasion and migration of human retinal microvascular endothelial cells (19). MMP-2 upregulation has been implicated in the pathophysiology of atherosclerosis (20).…”

Section: Discussionmentioning

confidence: 99%