Role of MMP-9 in the breakdown of barrier integrity of the corneal endothelium in response to TNF-α

Gangaraju, Rajashekhar; Shivanna, Mahesh; Kompella, Uday B.; Wang, Yueren; Srinivas, Sangly P.

doi:10.1016/j.exer.2014.03.004

Cited by 40 publications

(24 citation statements)

References 63 publications

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“…In addition, expression of TNFα mRNA, which is increased after BLM instillation in our model, has been shown to regulate MMP activity in other organ systems. [51] These data are supported by the current findings that MMP-2 mRNA expression and activity was increased in ASCs isolated from old mice and old humans when compared to ASCs from young donor.…”

Section: Discussionsupporting

confidence: 78%

Therapeutic benefits of young, but not old, adipose-derived mesenchymal stem cells in a chronic mouse model of bleomycin-induced pulmonary fibrosis

Tashiro

Elliot

Gerth

et al. 2015

Translational Research

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The observation that pulmonary inflammatory lesions and bleomycin (BLM)-induced pulmonary fibrosis spontaneously resolve in young mice, while remaining irreversible in aged mice, suggests that impairment of pulmonary regeneration and repair is associated with aging. Since mesenchymal stem cells (MSCs) may promote repair following injury, we postulated that differences in MSCs from aged mice may underlie post-injury fibrosis in aging. The potential for young-donor MSCs to inhibit BLM-induced pulmonary fibrosis in aged male mice (>22 months) has not been studied. Adipose-derived MSCs (ASCs) from young (4-month) and old (22-month) male mice were infused 1-day following intratracheal BLM administration. At 21-day sacrifice, aged BLM mice demonstrated lung fibrosis by Ashcroft score, collagen content, and αv-integrin mRNA expression. Lung tissue from aged BLM mice receiving young ASCs exhibited decreased fibrosis, matrix metalloproteinase (MMP)-2 activity, oxidative stress, and markers of apoptosis vs. BLM controls. Lung mRNA expression of TNFα was also decreased in aged BLM mice receiving young-donor ASCs vs. BLM controls. In contrast, old-donor ASC treatment in aged BLM mice did not reduce fibrosis and related markers. On examination of the cells, young-donor ASCs had decreased mRNA expression of MMP-2, insulin-like growth factor receptor, and AKT activation compared to old-donor ASCs. These results show that the BLM-induced pulmonary fibrosis in aged mice could be blocked by young-donor ASCs and that the mechanisms involve changes in collagen turnover and markers of inflammation.

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Section: Discussionsupporting

confidence: 78%

Therapeutic benefits of young, but not old, adipose-derived mesenchymal stem cells in a chronic mouse model of bleomycin-induced pulmonary fibrosis

Tashiro

Elliot

Gerth

et al. 2015

Translational Research

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“…MMPs regulate leukocyte recruitment and modulate cytokine and chemokine activity (38, 39). For example, MMP-9 induces endothelial barrier breakdown through degradation of endothelial junctions (40). MMP-9 also plays an important role in matrix remodeling during angiogenesis and mediates influx of proteins into angiogenic tissue (41, 42).…”

Section: Endothelial Cell Biology In a Nutshellmentioning

confidence: 99%

Endothelial Response to Glucocorticoids in Inflammatory Diseases

et al. 2016

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The endothelium plays a crucial role in inflammation. A balanced control of inflammation requires the action of glucocorticoids (GCs), steroidal hormones with potent cell-specific anti-inflammatory properties. Besides the classic anti-inflammatory effects of GCs on leukocytes, recent studies confirm that endothelial cells also represent an important target for GCs. GCs regulate different aspects of endothelial physiology including expression of adhesion molecules, production of pro-inflammatory cytokines and chemokines, and maintenance of endothelial barrier integrity. However, the regulation of endothelial GC sensitivity remains incompletely understood. In this review, we specifically examine the endothelial response to GCs in various inflammatory diseases ranging from multiple sclerosis, stroke, sepsis, and vasculitis to atherosclerosis. Shedding more light on the cross talk between GCs and endothelium will help to improve existing therapeutic strategies and develop new therapies better tailored to the needs of patients.

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“…Reduction of MMP-2 and MMP-9 gene expression (Rajashekhar, Shivanna, Kompella, Wang, & Srinivas, 2014;Xiao et al, 2012) RAR-β agonist AC55649 Primary rabbit corneal fibroblasts Incubation Reduction of MMP-2 and MMP-9 gene expression in a dose-dependent manner (Kimura et al, 2017) Female hormone 17β-estradiol Human corneal stromal cells Incubation Reduction of MMP-2 gene expression (Yin, Wan, Tian, Zhao, & Deng, 2018) Neuroprotectin D1 Herpes simplex virus (HSV)…”

Section: Alkali Burn Intraperitoneal Injectionmentioning

confidence: 99%

Regulation of matrix metalloproteinases 2 and 9 in corneal neovascularization

Zhang

Wang

et al. 2020

Chem Biol Drug Des

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Corneal neovascularization (CNV), a pathological process of angiogenesis, can lead to serious consequences in the cornea. CNV is generally proved to associate with inflammation in the cornea closely, which is mainly elicited by the disruption of equilibrium between angiogenic and antiangiogenic factors. Angiogenic factors including vascular endothelial growth factors (VEGFs), basic fibroblast growth factors (bFGFs), and matrix metalloproteinases (MMPs) are vital factors in the formation of CNV. Especially VEGFs are convinced to be the core angiogenic factors in CNV, and MMPs are proved to exert dual effects on the process. Strikingly, matrix metalloproteinase 2 (MMP-2) and matrix metalloproteinase 9 (MMP-9) are determined to play key roles in the formation of CNV, while the mechanism is still vague. In this review, the latest researches are reviewed to discuss the role of MMP-2 and MMP-9 in CNV, respectively, and some inhibitors of them are presented. We hope to provide a new direction of drug research for CNV. K E Y W O R D Scorneal neovascularization, matrix metalloproteinase 2, matrix metalloproteinase 9, vascular endothelial growth factor 486 | ZHANG et Al.How to cite this article: Zhang J, Wang S, He Y, Yao B, Zhang Y. Regulation of matrix metalloproteinases 2 and 9 in corneal neovascularization. Chem Biol Drug Des. 2020;95:485-492. https ://doi.

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Role of MMP-9 in the breakdown of barrier integrity of the corneal endothelium in response to TNF-α

Cited by 40 publications

References 63 publications

Therapeutic benefits of young, but not old, adipose-derived mesenchymal stem cells in a chronic mouse model of bleomycin-induced pulmonary fibrosis

Therapeutic benefits of young, but not old, adipose-derived mesenchymal stem cells in a chronic mouse model of bleomycin-induced pulmonary fibrosis

Endothelial Response to Glucocorticoids in Inflammatory Diseases

Regulation of matrix metalloproteinases 2 and 9 in corneal neovascularization

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