Generation of Endostatin by Matrix Metalloproteinase and Cathepsin from Human Limbocorneal Epithelial Cells Cultivated on Amniotic Membrane

Hui‐Kang, David; Yao, Jeng-Yuan; Kuo, Ming-Tse; See, Lai‐Chu; Lin, Kuei‐Ying; Chen, Shaochun; Chen, Jan‐Kan; Chao, An‐Shine; Wang, Sufang; Lin, Ken‐Kuo

doi:10.1167/iovs.06-0884

Cited by 27 publications

(12 citation statements)

References 40 publications

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“…Rather, our studies uncovered the ability of SorCS2 to facilitate production and/or release of endostatin from this cell type. Endostatin is cleaved from its precursor collagen XVIII by various proteases, including cathepsins and metalloproteinases (Felbor et al, ; Ferreras, Felbor, Lenhard, Olsen, & Delaissé, ; Ma et al, ). To date, it is not clear which protease plays the major role in generating endostatin in vivo and whether processing takes place intracellularly or in the extracellular space.…”

Section: Discussionmentioning

confidence: 99%

SorCS2 facilitates release of endostatin from astrocytes and controls post‐stroke angiogenesis

Malik

Lips

Gorniak‐Walas

et al. 2020

Glia

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SorCS2 is an intracellular sorting receptor of the VPS10P domain receptor gene family recently implicated in oxidative stress response. Here, we interrogated the relevance of stress‐related activities of SorCS2 in the brain by exploring its role in ischemic stroke in mouse models and in patients. Although primarily seen in neurons in the healthy brain, expression of SorCS2 was massively induced in astrocytes surrounding the ischemic core in mice following stroke. Post‐stroke induction was likely a result of increased levels of transforming growth factor β1 in damaged brain tissue, inducing Sorcs2 gene transcription in astrocytes but not neurons. Induced astrocytic expression of SorCS2 was also seen in stroke patients, substantiating the clinical relevance of this observation. In astrocytes in vitro and in the mouse brain in vivo, SorCS2 specifically controlled release of endostatin, a factor linked to post‐stroke angiogenesis. The ability of astrocytes to release endostatin acutely after stroke was lost in mice deficient for SorCS2, resulting in a blunted endostatin response which coincided with impaired vascularization of the ischemic brain. Our findings identified activated astrocytes as a source for endostatin in modulation of post‐stroke angiogenesis, and the importance of the sorting receptor SorCS2 in this brain stress response.

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Section: Discussionmentioning

confidence: 99%

SorCS2 facilitates release of endostatin from astrocytes and controls post‐stroke angiogenesis

Malik

Lips

Gorniak‐Walas

et al. 2020

Glia

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“…The majority of matrikines, such as angiostatin, arresten, canstatin, and tumstatin, exert anti-angiogenic functions by reducing endothelial cell proliferation. Cleavage of plasminogen by MMP2, MMP3, MMP7, MMP9, MMP12, and MMP19 generates angiostatin (Patterson and Sang 1997;Cornelius et al 1998;Lijnen et al 1998;Moses and O'Reilly 2003;Brauer et al 2011), and endostatin is generated through cleavage of collagen XVIII by MMP3, MMP9, and MMP13 (Ma et al 2007;Bendrik et al 2010;Fukuda et al 2011). Besides MMPs, different cathepsin family members, including the cysteine cathepsins L and S (Felbor et al 2000;Veillard et al 2011) and the aspartic cathepsin E (Shin et al 2007), have been shown to generate endostatin from collagen XVIII.…”

Section: Angiogenesismentioning

confidence: 99%

Pericellular proteolysis in cancer

2014

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Pericellular proteases have long been associated with cancer invasion and metastasis due to their ability to degrade extracellular matrix components. Recent studies demonstrate that proteases also modulate tumor progression and metastasis through highly regulated and complex processes involving cleavage, processing, or shedding of cell adhesion molecules, growth factors, cytokines, and kinases. In this review, we address how cancer cells, together with their surrounding microenvironment, regulate pericellular proteolysis. We dissect the multitude of mechanisms by which pericellular proteases contribute to cancer progression and discuss how this knowledge can be integrated into therapeutic opportunities.

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“…Collagen XVIII has been shown to be cleaved by several proteases, including MMP‐7, MMP‐14, and Cathepsin L, to generate endostatin‐containing fragments and endostatin [12–14]. MMP‐7 cleaves NC‐1 fragments of collagen XVIII to generate neostatin‐7, which contains an additional 60 amino acids at the N‐terminal of endostatin.…”

Section: Introductionmentioning

confidence: 99%

Neostatin‐7 regulates bFGF‐induced corneal lymphangiogenesis

2008

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Neostatin-7, with an anti-angiogenic potential, is generated from the proteolytic action of matrix metalloproteinase-7 on collagen XVIII. We previously reported that neostatin-7 inhibited angiogenesis in vitro and in vivo. Here we demonstrate that neostatin-7/collagen XVIII may possess anti-lymphangiogenic activities by: (1) corneal micropellet implantation of neostatin-7 reduced bFGF-induced corneal lymphangiogenesis; (2) neostatin-7 bound to VEGF receptor-3 in vitro; and (3) enhanced corneal lymphangiogenesis and VEGF-C expression in collagen XVIII knockout mice in a corneal wounding model. Understanding the mechanism of neostatin-7/collagen XVIII on corneal lymphangiogenesis may provide therapeutic interventions to treat lymphangiogenesis-related disorders, such as lymphedema, transplantation rejection and cancers. Published by Elsevier B.V. on behalf of the Federation of European Biochemical Societies.

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Generation of Endostatin by Matrix Metalloproteinase and Cathepsin from Human Limbocorneal Epithelial Cells Cultivated on Amniotic Membrane

Abstract: MMP-7 and cathepsins B and V are involved in the generation of endostatin by HLE cells. Facilitating endostatin generation may be a novel physiological function of the cornea-specific cathepsin V.

Cited by 27 publications

References 40 publications

SorCS2 facilitates release of endostatin from astrocytes and controls post‐stroke angiogenesis

SorCS2 facilitates release of endostatin from astrocytes and controls post‐stroke angiogenesis

Pericellular proteolysis in cancer

Neostatin‐7 regulates bFGF‐induced corneal lymphangiogenesis

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