corneal neovascularization/protease

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Diurnal variations in angiostatin in human tear fluid: a possible role in prevention of corneal neovascularization.

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OBJECTIVE Although overnight eye closure is known to result in hypoxia and release of potent angiogenic factors, even prolonged eye closure does not result in corneal neovascularization. This suggests that the closed eye tear film may contain factors that can impede neovascularization. Closed eye

PEDF-derived peptide inhibits corneal angiogenesis by suppressing VEGF expression.

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Pigment epithelium-derived factor (PEDF) a glycoprotein that belongs to the superfamily of serine protease inhibitors, has been recently shown to be the most potent inhibitor of angiogenesis in the mammalian eye. However, which active domain of PEDF protein could be involved in its anti-angiogenic

Involvement of cysteine proteases in bFGF-induced angiogenesis in guinea pig and rat cornea.

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Overexpression and activation of matrix metalloprotease (MMP) have been implicated in angiogenesis. However, the involvement of cysteine proteases, such as calpains (EC 34.22.17), is obscure. Thus, the purpose of this experiment was to study the involvement of cysteine proteases in angiogenesis

Antiangiogenic and antivascular effects of a recombinant tumstatin-derived peptide in a corneal neovascularization model.

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Tumstatin, a cleavage fragment of collagen IV, is a potent endogenous inhibitor of angiogenesis. Tumstatin-derived peptide T8 possesses all angiostatic properties of full-length tumstatin and indirectly suppresses tumor growth. The potential of T8 to block pathological angiogenesis in the eye has

Corneal angiogenesis modulation by cysteine cathepsins: In vitro and in vivo studies.

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Corneal avascularization is essential for normal vision. Several antiangiogenic factors were identified in cornea such as endostatin and angiostatin. Cathepsin V, which is highly expressed in the cornea, can hydrolyze human plasminogen to release angiostatin fragments. Herein, we describe a detailed

The inhibition of corneal vascularization with aortic extracts in rabbits.

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A low molecular weight fraction of bovine aortic extract inhibited corneal vascularization and edema in rabbits when administered either subconjunctivally or topically as long as 48 hours after injury. The extract also appeared to enhance the regression of newly formed corneal vessels. Topical

Transglutaminase binding fusion protein linked to SLPI reduced corneal inflammation and neovascularization.

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BACKGROUND To study the effect of topical administration of a fusion protein (PF-MC) made up of N-terminal portion of the protease inhibitor Trappin-2 (which is a substrate of transglutaminasa-2) and SLPI (protein with anti-inflammatory, anti-bacterial and anti-viral ability), in an animal model of

Peptides derived from two separate domains of the matrix protein thrombospondin-1 have anti-angiogenic activity.

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Thrombospondin-1 (TSP1) is a large modular matrix protein containing three identical disulfide-linked 180-kD chains that inhibits neovascularization in vivo (Good et al., 1990). To determine which of the structural motifs present in the 180-kD TSP1 polypeptide mediate the anti-angiogenic activity, a

Suppression of angiogenesis and tumor growth by the inhibitor K1-5 generated by plasmin-mediated proteolysis.

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Proteolytic enzymes are involved in generation of a number of endogenous angiogenesis inhibitors. Previously, we reported that angiostatin, a potent angiogenesis inhibitor, is a proteolytic fragment containing the first four kringle modules of plasminogen. In this report, we demonstrate that

The annexin A2 system and angiogenesis.

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The formation of new blood vessels from pre-existing vasculature, the process known as angiogenesis, is highly regulated by pro- and anti-angiogenic signaling molecules including growth factors and proteases. As an endothelial cell-surface co-receptor for plasminogen and tissue plasminogen

Thrombospondins 1 and 2 function as inhibitors of angiogenesis.

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Thrombospondins (TSPs) 1 and 2 are matricellular proteins with the well-characterized ability to inhibit angiogenesis in vivo, and the migration and proliferation of cultured microvascular endothelial cells (ECs). Angiogenesis in developing tumors and in various models of wound healing is diminished

Towards a closed eye model of the pre-ocular tear layer.

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Although the tear film has been extensively studied as it exists in the open eye state, until recently very little was known as to what happens to the tear film on eye closure. Recent studies have shown that eye closure results in a profound change in the composition, origins, turnover and

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