A C-terminal fragment BIGH3 protein with an RGDRGD motif inhibits corneal neovascularization in vitro and in vivo

Ge, Heng; Tian, Peng; Guan, Lan; Yin, Xiu-li; Liu, Hanruo; Xiao, Nan; Luo, Xin; Sun, Yunduan; Qi, Donghua; Ni, Shuang; Liu, Ping

doi:10.1016/j.exer.2013.03.014

Cited by 11 publications

(6 citation statements)

References 43 publications

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“…In addition, these authors also showed that TGFBI could inhibit angiogenesis (J. E. Kim et al, ). This was later confirmed by expressing a recombinant TGFBI containing an RGDRGD modified C‐terminal fragment (Ge et al, ).…”

Section: Tgfbi Expression Role and Pathology In The Eye Of Humans Amentioning

confidence: 89%

Mutation update:TGFBIpathogenic and likely pathogenic variants in corneal dystrophies

et al. 2019

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Human transforming growth factor β‐induced (TGFBI), is a gene responsible for various corneal dystrophies. TGFBI produces a protein called TGFBI, which is involved in cell adhesion and serves as a recognition sequence for integrins. An alteration in cell surface interactions could be the underlying cause for the progressive accumulation of extracellular deposits in different layers of the cornea with the resulting changes of refractive index and transparency. To this date, 69 different pathogenic or likely pathogenic variants in TGFBI have been identified in a heterozygous or homozygous state in various corneal dystrophies, including a novel variant reported here. All disease‐associated variants were inherited as autosomal‐dominant traits but one; this latter was inherited as an autosomal recessive trait. Most corneal dystrophy‐associated variants are located at amino acids Arg124 and Arg555. To keep the list of corneal dystrophy‐associated variant current, we generated a locus‐specific database for TGFBI (http://databases.lovd.nl/shared/variants/TGFBI) containing all pathogenic and likely pathogenic variants reported so far. Non‐disease‐associated variants are described in specific databases, like gnomAD and ExAC but are not listed here. This article presents the most recent up‐to‐date list of disease‐associated variants.

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Section: Tgfbi Expression Role and Pathology In The Eye Of Humans Amentioning

confidence: 89%

Mutation update:TGFBIpathogenic and likely pathogenic variants in corneal dystrophies

et al. 2019

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“…Another downregulated transcript in dHUVEC was WNT5a that activates WNT signaling via non-canonical WNT pathways and in human endothelial cells it induces their proliferation, survival under serum-starved conditions, migration and tube formation [28]. ␤ig-h3 (a collagenbinding extracellular matrix protein), a direct target of TGF-␤1 [29], is an adhesive molecule that interacts with integrins and modulate adhesion, spreading, migration, and proliferation of vascular cells [30][31][32]. Finally, collagen, type III, ␣1 is a major collagen found in connective tissues and it plays a role in blood vessel development [33].…”

Section: Effects Of Exogenous Tgf-ˇ1 On Gene Expression Profile Of Dhmentioning

confidence: 99%

Dysregulation of gene expression in human fetal endothelial cells from gestational diabetes in response to TGF-β1

Marcantoni

Dovizio

Ó’Gaora

et al. 2015

Prostaglandins & Other Lipid Mediators

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“…Consequently, corneal neovascularization is one of the most common causes of visual impairment and is also a high-risk factor for rejection of corneal allografts by facilitating the exposure of antigens in the donor cornea to the immune system. This process involves changes in vascular permeability, endothelial cell adhesion, migration, proliferation and differentiation (Lai et al 2007;Ge, et al 2013).…”

Section: Type XVIII Collagenmentioning

confidence: 99%

Collagens and proteoglycans of the cornea: importance in transparency and visual disorders

Massoudi¹,

Malecaze²,

Galiacy³

2015

Cell Tissue Res

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The cornea represents the external part of the eye and consists of an epithelium, a stroma and an endothelium. Due to its curvature and transparency this structure makes up approximately 70% of the total refractive power of the eye. This function is partly made possible by the particular organization of the collagen extracellular matrix contained in the corneal stroma that allows a constant refractive power. The maintenance of such an organization involves other molecules such as type V collagen, FACITs (fibril-associated collagens with interrupted triple helices) and SLRPs (small leucine-rich proteoglycans). These components play crucial roles in the preservation of the correct organization and function of the cornea since their absence or modification leads to abnormalities such as corneal opacities. Thus, the aim of this review is to describe the different corneal collagens and proteoglycans by highlighting their importance in corneal transparency as well as their implication in corneal visual disorders.

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A C-terminal fragment BIGH3 protein with an RGDRGD motif inhibits corneal neovascularization in vitro and in vivo

Cited by 11 publications

References 43 publications

Mutation update:TGFBIpathogenic and likely pathogenic variants in corneal dystrophies

Mutation update:TGFBIpathogenic and likely pathogenic variants in corneal dystrophies

Dysregulation of gene expression in human fetal endothelial cells from gestational diabetes in response to TGF-β1

Collagens and proteoglycans of the cornea: importance in transparency and visual disorders

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