Extracellular matrix alterations in human corneas with bullous keratopathy.

A V Ljubimov; R E Burgeson; R J Butkowski; J R Couchman; R R Wu; Y Ninomiya; Y Sado; E Maguen; A B Nesburn; M C Kenney

Extracellular matrix alterations in human corneas with bullous keratopathy.

A V Ljubimov, R E Burgeson, R J Butkowski, J R Couchman, R R Wu, Y Ninomiya, Y Sado, E Maguen, A B Nesburn, M C Kenney

Nutritional Immunology

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › peer review

133 Citationer (Scopus)

Abstract

Udgivelsesdato: 1996-May

Originalsprog	Engelsk
Tidsskrift	Investigative Ophthalmology & Visual Science
Vol/bind	37
Udgave nummer	6
Sider (fra-til)	997-1007
Antal sider	10
ISSN	0146-0404
Status	Udgivet - 1996

Bibliografisk note

Keywords: Aged; Aged, 80 and over; Basement Membrane; Cataract Extraction; Cornea; Corneal Diseases; Corneal Transplantation; Extracellular Matrix; Extracellular Matrix Proteins; Female; Fibrosis; Fluorescent Antibody Technique; Humans; Male; Middle Aged

Citationsformater

@article{485938d0597711dd8d9f000ea68e967b,

title = "Extracellular matrix alterations in human corneas with bullous keratopathy.",

abstract = "PURPOSE. To uncover abnormalities of extracellular matrix (ECM) distribution in human corneas with pseudophakic and aphakic bullous keratopathy (PBK/ABK). METHODS. Indirect immunofluorescence with antibodies to 27 ECM components was used on frozen sections of 14 normal and 20 PBK/ABK corneas. RESULTS. Fibrillar deposits of an antiadhesive glycoprotein tenascin in the anterior and posterior stroma, epithelial basement membrane (BM), bullae and subepithelial fibrosis (SEF) areas, and posterior collagenous layer (PCL) were revealed in disease corneas. Tenascin in midstroma, which was observed in some cases, correlated with decreased visual acuity. In normal central corneas, tenascin was never found. Other major ECM abnormalities in PBK/ABK corneas compared to normals included: discontinuous epithelial BM straining for laminin-1 (alpha 1 beta 1 gamma 1), entactin/nidogen and fibronectin; accumulation of fibronectin and alpha 1-alpha 2 type IV collagen on the endothelial face of the Descemet's membrane; and abnormal deposition of stromal ECM (tenascin, fibronectin, decorin, types I, III, V, VI, VIII, XII, XIV collagen) and BM components (type IV, collagen, perlecan, bamacan, laminin-1, entactin-nidogen, fibronectin) in SEF areas and in PCL. CONCLUSIONS. The study provides a molecular description of an ongoing fibrosis on the epithelial, stomal, and endothelial levels in PBK/ABK corneas. These fibrotic changes may follow initial endothelial damage after cataract surgery, may be caused by the upregulation of fibrogenic cytokines, and may play a significant role in the progression of bullous keratopathy.",

author = "Ljubimov, {A V} and Burgeson, {R E} and Butkowski, {R J} and Couchman, {J R} and Wu, {R R} and Y Ninomiya and Y Sado and E Maguen and Nesburn, {A B} and Kenney, {M C}",

note = "Keywords: Aged; Aged, 80 and over; Basement Membrane; Cataract Extraction; Cornea; Corneal Diseases; Corneal Transplantation; Extracellular Matrix; Extracellular Matrix Proteins; Female; Fibrosis; Fluorescent Antibody Technique; Humans; Male; Middle Aged",

year = "1996",

language = "English",

volume = "37",

pages = "997--1007",

journal = "Investigative Ophthalmology & Visual Science",

issn = "0146-0404",

publisher = "Association for Research in Vision and Ophthalmology",

number = "6",

}

TY - JOUR

T1 - Extracellular matrix alterations in human corneas with bullous keratopathy.

AU - Ljubimov, A V

AU - Burgeson, R E

AU - Butkowski, R J

AU - Couchman, J R

AU - Wu, R R

AU - Ninomiya, Y

AU - Sado, Y

AU - Maguen, E

AU - Nesburn, A B

AU - Kenney, M C

N1 - Keywords: Aged; Aged, 80 and over; Basement Membrane; Cataract Extraction; Cornea; Corneal Diseases; Corneal Transplantation; Extracellular Matrix; Extracellular Matrix Proteins; Female; Fibrosis; Fluorescent Antibody Technique; Humans; Male; Middle Aged

PY - 1996

Y1 - 1996

N2 - PURPOSE. To uncover abnormalities of extracellular matrix (ECM) distribution in human corneas with pseudophakic and aphakic bullous keratopathy (PBK/ABK). METHODS. Indirect immunofluorescence with antibodies to 27 ECM components was used on frozen sections of 14 normal and 20 PBK/ABK corneas. RESULTS. Fibrillar deposits of an antiadhesive glycoprotein tenascin in the anterior and posterior stroma, epithelial basement membrane (BM), bullae and subepithelial fibrosis (SEF) areas, and posterior collagenous layer (PCL) were revealed in disease corneas. Tenascin in midstroma, which was observed in some cases, correlated with decreased visual acuity. In normal central corneas, tenascin was never found. Other major ECM abnormalities in PBK/ABK corneas compared to normals included: discontinuous epithelial BM straining for laminin-1 (alpha 1 beta 1 gamma 1), entactin/nidogen and fibronectin; accumulation of fibronectin and alpha 1-alpha 2 type IV collagen on the endothelial face of the Descemet's membrane; and abnormal deposition of stromal ECM (tenascin, fibronectin, decorin, types I, III, V, VI, VIII, XII, XIV collagen) and BM components (type IV, collagen, perlecan, bamacan, laminin-1, entactin-nidogen, fibronectin) in SEF areas and in PCL. CONCLUSIONS. The study provides a molecular description of an ongoing fibrosis on the epithelial, stomal, and endothelial levels in PBK/ABK corneas. These fibrotic changes may follow initial endothelial damage after cataract surgery, may be caused by the upregulation of fibrogenic cytokines, and may play a significant role in the progression of bullous keratopathy.

AB - PURPOSE. To uncover abnormalities of extracellular matrix (ECM) distribution in human corneas with pseudophakic and aphakic bullous keratopathy (PBK/ABK). METHODS. Indirect immunofluorescence with antibodies to 27 ECM components was used on frozen sections of 14 normal and 20 PBK/ABK corneas. RESULTS. Fibrillar deposits of an antiadhesive glycoprotein tenascin in the anterior and posterior stroma, epithelial basement membrane (BM), bullae and subepithelial fibrosis (SEF) areas, and posterior collagenous layer (PCL) were revealed in disease corneas. Tenascin in midstroma, which was observed in some cases, correlated with decreased visual acuity. In normal central corneas, tenascin was never found. Other major ECM abnormalities in PBK/ABK corneas compared to normals included: discontinuous epithelial BM straining for laminin-1 (alpha 1 beta 1 gamma 1), entactin/nidogen and fibronectin; accumulation of fibronectin and alpha 1-alpha 2 type IV collagen on the endothelial face of the Descemet's membrane; and abnormal deposition of stromal ECM (tenascin, fibronectin, decorin, types I, III, V, VI, VIII, XII, XIV collagen) and BM components (type IV, collagen, perlecan, bamacan, laminin-1, entactin-nidogen, fibronectin) in SEF areas and in PCL. CONCLUSIONS. The study provides a molecular description of an ongoing fibrosis on the epithelial, stomal, and endothelial levels in PBK/ABK corneas. These fibrotic changes may follow initial endothelial damage after cataract surgery, may be caused by the upregulation of fibrogenic cytokines, and may play a significant role in the progression of bullous keratopathy.

M3 - Journal article

C2 - 8631643

SN - 0146-0404

VL - 37

SP - 997

EP - 1007

JO - Investigative Ophthalmology & Visual Science

JF - Investigative Ophthalmology & Visual Science

IS - 6

ER -