The role of NF-kB in retinal neovascularization in the rat

Possible involvement of cytokine-induced neutrophil chemoattractant (CINC), a member of the interleukin-8 family

Ayako Yoshida, Shigeo Yoshida, Yasuaki Hata, Ahmad K. Khalil, Tatsuro Ishibashi, Hajime Inomata

Research output: Contribution to journalArticle

37 Citations (Scopus)

Abstract

Hypoxia precedes neovascularization in many retinal diseases that can lead to irreversible vision loss. The transcription factor NF-KB is activated by hypoxia and regulates the expression of many genes, including angiogenic factors. The relation between the NF-kB activation and the cytokine-induced neutrophil chemoattractant (CINC), a member of the interleukin-8 (IL-8) family, was investigated by immunohistochemistry in a rat model of proliferative retinopathy presumably caused by relative hypoxia. Activated NF-KB and CINC immunoreactivity was detected in retinal glial cells in the nonperfused retina and in neovascular cells. Activated NF-kB was detected before the CINC staining, and both of these events occurred before the development of neovascularization. The intensity of both activated NF-KB and CINC staining remained increased during the development of neovascularization and then declined as neovascularization regressed. In rat retinal glial cells in vitro, dexamethasone, an inhibitor of NF-kB activation, prevented the hypoxia-induced increase in the amount of CINC mRNA. Furthermore, CINC induced neovascularization in a rat corneal pocket model. These results suggest that hypoxia-induced activation of NF-kB results in CINC production and participates in the induction of retinal neovascularization.

Original languageEnglish
Pages (from-to)429-436
Number of pages8
JournalJournal of Histochemistry and Cytochemistry
Volume46
Issue number4
DOIs
Publication statusPublished - Jan 1 1998

Fingerprint

Retinal Neovascularization
NF-kappa B
Chemotactic Factors
Interleukin-8
Neutrophils
Cytokines
Neuroglia
Staining and Labeling
Retinal Diseases
Angiogenesis Inducing Agents
Dexamethasone
Retina
Transcription Factors
Immunohistochemistry
Hypoxia
Gene Expression
Messenger RNA

All Science Journal Classification (ASJC) codes

  • Anatomy
  • Histology

Cite this

The role of NF-kB in retinal neovascularization in the rat : Possible involvement of cytokine-induced neutrophil chemoattractant (CINC), a member of the interleukin-8 family. / Yoshida, Ayako; Yoshida, Shigeo; Hata, Yasuaki; Khalil, Ahmad K.; Ishibashi, Tatsuro; Inomata, Hajime.

In: Journal of Histochemistry and Cytochemistry, Vol. 46, No. 4, 01.01.1998, p. 429-436.

Research output: Contribution to journalArticle

@article{3563b9804b9b44b8a824cca4064bcd6d,
title = "The role of NF-kB in retinal neovascularization in the rat: Possible involvement of cytokine-induced neutrophil chemoattractant (CINC), a member of the interleukin-8 family",
abstract = "Hypoxia precedes neovascularization in many retinal diseases that can lead to irreversible vision loss. The transcription factor NF-KB is activated by hypoxia and regulates the expression of many genes, including angiogenic factors. The relation between the NF-kB activation and the cytokine-induced neutrophil chemoattractant (CINC), a member of the interleukin-8 (IL-8) family, was investigated by immunohistochemistry in a rat model of proliferative retinopathy presumably caused by relative hypoxia. Activated NF-KB and CINC immunoreactivity was detected in retinal glial cells in the nonperfused retina and in neovascular cells. Activated NF-kB was detected before the CINC staining, and both of these events occurred before the development of neovascularization. The intensity of both activated NF-KB and CINC staining remained increased during the development of neovascularization and then declined as neovascularization regressed. In rat retinal glial cells in vitro, dexamethasone, an inhibitor of NF-kB activation, prevented the hypoxia-induced increase in the amount of CINC mRNA. Furthermore, CINC induced neovascularization in a rat corneal pocket model. These results suggest that hypoxia-induced activation of NF-kB results in CINC production and participates in the induction of retinal neovascularization.",
author = "Ayako Yoshida and Shigeo Yoshida and Yasuaki Hata and Khalil, {Ahmad K.} and Tatsuro Ishibashi and Hajime Inomata",
year = "1998",
month = "1",
day = "1",
doi = "10.1177/002215549804600402",
language = "English",
volume = "46",
pages = "429--436",
journal = "Journal of Histochemistry and Cytochemistry",
issn = "0022-1554",
publisher = "Histochemical Society Inc.",
number = "4",

}

TY - JOUR

T1 - The role of NF-kB in retinal neovascularization in the rat

T2 - Possible involvement of cytokine-induced neutrophil chemoattractant (CINC), a member of the interleukin-8 family

AU - Yoshida, Ayako

AU - Yoshida, Shigeo

AU - Hata, Yasuaki

AU - Khalil, Ahmad K.

AU - Ishibashi, Tatsuro

AU - Inomata, Hajime

PY - 1998/1/1

Y1 - 1998/1/1

N2 - Hypoxia precedes neovascularization in many retinal diseases that can lead to irreversible vision loss. The transcription factor NF-KB is activated by hypoxia and regulates the expression of many genes, including angiogenic factors. The relation between the NF-kB activation and the cytokine-induced neutrophil chemoattractant (CINC), a member of the interleukin-8 (IL-8) family, was investigated by immunohistochemistry in a rat model of proliferative retinopathy presumably caused by relative hypoxia. Activated NF-KB and CINC immunoreactivity was detected in retinal glial cells in the nonperfused retina and in neovascular cells. Activated NF-kB was detected before the CINC staining, and both of these events occurred before the development of neovascularization. The intensity of both activated NF-KB and CINC staining remained increased during the development of neovascularization and then declined as neovascularization regressed. In rat retinal glial cells in vitro, dexamethasone, an inhibitor of NF-kB activation, prevented the hypoxia-induced increase in the amount of CINC mRNA. Furthermore, CINC induced neovascularization in a rat corneal pocket model. These results suggest that hypoxia-induced activation of NF-kB results in CINC production and participates in the induction of retinal neovascularization.

AB - Hypoxia precedes neovascularization in many retinal diseases that can lead to irreversible vision loss. The transcription factor NF-KB is activated by hypoxia and regulates the expression of many genes, including angiogenic factors. The relation between the NF-kB activation and the cytokine-induced neutrophil chemoattractant (CINC), a member of the interleukin-8 (IL-8) family, was investigated by immunohistochemistry in a rat model of proliferative retinopathy presumably caused by relative hypoxia. Activated NF-KB and CINC immunoreactivity was detected in retinal glial cells in the nonperfused retina and in neovascular cells. Activated NF-kB was detected before the CINC staining, and both of these events occurred before the development of neovascularization. The intensity of both activated NF-KB and CINC staining remained increased during the development of neovascularization and then declined as neovascularization regressed. In rat retinal glial cells in vitro, dexamethasone, an inhibitor of NF-kB activation, prevented the hypoxia-induced increase in the amount of CINC mRNA. Furthermore, CINC induced neovascularization in a rat corneal pocket model. These results suggest that hypoxia-induced activation of NF-kB results in CINC production and participates in the induction of retinal neovascularization.

UR - http://www.scopus.com/inward/record.url?scp=0031594736&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0031594736&partnerID=8YFLogxK

U2 - 10.1177/002215549804600402

DO - 10.1177/002215549804600402

M3 - Article

VL - 46

SP - 429

EP - 436

JO - Journal of Histochemistry and Cytochemistry

JF - Journal of Histochemistry and Cytochemistry

SN - 0022-1554

IS - 4

ER -