Protection of thymosin beta-4 on corneal endothelial cells from UVB-induced apoptosis

Jennifer Hui Chun Ho, Yeu Su, Ko Hua Chen, Oscar Kuang Sheng Lee

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

Cornea absorbs most of daily ultraviolet (UV) light. An excess of UV damages results in not only keratopathy and cataract but also maculopathy. It has been reported that thymosin beta-4 (Tβ 4) promotes wound healing, decreases inflammatory response and prevents apoptosis of corneal epithelial cells. However, it is not clear whether Tβ 4 protects UVB-induced corneal injury, particularly in corneal endothelial cells because of its non-proliferation in nature. The purpose of this study is to compare the protective effects of Tβ 4 on bovine corneal endothelial (BCE) cells from low- and high-dose UVB damage. In this study, 1 μg/ml of Tβ 4 was added to BCE cells 2 h before low (12.5 mj/cm 2) or high dosage (100 mj/cm 2) UVB exposure. Using a fluorogenic substrate cleavage assay, we found that Tβ 4 diminished the reactive oxygen species level in BCE cells elicited by UVB. However, the protection of viability by Tβ 4 could only be detected under low-dose UVB exposure. Moreover, both caspase-9 activity and annexin V/propidium iodine staining demonstrated that Tβ 4 only protected BCE cells from low-dose UVBinduced apoptosis but not high-dose UVB-induced necrosis. Together, Tβ 4 protected corneal endothelial cells from UVB-induced oxidative stress and apoptosis after low-dose UVB exposure. The results support further investigation towards topical use or anterior chamber injection of this small hydrophilic peptide in treating and preventing UVB-induced corneal endothelial damage.

Original languageEnglish
Pages (from-to)190-195
Number of pages6
JournalChinese Journal of Physiology
Volume53
Issue number3
DOIs
Publication statusPublished - 2010

Fingerprint

Endothelial Cells
Apoptosis
Caspase 9
Propidium
Annexin A5
Anterior Chamber
Ultraviolet Rays
Fluorescent Dyes
Iodine
Wound Healing
Cornea
Cataract
thymosin beta(4)
Reactive Oxygen Species
Oxidative Stress
Necrosis
Epithelial Cells
Staining and Labeling
Peptides
Injections

Keywords

  • Corneal endothelial cells
  • Thymosin ß
  • Ultraviolet B

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

Cite this

Protection of thymosin beta-4 on corneal endothelial cells from UVB-induced apoptosis. / Ho, Jennifer Hui Chun; Su, Yeu; Chen, Ko Hua; Lee, Oscar Kuang Sheng.

In: Chinese Journal of Physiology, Vol. 53, No. 3, 2010, p. 190-195.

Research output: Contribution to journalArticle

Ho, Jennifer Hui Chun ; Su, Yeu ; Chen, Ko Hua ; Lee, Oscar Kuang Sheng. / Protection of thymosin beta-4 on corneal endothelial cells from UVB-induced apoptosis. In: Chinese Journal of Physiology. 2010 ; Vol. 53, No. 3. pp. 190-195.
@article{499cd128d8ea44609911504e9232e981,
title = "Protection of thymosin beta-4 on corneal endothelial cells from UVB-induced apoptosis",
abstract = "Cornea absorbs most of daily ultraviolet (UV) light. An excess of UV damages results in not only keratopathy and cataract but also maculopathy. It has been reported that thymosin beta-4 (Tβ 4) promotes wound healing, decreases inflammatory response and prevents apoptosis of corneal epithelial cells. However, it is not clear whether Tβ 4 protects UVB-induced corneal injury, particularly in corneal endothelial cells because of its non-proliferation in nature. The purpose of this study is to compare the protective effects of Tβ 4 on bovine corneal endothelial (BCE) cells from low- and high-dose UVB damage. In this study, 1 μg/ml of Tβ 4 was added to BCE cells 2 h before low (12.5 mj/cm 2) or high dosage (100 mj/cm 2) UVB exposure. Using a fluorogenic substrate cleavage assay, we found that Tβ 4 diminished the reactive oxygen species level in BCE cells elicited by UVB. However, the protection of viability by Tβ 4 could only be detected under low-dose UVB exposure. Moreover, both caspase-9 activity and annexin V/propidium iodine staining demonstrated that Tβ 4 only protected BCE cells from low-dose UVBinduced apoptosis but not high-dose UVB-induced necrosis. Together, Tβ 4 protected corneal endothelial cells from UVB-induced oxidative stress and apoptosis after low-dose UVB exposure. The results support further investigation towards topical use or anterior chamber injection of this small hydrophilic peptide in treating and preventing UVB-induced corneal endothelial damage.",
keywords = "Corneal endothelial cells, Thymosin {\ss}, Ultraviolet B",
author = "Ho, {Jennifer Hui Chun} and Yeu Su and Chen, {Ko Hua} and Lee, {Oscar Kuang Sheng}",
year = "2010",
doi = "10.4077/CJP.2010.AMH091",
language = "English",
volume = "53",
pages = "190--195",
journal = "Chinese Journal of Physiology",
issn = "0304-4920",
publisher = "Chinese Physiological Society",
number = "3",

}

TY - JOUR

T1 - Protection of thymosin beta-4 on corneal endothelial cells from UVB-induced apoptosis

AU - Ho, Jennifer Hui Chun

AU - Su, Yeu

AU - Chen, Ko Hua

AU - Lee, Oscar Kuang Sheng

PY - 2010

Y1 - 2010

N2 - Cornea absorbs most of daily ultraviolet (UV) light. An excess of UV damages results in not only keratopathy and cataract but also maculopathy. It has been reported that thymosin beta-4 (Tβ 4) promotes wound healing, decreases inflammatory response and prevents apoptosis of corneal epithelial cells. However, it is not clear whether Tβ 4 protects UVB-induced corneal injury, particularly in corneal endothelial cells because of its non-proliferation in nature. The purpose of this study is to compare the protective effects of Tβ 4 on bovine corneal endothelial (BCE) cells from low- and high-dose UVB damage. In this study, 1 μg/ml of Tβ 4 was added to BCE cells 2 h before low (12.5 mj/cm 2) or high dosage (100 mj/cm 2) UVB exposure. Using a fluorogenic substrate cleavage assay, we found that Tβ 4 diminished the reactive oxygen species level in BCE cells elicited by UVB. However, the protection of viability by Tβ 4 could only be detected under low-dose UVB exposure. Moreover, both caspase-9 activity and annexin V/propidium iodine staining demonstrated that Tβ 4 only protected BCE cells from low-dose UVBinduced apoptosis but not high-dose UVB-induced necrosis. Together, Tβ 4 protected corneal endothelial cells from UVB-induced oxidative stress and apoptosis after low-dose UVB exposure. The results support further investigation towards topical use or anterior chamber injection of this small hydrophilic peptide in treating and preventing UVB-induced corneal endothelial damage.

AB - Cornea absorbs most of daily ultraviolet (UV) light. An excess of UV damages results in not only keratopathy and cataract but also maculopathy. It has been reported that thymosin beta-4 (Tβ 4) promotes wound healing, decreases inflammatory response and prevents apoptosis of corneal epithelial cells. However, it is not clear whether Tβ 4 protects UVB-induced corneal injury, particularly in corneal endothelial cells because of its non-proliferation in nature. The purpose of this study is to compare the protective effects of Tβ 4 on bovine corneal endothelial (BCE) cells from low- and high-dose UVB damage. In this study, 1 μg/ml of Tβ 4 was added to BCE cells 2 h before low (12.5 mj/cm 2) or high dosage (100 mj/cm 2) UVB exposure. Using a fluorogenic substrate cleavage assay, we found that Tβ 4 diminished the reactive oxygen species level in BCE cells elicited by UVB. However, the protection of viability by Tβ 4 could only be detected under low-dose UVB exposure. Moreover, both caspase-9 activity and annexin V/propidium iodine staining demonstrated that Tβ 4 only protected BCE cells from low-dose UVBinduced apoptosis but not high-dose UVB-induced necrosis. Together, Tβ 4 protected corneal endothelial cells from UVB-induced oxidative stress and apoptosis after low-dose UVB exposure. The results support further investigation towards topical use or anterior chamber injection of this small hydrophilic peptide in treating and preventing UVB-induced corneal endothelial damage.

KW - Corneal endothelial cells

KW - Thymosin ß

KW - Ultraviolet B

UR - http://www.scopus.com/inward/record.url?scp=78149430429&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=78149430429&partnerID=8YFLogxK

U2 - 10.4077/CJP.2010.AMH091

DO - 10.4077/CJP.2010.AMH091

M3 - Article

VL - 53

SP - 190

EP - 195

JO - Chinese Journal of Physiology

JF - Chinese Journal of Physiology

SN - 0304-4920

IS - 3

ER -