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Glucose transporter 1 expression is enhanced during corneal epithelial wound repair.
Exp Eye Res 1996; 63(6):649-59EE

Abstract

Corneal epithelial wound healing involves a number of metabolically demanding processes such as cell migration and proliferation. The energy for those processes is known to be provided by glycolysis. Thus, it was hypothesized that migrating epithelium would require high levels of glucose to provide a substrate for glycolysis. It is well established that glucose is transported into virtually all mammalian cells by the facilitated glucose transport protein, glucose transporter (GLUT). We sought to investigate the expression of one of the isoforms of glucose transporter, GLUT1, in corneal epithelium after epithelial debridement in the rat. Three-millimeter debridement wounds were made on central rat cornea and allowed to heal from 1 hr to 21 days. To quantitate changes in GLUT1 mRNA and protein levels, whole corneal epithelium was harvested and analysed by reverse transcription-polymerase chain reaction, northern blot, and western blot analysis. GLUT1 protein localization was also observed immunohistochemically. Expression of GLUT1 protein rapidly increased following wounding and was 2.4-fold higher than control at 4 hr post debridement. GLUT1 protein levels continued to increase even after epithelial wound closure (24 hr) and peaked at 2 days post debridement, 5.8-fold higher than control. The increase in GLUT1 protein levels coincided with enhanced GLUT1 mRNA levels (3.7-fold higher than control at 4 hr post debridement). Immunofluorescence microscopy showed increased binding of anti-GLUT1 concentrated in the membranes of the basal cells from limbus-to-limbus until 24 hr post wounding. After 24 hr. binding remained enhanced in the wound area, while binding to the limbal basal cells returned to the control level. In conclusion, the expression of GLUT1 mRNA and protein are rapidly enhanced after wounding. This may allow the increased transport of glucose, providing the metabolic energy necessary for cell migration and proliferation.

Authors+Show Affiliations

Schepens Eye Research Institute, Boston, MA, USA.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

9068372

Citation

Takahashi, H, et al. "Glucose Transporter 1 Expression Is Enhanced During Corneal Epithelial Wound Repair." Experimental Eye Research, vol. 63, no. 6, 1996, pp. 649-59.
Takahashi H, Kaminski AE, Zieske JD. Glucose transporter 1 expression is enhanced during corneal epithelial wound repair. Exp Eye Res. 1996;63(6):649-59.
Takahashi, H., Kaminski, A. E., & Zieske, J. D. (1996). Glucose transporter 1 expression is enhanced during corneal epithelial wound repair. Experimental Eye Research, 63(6), pp. 649-59.
Takahashi H, Kaminski AE, Zieske JD. Glucose Transporter 1 Expression Is Enhanced During Corneal Epithelial Wound Repair. Exp Eye Res. 1996;63(6):649-59. PubMed PMID: 9068372.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Glucose transporter 1 expression is enhanced during corneal epithelial wound repair. AU - Takahashi,H, AU - Kaminski,A E, AU - Zieske,J D, PY - 1996/12/1/pubmed PY - 1996/12/1/medline PY - 1996/12/1/entrez SP - 649 EP - 59 JF - Experimental eye research JO - Exp. Eye Res. VL - 63 IS - 6 N2 - Corneal epithelial wound healing involves a number of metabolically demanding processes such as cell migration and proliferation. The energy for those processes is known to be provided by glycolysis. Thus, it was hypothesized that migrating epithelium would require high levels of glucose to provide a substrate for glycolysis. It is well established that glucose is transported into virtually all mammalian cells by the facilitated glucose transport protein, glucose transporter (GLUT). We sought to investigate the expression of one of the isoforms of glucose transporter, GLUT1, in corneal epithelium after epithelial debridement in the rat. Three-millimeter debridement wounds were made on central rat cornea and allowed to heal from 1 hr to 21 days. To quantitate changes in GLUT1 mRNA and protein levels, whole corneal epithelium was harvested and analysed by reverse transcription-polymerase chain reaction, northern blot, and western blot analysis. GLUT1 protein localization was also observed immunohistochemically. Expression of GLUT1 protein rapidly increased following wounding and was 2.4-fold higher than control at 4 hr post debridement. GLUT1 protein levels continued to increase even after epithelial wound closure (24 hr) and peaked at 2 days post debridement, 5.8-fold higher than control. The increase in GLUT1 protein levels coincided with enhanced GLUT1 mRNA levels (3.7-fold higher than control at 4 hr post debridement). Immunofluorescence microscopy showed increased binding of anti-GLUT1 concentrated in the membranes of the basal cells from limbus-to-limbus until 24 hr post wounding. After 24 hr. binding remained enhanced in the wound area, while binding to the limbal basal cells returned to the control level. In conclusion, the expression of GLUT1 mRNA and protein are rapidly enhanced after wounding. This may allow the increased transport of glucose, providing the metabolic energy necessary for cell migration and proliferation. SN - 0014-4835 UR - https://www.unboundmedicine.com/medline/citation/9068372/Glucose_transporter_1_expression_is_enhanced_during_corneal_epithelial_wound_repair_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0014-4835(96)90159-1 DB - PRIME DP - Unbound Medicine ER -