Galectins-3 and -7, but not galectin-1, play a role in re-epithelialization of wounds

Zhiyi Cao, Neveen Said, Shalin Amin, Helen K. Wu, Amenda Bruce, Marco Garate, Daniel K. Hsu, Ichiro Kuwabara, Fu-Tong Liu, Noorjahan Panjwani

Research output: Contribution to journalArticle

138 Citations (Scopus)

Abstract

Disorders of wound healing characterized by impaired or delayed re-epithelialization are a serious medical problem. These conditions affect many tissues, are painful, and are difficult to treat. In this study, using cornea as a model, we demonstrate for the first time the importance of carbohydrate-binding proteins galectins-3 and -7 in re-epithelialization of wounds. In two different models of corneal wound healing, re-epithelialization of wounds was significantly slower in galectin-3-deficient (gal3-/-) mice compared with wild-type (gal3+/+) mice. In contrast, there was no difference in corneal epithelial wound closure rates between galectin-l-deficient and wild-type mice. Quantitation of the bromodeoxyuridine-labeled cells in gal3+/+ and gal3-/- corneas revealed that corneal epithelial cell proliferation rate is not perturbed in gal3-/- corneas. Exogenous galectin-3 accelerated re-epithelialization of wounds in gal3+/+ mice but, surprisingly, not in the gal3-/- mice. Gene expression analysis using cDNA microarrays revealed that healing corneas of gal3-/- mice contain markedly reduced levels of galectin-7 compared with those of gal3+/+ mice. More importantly, unlike galectin-3, galectin-7 accelerated re-epithelialization of wounds in both gal3-/- and gal3+/+ mice. In corresponding experiments, recombinant galectin-1 did not stimulate the corneal epithelial wound closure rate. The extent of acceleration of re-epithelialization of wounds with both galectin-3 and galectin-7 was greater than that observed in most of the published studies using growth factors. These findings have broad implications for developing novel therapeutic strategies for treating nonhealing wounds.

Original languageEnglish (US)
Pages (from-to)42299-42305
Number of pages7
JournalJournal of Biological Chemistry
Volume277
Issue number44
DOIs
StatePublished - Nov 1 2002
Externally publishedYes

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Galectin 1
Re-Epithelialization
Galectin 3
Wounds and Injuries
Galectins
Cornea
Wound Healing
Cell proliferation
Bromodeoxyuridine
Microarrays
Medical problems
Oligonucleotide Array Sequence Analysis
Gene expression
Intercellular Signaling Peptides and Proteins
Complementary DNA
Epithelial Cells
Cell Proliferation

ASJC Scopus subject areas

  • Biochemistry

Cite this

Cao, Z., Said, N., Amin, S., Wu, H. K., Bruce, A., Garate, M., ... Panjwani, N. (2002). Galectins-3 and -7, but not galectin-1, play a role in re-epithelialization of wounds. Journal of Biological Chemistry, 277(44), 42299-42305. https://doi.org/10.1074/jbc.M200981200

Galectins-3 and -7, but not galectin-1, play a role in re-epithelialization of wounds. / Cao, Zhiyi; Said, Neveen; Amin, Shalin; Wu, Helen K.; Bruce, Amenda; Garate, Marco; Hsu, Daniel K.; Kuwabara, Ichiro; Liu, Fu-Tong; Panjwani, Noorjahan.

In: Journal of Biological Chemistry, Vol. 277, No. 44, 01.11.2002, p. 42299-42305.

Research output: Contribution to journalArticle

Cao, Z, Said, N, Amin, S, Wu, HK, Bruce, A, Garate, M, Hsu, DK, Kuwabara, I, Liu, F-T & Panjwani, N 2002, 'Galectins-3 and -7, but not galectin-1, play a role in re-epithelialization of wounds', Journal of Biological Chemistry, vol. 277, no. 44, pp. 42299-42305. https://doi.org/10.1074/jbc.M200981200
Cao, Zhiyi ; Said, Neveen ; Amin, Shalin ; Wu, Helen K. ; Bruce, Amenda ; Garate, Marco ; Hsu, Daniel K. ; Kuwabara, Ichiro ; Liu, Fu-Tong ; Panjwani, Noorjahan. / Galectins-3 and -7, but not galectin-1, play a role in re-epithelialization of wounds. In: Journal of Biological Chemistry. 2002 ; Vol. 277, No. 44. pp. 42299-42305.
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AU - Bruce, Amenda

AU - Garate, Marco

AU - Hsu, Daniel K.

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AB - Disorders of wound healing characterized by impaired or delayed re-epithelialization are a serious medical problem. These conditions affect many tissues, are painful, and are difficult to treat. In this study, using cornea as a model, we demonstrate for the first time the importance of carbohydrate-binding proteins galectins-3 and -7 in re-epithelialization of wounds. In two different models of corneal wound healing, re-epithelialization of wounds was significantly slower in galectin-3-deficient (gal3-/-) mice compared with wild-type (gal3+/+) mice. In contrast, there was no difference in corneal epithelial wound closure rates between galectin-l-deficient and wild-type mice. Quantitation of the bromodeoxyuridine-labeled cells in gal3+/+ and gal3-/- corneas revealed that corneal epithelial cell proliferation rate is not perturbed in gal3-/- corneas. Exogenous galectin-3 accelerated re-epithelialization of wounds in gal3+/+ mice but, surprisingly, not in the gal3-/- mice. Gene expression analysis using cDNA microarrays revealed that healing corneas of gal3-/- mice contain markedly reduced levels of galectin-7 compared with those of gal3+/+ mice. More importantly, unlike galectin-3, galectin-7 accelerated re-epithelialization of wounds in both gal3-/- and gal3+/+ mice. In corresponding experiments, recombinant galectin-1 did not stimulate the corneal epithelial wound closure rate. The extent of acceleration of re-epithelialization of wounds with both galectin-3 and galectin-7 was greater than that observed in most of the published studies using growth factors. These findings have broad implications for developing novel therapeutic strategies for treating nonhealing wounds.

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