Targeted disruption of the galectin-3 gene results in decreased susceptibility to multiple low dose streptozotocin-induced diabetes in mice

E. P K Mensah-Brown; Z. Al Rabesi; A. Shahin; M. Al Shamsi; N. Arsenijevic; D. K. Hsu; Fu-Tong Liu; M. L. Lukic

doi:10.1016/j.clim.2008.08.024

Targeted disruption of the galectin-3 gene results in decreased susceptibility to multiple low dose streptozotocin-induced diabetes in mice

E. P K Mensah-Brown, Z. Al Rabesi, A. Shahin, M. Al Shamsi, N. Arsenijevic, D. K. Hsu, Fu-Tong Liu, M. L. Lukic

Dermatology

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Abstract

Galectin 3 (Gal-3) is an antiapoptotic and a proinflammatory lectin. We hypothesized that the proinflammatory properties of Gal-3 may influence disease induction in the multiple low doses of streptozotocin model of diabetes. Diabetes was induced in C57BL/6 Gal-3^+/+ and Gal-3^-/- mice and disease monitored by blood glucose level, immuno-histology, insulin content of islets and expression of the proinflammatory cytokines, TNF-α, IFN-γ, IL-17, and iNOS in pancreatic lymph nodes. Gal-3^+/+ mice developed delayed and sustained hyperglycemia, mononuclear cellular infiltration and reduced insulin content of islets accompanied with expression of proinflammatory cytokines. Gal-3^-/^- mice were relatively resistant to diabetogenesis as evaluated by glycemia, quantitative histology and insulin content. Further, we observed the weaker expression of IFN-γ and complete absence of TNF-α, and IL-17 in draining pancreatic lymph nodes. Macrophages, the first cells that infiltrate the islet in this model of diabetes, produce less TNF-α and NO in Gal-3^-/- mice. Thus, Gal-3 is involved in immune mediated β cell damage and is required for diabetogenesis in this model of disease.

Original language	English (US)
Pages (from-to)	83-88
Number of pages	6
Journal	Clinical Immunology
Volume	130
Issue number	1
DOIs	https://doi.org/10.1016/j.clim.2008.08.024
State	Published - Jan 2009

Keywords

Autoimmunity;
Inducible nitric oxide synthase;
Interferon-gamma;
Interleukin-17
Proinflammatory cytokines;

ASJC Scopus subject areas

Immunology
Immunology and Allergy

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10.1016/j.clim.2008.08.024

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Targeted disruption of the galectin-3 gene results in decreased susceptibility to multiple low dose streptozotocin-induced diabetes in mice. / Mensah-Brown, E. P K; Al Rabesi, Z.; Shahin, A.; Al Shamsi, M.; Arsenijevic, N.; Hsu, D. K.; Liu, Fu-Tong; Lukic, M. L.

In: Clinical Immunology, Vol. 130, No. 1, 01.2009, p. 83-88.

Research output: Contribution to journal › Article › peer-review

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abstract = "Galectin 3 (Gal-3) is an antiapoptotic and a proinflammatory lectin. We hypothesized that the proinflammatory properties of Gal-3 may influence disease induction in the multiple low doses of streptozotocin model of diabetes. Diabetes was induced in C57BL/6 Gal-3+/+ and Gal-3-/- mice and disease monitored by blood glucose level, immuno-histology, insulin content of islets and expression of the proinflammatory cytokines, TNF-α, IFN-γ, IL-17, and iNOS in pancreatic lymph nodes. Gal-3+/+ mice developed delayed and sustained hyperglycemia, mononuclear cellular infiltration and reduced insulin content of islets accompanied with expression of proinflammatory cytokines. Gal-3-/- mice were relatively resistant to diabetogenesis as evaluated by glycemia, quantitative histology and insulin content. Further, we observed the weaker expression of IFN-γ and complete absence of TNF-α, and IL-17 in draining pancreatic lymph nodes. Macrophages, the first cells that infiltrate the islet in this model of diabetes, produce less TNF-α and NO in Gal-3-/- mice. Thus, Gal-3 is involved in immune mediated β cell damage and is required for diabetogenesis in this model of disease.",

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author = "Mensah-Brown, {E. P K} and {Al Rabesi}, Z. and A. Shahin and {Al Shamsi}, M. and N. Arsenijevic and Hsu, {D. K.} and Fu-Tong Liu and Lukic, {M. L.}",

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AU - Al Rabesi, Z.

AU - Shahin, A.

AU - Al Shamsi, M.

AU - Arsenijevic, N.

AU - Hsu, D. K.

AU - Liu, Fu-Tong

AU - Lukic, M. L.

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AB - Galectin 3 (Gal-3) is an antiapoptotic and a proinflammatory lectin. We hypothesized that the proinflammatory properties of Gal-3 may influence disease induction in the multiple low doses of streptozotocin model of diabetes. Diabetes was induced in C57BL/6 Gal-3+/+ and Gal-3-/- mice and disease monitored by blood glucose level, immuno-histology, insulin content of islets and expression of the proinflammatory cytokines, TNF-α, IFN-γ, IL-17, and iNOS in pancreatic lymph nodes. Gal-3+/+ mice developed delayed and sustained hyperglycemia, mononuclear cellular infiltration and reduced insulin content of islets accompanied with expression of proinflammatory cytokines. Gal-3-/- mice were relatively resistant to diabetogenesis as evaluated by glycemia, quantitative histology and insulin content. Further, we observed the weaker expression of IFN-γ and complete absence of TNF-α, and IL-17 in draining pancreatic lymph nodes. Macrophages, the first cells that infiltrate the islet in this model of diabetes, produce less TNF-α and NO in Gal-3-/- mice. Thus, Gal-3 is involved in immune mediated β cell damage and is required for diabetogenesis in this model of disease.

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Targeted disruption of the galectin-3 gene results in decreased susceptibility to multiple low dose streptozotocin-induced diabetes in mice

Abstract

Keywords

ASJC Scopus subject areas

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