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Increased Expression of Intercellular Adhesion Molecule-1 (ICAM-1) in Diabetic Rat Glomeruli: Glomerular Hyperfiltration Is a Potential Mechanism of ICAM-1 Upregulation
Abstract
Mononuclear cells, including monocytes/macrophages and T-cells, are considered to be involved in the progression of diabetic nephropathy, although the mechanism of their recruitment into diabetic glomeruli is unclear. The intercellular adhesion molecule-1 (ICAM-1) promotes the infiltration of leukocytes into atherosclerotic lesions as well as inflammatory tissues. In the present study, we investigated the expression of ICAM-1 in the glomeruli of streptozotocin-induced diabetic rats. The expression of ICAM-1 was increased significantly during the early stage of diabetes. The number of mononuclear cells, primarily monocytes/macrophages and lymphocytes, was significantly increased in diabetic glomeruli. Mononuclear cell infiltration into diabetic glomeruli was prevented by anti-ICAM-1 monoclonal antibody. Insulin treatment decreased ICAM-1 expression and mononuclear cell infiltration. The ICAM-1 expression on cultured human umbilical vein endothelial cells was not induced under high glucose culture conditions. Glomerular hyperfiltration is a characteristic change in the early stage of diabetic nephropathy. Treatment with aldose reductase inhibitor, which prevented glomerular hyperfiltration without changes in blood glucose levels, decreased ICAM-1 expression and mononuclear cell infiltration. Moreover, we examined the ICAM-1 expression in the glomeruli of the 5/6 nephrectomized rat, which is a model for glomerular hyperfiltration without hyperglycemia. The ICAM-1 expression and infiltration of mononuclear cells was significantly increased in the glomeruli of 5/6 nephrectomized rats. We conclude that ICAM-1 is upregulated and promotes the recruitment of mononuclear cells in diabetic glomeruli. Moreover, glomerular hyperfiltration that occurs in the early stage of diabetic glomeruli may be one of the potential mechanisms of ICAM-1 upregulation in diabetic nephropathy.
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Cited by
Kodera, R., Shikata, K., Kataoka, H. U., Takatsuka, T., Miyamoto, S., Sasaki, M., Kajitani, N., Nishishita, S., Sarai, K., Hirota, D., et al. (2011) · Diabetologia · doi:10.1007/s00125-010-2028-x · Cited by 394
Self-citationDiabetes-Induced Reactive Oxygen Species: Mechanism of Their Generation and Role in Renal Injury
Fakhruddin, S., Alanazi, W., & Jackson, K. E. (2017) · Journal of Diabetes Research · doi:10.1155/2017/8379327 · Cited by 292
Kitada, M., Takeda, A., Nagai, T., Ito, H., Kanasaki, K., & Koya, D. (2011) · Experimental Diabetes Research · doi:10.1155/2011/908185 · Cited by 213
Immune responses in diabetic nephropathy: Pathogenic mechanisms and therapeutic target
Chen, J., Liu, Q., He, J., & Li, Y. (2022) · Frontiers in Immunology · doi:10.3389/fimmu.2022.958790 · Cited by 164
Ojima, A., Ishibashi, Y., Matsui, T., Maeda, S., Nishino, Y., Takeuchi, M., Fukami, K., & Yamagishi, S.-I. (2013) · The American Journal of Pathology · doi:10.1016/j.ajpath.2012.09.016 · Cited by 156
Metadata
- Authors
- Sugimoto, H., Shikata, K., Hirata, K., Akiyama, K., Matsuda, M., Kushiro, M., Shikata, Y., Miyatake, N., Miyasaka, M., & Makino, H.
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 1997-12-01
- Volume
- 46
- Issue
- 12
- Pages
- 2075-2081
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2079785479
- Cited by
- 193
- References
- 0
- FWCI
- 3.20
- Type
- journal article
- Language
- en
- Open access
- closed
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- CoChat. (2026). Citation check: Increased Expression of Intercellular Adhesion Molecule-1 (ICAM-1) in Diabetic Rat Glomeruli: Glomerular Hyperfiltration Is a Potential Mechanism of ICAM-1 Upregulation. https://app.cochat.ai/papers/10.2337/diab.46.12.2075
- The paper
- Sugimoto, H., Shikata, K., Hirata, K., Akiyama, K., Matsuda, M., Kushiro, M., Shikata, Y., Miyatake, N., Miyasaka, M., & Makino, H. (1997). Increased Expression of Intercellular Adhesion Molecule-1 (ICAM-1) in Diabetic Rat Glomeruli: Glomerular Hyperfiltration Is a Potential Mechanism of ICAM-1 Upregulation. Diabetes. https://doi.org/10.2337/diab.46.12.2075
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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