High glucose and angiotensin II increase β1 integrin and integrin-linked kinase synthesis in cultured mouse podocytes

Sang Youb Han, Young Sun Kang, Yi Hwa Jee, Kum Hyun Han, Dae-Ryong Cha, Shin Wook Kang, Dae Suk Han

Research output: Contribution to journalArticle

33 Citations (Scopus)

Abstract

Alterations of integrin α3β1 may play a role in the development of diabetic nephropathy. We have investigated the effects of high glucose and angiotensin II on the expression of integrin α3 and β1, and whether these changes are associated with integrin-linked kinase (ILK) in cultured mouse podocytes. Integrin β1 and ILK mRNA expression and protein production were rapidly up-regulated in a dose-dependent manner by high glucose and angiotensin II stimulation. ILK mRNA levels in the mouse podocytes exposed to 30 mmol/1 glucose were 1.66, 1.89, and 1.28 times higher than those in control cells at 6, 24, and 72 h exposure, respectively. ILK mRNA levels in mouse podocytes exposed to 1 nM, 10 nM, and 100 nM angiotensin II for 6 h were 1.38, 1.55, and 1.93 times higher, respectively, than those in control cells. Angiotensin-II-induced integrin β1 and ILK mRNA expression was significantly inhibited by treatment with losartan (100 μM). In addition, the up-regulation of ILK synthesis induced by these stimuli was related to β1 integrin synthesis and increased ILK kinase activity. Cell adhesion assay displayed inhibitory effects when podocytes were exposed to high concentrations of angiotensin II. Interestingly, glucose and angiotensin II stimulation induced shrinkage of the cell body and elongation of the podocyte processes, a phenotype similar to that of immature podocytes. In addition, β1 integrin showed higher levels of staining on both the cell membranes and the cell-cell contact areas. Thus, high glucose and angiotensin II may affect the regulation of the integrin-ILK system in podocytes; this system may therefore play a role in the pathogenesis of diabetic nephropathy and other renal diseases affecting podocytes.

Original languageEnglish
Pages (from-to)321-332
Number of pages12
JournalCell and Tissue Research
Volume323
Issue number2
DOIs
Publication statusPublished - 2006 Feb 1

Fingerprint

Podocytes
Integrins
Angiotensin II
Glucose
Messenger RNA
Diabetic Nephropathies
Losartan
integrin-linked kinase
Cell adhesion
Cell membranes
Cell Adhesion
Elongation
Assays
Phosphotransferases
Up-Regulation
Cells
Cell Membrane
Staining and Labeling
Phenotype
Kidney

Keywords

  • Diabetes mellitus
  • Integrin beta 1
  • Integrin-linked kinase
  • Mouse (immortalized podocyte cell line)
  • Podocyte

ASJC Scopus subject areas

  • Anatomy
  • Clinical Biochemistry
  • Cell Biology

Cite this

High glucose and angiotensin II increase β1 integrin and integrin-linked kinase synthesis in cultured mouse podocytes. / Han, Sang Youb; Kang, Young Sun; Jee, Yi Hwa; Han, Kum Hyun; Cha, Dae-Ryong; Kang, Shin Wook; Han, Dae Suk.

In: Cell and Tissue Research, Vol. 323, No. 2, 01.02.2006, p. 321-332.

Research output: Contribution to journalArticle

Han, Sang Youb ; Kang, Young Sun ; Jee, Yi Hwa ; Han, Kum Hyun ; Cha, Dae-Ryong ; Kang, Shin Wook ; Han, Dae Suk. / High glucose and angiotensin II increase β1 integrin and integrin-linked kinase synthesis in cultured mouse podocytes. In: Cell and Tissue Research. 2006 ; Vol. 323, No. 2. pp. 321-332.
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AB - Alterations of integrin α3β1 may play a role in the development of diabetic nephropathy. We have investigated the effects of high glucose and angiotensin II on the expression of integrin α3 and β1, and whether these changes are associated with integrin-linked kinase (ILK) in cultured mouse podocytes. Integrin β1 and ILK mRNA expression and protein production were rapidly up-regulated in a dose-dependent manner by high glucose and angiotensin II stimulation. ILK mRNA levels in the mouse podocytes exposed to 30 mmol/1 glucose were 1.66, 1.89, and 1.28 times higher than those in control cells at 6, 24, and 72 h exposure, respectively. ILK mRNA levels in mouse podocytes exposed to 1 nM, 10 nM, and 100 nM angiotensin II for 6 h were 1.38, 1.55, and 1.93 times higher, respectively, than those in control cells. Angiotensin-II-induced integrin β1 and ILK mRNA expression was significantly inhibited by treatment with losartan (100 μM). In addition, the up-regulation of ILK synthesis induced by these stimuli was related to β1 integrin synthesis and increased ILK kinase activity. Cell adhesion assay displayed inhibitory effects when podocytes were exposed to high concentrations of angiotensin II. Interestingly, glucose and angiotensin II stimulation induced shrinkage of the cell body and elongation of the podocyte processes, a phenotype similar to that of immature podocytes. In addition, β1 integrin showed higher levels of staining on both the cell membranes and the cell-cell contact areas. Thus, high glucose and angiotensin II may affect the regulation of the integrin-ILK system in podocytes; this system may therefore play a role in the pathogenesis of diabetic nephropathy and other renal diseases affecting podocytes.

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