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Article

Partial deletion of the ROCK2 protein fails to reduce renal fibrosis in a unilateral ureteral obstruction model in mice

  • Authors:
    • Itsuko Baba
    • Yasuhiro Egi
    • Kazuo Suzuki
  • View Affiliations / Copyright

    Affiliations: Pharmacology Research Laboratories II, Research Division, Mitsubishi Tanabe Pharma Corporation, Toda‑Shi, Saitama 335‑8505, Japan
  • Pages: 231-236
    |
    Published online on: November 16, 2015
       https://doi.org/10.3892/mmr.2015.4569
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Abstract

Renal fibrosis is a well‑known cause for the progression of chronic kidney disease. Rho/Rho‑associated coiled‑coil kinase (ROCK) signaling is involved in renal fibrotic processes. Non‑selective ROCK1/2 inhibitors have been reported to reduce renal interstitial fibrosis in a rodent unilateral ureteral obstruction (UUO) model. To clarify the role and contribution of ROCK2 in renal fibrosis, the present study used ROCK2 heterozygous knockout (HKO) mice to assess collagen deposition and fibrosis‑associated gene expression in the kidney of the UUO model. In the ROCK2 HKO mice, the expression level of ROCK2 in the normal kidney was half of that in the kidney of wild‑type (WT) mice. The expression levels of ROCK1 in the ROCK2 HKO mice and WT mice were equivalent. Furthermore, in the ROCK2 HKO and the WT mice, the hydroxyproline content and the gene expression levels of collagen I and transforming growth factor‑β1 in the obstructed kidneys were augmented following UUO. By contrast, the mRNA expression of α‑smooth muscle actin decreased in the ROCK2 HKO mice, compared with that in the WT mice. The activity of ROCK in the obstructed kidneys, indicated by the phosphorylation of myosin phosphatase target subunit‑1, which is a non‑selective substrate of ROCK1 and ROCK2, was equivalent among the ROCK2 HKO and WT mice. In conclusion, no differences in renal interstitial fibrosis or UUO‑induced ROCK activity were identified between the ROCK2 HKO and WT mice, indicating that the genetic partial disruption of ROCK2 is insufficient for protecting against renal fibrosis.
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Copy and paste a formatted citation
Spandidos Publications style
Baba I, Egi Y and Suzuki K: Partial deletion of the ROCK2 protein fails to reduce renal fibrosis in a unilateral ureteral obstruction model in mice. Mol Med Rep 13: 231-236, 2016.
APA
Baba, I., Egi, Y., & Suzuki, K. (2016). Partial deletion of the ROCK2 protein fails to reduce renal fibrosis in a unilateral ureteral obstruction model in mice. Molecular Medicine Reports, 13, 231-236. https://doi.org/10.3892/mmr.2015.4569
MLA
Baba, I., Egi, Y., Suzuki, K."Partial deletion of the ROCK2 protein fails to reduce renal fibrosis in a unilateral ureteral obstruction model in mice". Molecular Medicine Reports 13.1 (2016): 231-236.
Chicago
Baba, I., Egi, Y., Suzuki, K."Partial deletion of the ROCK2 protein fails to reduce renal fibrosis in a unilateral ureteral obstruction model in mice". Molecular Medicine Reports 13, no. 1 (2016): 231-236. https://doi.org/10.3892/mmr.2015.4569
Copy and paste a formatted citation
x
Spandidos Publications style
Baba I, Egi Y and Suzuki K: Partial deletion of the ROCK2 protein fails to reduce renal fibrosis in a unilateral ureteral obstruction model in mice. Mol Med Rep 13: 231-236, 2016.
APA
Baba, I., Egi, Y., & Suzuki, K. (2016). Partial deletion of the ROCK2 protein fails to reduce renal fibrosis in a unilateral ureteral obstruction model in mice. Molecular Medicine Reports, 13, 231-236. https://doi.org/10.3892/mmr.2015.4569
MLA
Baba, I., Egi, Y., Suzuki, K."Partial deletion of the ROCK2 protein fails to reduce renal fibrosis in a unilateral ureteral obstruction model in mice". Molecular Medicine Reports 13.1 (2016): 231-236.
Chicago
Baba, I., Egi, Y., Suzuki, K."Partial deletion of the ROCK2 protein fails to reduce renal fibrosis in a unilateral ureteral obstruction model in mice". Molecular Medicine Reports 13, no. 1 (2016): 231-236. https://doi.org/10.3892/mmr.2015.4569
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