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Article

Akt/hypoxia-inducible factor-1α signaling deficiency compromises skin wound healing in a type 1 diabetes mouse model

  • Authors:
    • Lifeng Jing
    • Shuang Li
    • Qin Li
  • View Affiliations / Copyright

    Affiliations: Graduate School of Southern Medical University, Guangzhou, Guangdong 510515, P.R. China, Department of Plastic Surgery, General Hospital of Guangzhou Military Command, Guangzhou, Guangdong 510010, P.R. China
  • Pages: 2141-2146
    |
    Published online on: March 30, 2015
       https://doi.org/10.3892/etm.2015.2394
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Abstract

The aim of the present study was to investigate the mechanisms for impaired skin wound healing in subjects with diabetes. Type 1 diabetes (T1DM) was induced in BALB/c mice using streptozotocin. One month after the establishment of the T1DM mouse model, a wound was formed on the back of the mice, and tissues from the wounds and the margins were collected on days 0, 3, 7 and 10. Protein levels of cluster of differentiation 31 (CD31) were detected using immunohistochemistry, and the mRNA levels of Akt, hypoxia‑inducible factor‑1α (Hif‑1α), vascular endothelial growth factor (Vegf), VEGF receptor 2 (Vegfr2), stromal cell‑derived growth factor‑1α (Sdf‑1α) and CXC chemokine receptor 4 (Cxcr4) were determined using reverse transcription‑quantitative polymerase chain reaction analysis. The corresponding protein levels were determined using western blotting. The skin wound healing rate in the T1DM mice was significantly lower than that in the control mice, and the protein level of CD31 in the wounded skin of the T1DM mice was significantly decreased. Furthermore, the overall mRNA levels of Akt, Hif‑1α, Vegf, Vegfr2, Sdf‑1α and Cxcr4 in the T1DM mice were significantly lower than those in the control mice, and similar trends were observed in the protein levels. In conclusion, skin wound healing was impaired in the T1DM mice, and this may have been caused by a deficiency of Akt/HIF‑1α and downstream signaling, as well as delayed angiogenesis.
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Copy and paste a formatted citation
Spandidos Publications style
Jing L, Li S and Li Q: Akt/hypoxia-inducible factor-1α signaling deficiency compromises skin wound healing in a type 1 diabetes mouse model. Exp Ther Med 9: 2141-2146, 2015.
APA
Jing, L., Li, S., & Li, Q. (2015). Akt/hypoxia-inducible factor-1α signaling deficiency compromises skin wound healing in a type 1 diabetes mouse model. Experimental and Therapeutic Medicine, 9, 2141-2146. https://doi.org/10.3892/etm.2015.2394
MLA
Jing, L., Li, S., Li, Q."Akt/hypoxia-inducible factor-1α signaling deficiency compromises skin wound healing in a type 1 diabetes mouse model". Experimental and Therapeutic Medicine 9.6 (2015): 2141-2146.
Chicago
Jing, L., Li, S., Li, Q."Akt/hypoxia-inducible factor-1α signaling deficiency compromises skin wound healing in a type 1 diabetes mouse model". Experimental and Therapeutic Medicine 9, no. 6 (2015): 2141-2146. https://doi.org/10.3892/etm.2015.2394
Copy and paste a formatted citation
x
Spandidos Publications style
Jing L, Li S and Li Q: Akt/hypoxia-inducible factor-1α signaling deficiency compromises skin wound healing in a type 1 diabetes mouse model. Exp Ther Med 9: 2141-2146, 2015.
APA
Jing, L., Li, S., & Li, Q. (2015). Akt/hypoxia-inducible factor-1α signaling deficiency compromises skin wound healing in a type 1 diabetes mouse model. Experimental and Therapeutic Medicine, 9, 2141-2146. https://doi.org/10.3892/etm.2015.2394
MLA
Jing, L., Li, S., Li, Q."Akt/hypoxia-inducible factor-1α signaling deficiency compromises skin wound healing in a type 1 diabetes mouse model". Experimental and Therapeutic Medicine 9.6 (2015): 2141-2146.
Chicago
Jing, L., Li, S., Li, Q."Akt/hypoxia-inducible factor-1α signaling deficiency compromises skin wound healing in a type 1 diabetes mouse model". Experimental and Therapeutic Medicine 9, no. 6 (2015): 2141-2146. https://doi.org/10.3892/etm.2015.2394
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