To characterize a streptozotocin-induced diabetic porcine model of full-thickness wound healing and compare transcriptomic differences between diabetic and non-diabetic wounds.
Approach:
Diabetes Induction: Diabetes was induced in Yucatan minipigs via intravenous infusion of STZ, followed by a maturation period and creation of full-thickness skin wounds.
Wound Healing Assessment: Wound area was measured over 10 days, and differences in inflammation, granulation tissue formation, and re-epithelialization were assessed.
Transcriptomic Analysis: Bulk RNA sequencing was performed on diabetic and non-diabetic wounds to identify differential gene expression.
Key Findings:
Diabetic wounds exhibited significant delays in wound closure and contraction compared to non-diabetic wounds.
A total of 1015 genes showed differential expression between diabetic and non-diabetic wounds, with notable pathways related to metabolism, inflammation, and oxidative stress.
Increased immune cell infiltration and dysregulated immune responses were observed in diabetic wounds.
Oxidative stress markers were elevated in diabetic wounds, indicating increased DNA oxidative damage.
Interpretation:
Limitations:
The study was conducted on a limited number of animals, which may affect the generalizability of the findings.
The early time point of assessment may not capture the full spectrum of wound healing processes.
Conclusion:
The study provides insights into the molecular mechanisms underlying impaired wound healing in diabetes, emphasizing the relevance of the porcine model for future therapeutic research.
