Diabetes, as a fast growing non-communicable disease, is one of the major health problems of the twenty-first century. Several complications such as cardiovascular disease and renal failure are accompanying diabetes. The chronic cutaneous wound is another diabetes complication, results from the reduced body healing potential. At genome level, diabetic wound environment displays disorganized gene functions emphasizing the critical role of gene regulatory networks in the control of chronic wound repair. MicroRNAs, major regulators of gene activity, have been shown to be impaired in several pathological conditions such as chronic wounds. A reason behind that can be sought in the impaired activity of enzymes involved in the development and production of miRNAs. In current study, streptozocin-induced diabetic rats and non-diabetic controls were used to study the effect of diabetes on Dicer presence in wound environment. Unwounded skin of diabetic animals showed significantly lower level of Dicer expression compared with non-diabetic animal-derived skin. However, at day 7 post-wounding, diabetic animal-derived wounds contained a higher level of Dicer expression compared with non-diabetic ones. Parallel to these findings, the granulation tissue formation and wound closure are impaired in diabetic wounds. This study highlights the dysregulated presence of Dicer at different stages of the diabetic cutaneous wound.
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