Abstract
One of the major complications in diabetes is impaired wound healing. Unfortunately, effective therapies are currently lacking. Epithelial to mesenchymal transition (EMT) is a critical process involved in cutaneous wound healing. In response to injury, EMT is required to activate and mobilize stationary keratinocytes in the skin toward the wound bed, which allows for re-epithelialization. This process is stalled in diabetic wounds. In this study, we investigate the role of long non-coding RNA (lncRNA), MALAT1, in transforming growth factor beta 1(TGF-β1)-induced EMT of human keratinocyte (HaCaT) cells. Initially, we detected MALAT1 and TGF-β1 expression in non-diabetic and diabetic wounds and found that these expression are significantly up-regulated in diabetic wounds. Then, HaCaT cells were cultured and exposed to TGF-β1. The EMT of HaCaT cells were confirmed by the increased expression of CDH2, KRT10, and ACTA2, in addition to the down-regulation of CDH1. Knockdown of MALAT1 was achieved by transfecting a small interfering RNA (SiRNA). MALAT1 silencing attenuates TGFβ1-induced EMT. Mechanistically, MALAT1 is involved in TGF-β1 mediated EMT through significantly induced ZEB1 expression, a critical transcription factor for EMT. In summary, lncRNA MALAT1 is involved in TGFβ1-induced EMT of human HaCaT cells and provides new understanding for the pathogenesis of diabetic wounds.
Highlights
TGF-β1 and metastasisassociated lung adenocarcinoma transcript 1 (MALAT1) Expression Is Significantly Higher in Diabetic Wounds
We compared the expression of TGF-β1 and MALAT1 in non-diabetic and diabetic wounds at day 3 and day 7 after injury
Results from Realtime qPCR showed that the expression of TGF-β1 and MALAT1 were significantly up-regulated in diabetic wounds compared to non-diabetic wounds at both day 3 and day 7 after injury (Figure 1)
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. It is currently estimated that the number of diabetic patients will reach approximately 700 million by the year 2045 [1]. Diabetic complications, including that of impaired wound healing, represent a significant medical problem in society today. The annual cost of diabetic lower extremity ulcers alone exceeds 1.5 billion dollars annually [2]. More than one-third of diabetic patients suffer from diabetic foot ulcers(DFU) [1], which are known to be the number one cause of non-traumatic lower extremity amputation. Despite the enormous impact of these chronic wounds on both individuals and society, effective therapies are lacking at the current time
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