Wound Healing and Regenerative Medicine Research Program, Dr Phillip Frost Department of Dermatology and Cutaneous Surgery, University of Miami Miller School of Medicine, Miami, FL, USA.
Department of Cell, Molecular, and Developmental Biology, Sackler School of Graduate Biomedical Sciences, Tufts University, Boston, MA, USA.
Exp Dermatol. 2021 Aug;30(8):1065-1072. doi: 10.1111/exd.14405. Epub 2021 Jun 11.
Diabetic foot ulcers (DFUs), a prevalent complication of diabetes, constitute a major medical challenge with a critical need for development of cell-based therapies. We previously generated induced pluripotent stem cells (iPSCs) from dermal fibroblasts derived from the DFU patients, location-matched skin of diabetic patients and normal healthy donors and re-differentiated them into fibroblasts. To assess the epigenetic microRNA (miR) regulated changes triggered by cellular reprogramming, we performed miRs expression profiling. We found let-7c, miR-26b-5p, -29c-3p, -148a-3p, -196a-5p, -199b-5p and -374a-5p suppressed in iPSC-derived fibroblasts in vitro and in 3D dermis-like self-assembly tissue, whereas their corresponding targets involved in cellular migration were upregulated. Moreover, targets involved in organization of extracellular matrix were induced after fibroblast reprogramming. PLAT gene, the crucial fibrinolysis factor, was upregulated in iPSC-derived fibroblasts and was confirmed as a direct target of miR-196a-5p. miR-197-3p and miR-331-3p were found upregulated specifically in iPSC-derived diabetic fibroblasts, while their targets CAV1 and CDKN3 were suppressed. CAV1, an important negative regulator of wound healing, was confirmed as a direct miR-197-3p target. Together, our findings demonstrate that iPSC reprogramming is an effective approach for erasing the diabetic non-healing miR-mediated epigenetic signature and promoting a pro-healing cellular phenotype.
糖尿病足溃疡 (DFU) 是糖尿病的一种常见并发症,是一个重大的医学挑战,因此急需开发基于细胞的治疗方法。我们之前从 DFU 患者、糖尿病患者和正常健康供体的皮肤中生成了诱导多能干细胞 (iPSC),并将其重新分化为成纤维细胞。为了评估细胞重编程引发的表观遗传微小 RNA (miR) 调控变化,我们进行了 miR 表达谱分析。我们发现,let-7c、miR-26b-5p、-29c-3p、-148a-3p、-196a-5p、-199b-5p 和 -374a-5p 在体外和 3D 真皮样自组装组织中 iPSC 衍生的成纤维细胞中受到抑制,而其对应的参与细胞迁移的靶基因则上调。此外,细胞外基质组织的靶基因在成纤维细胞重编程后被诱导。PLAT 基因是关键的纤维蛋白溶解因子,在 iPSC 衍生的成纤维细胞中上调,并被证实是 miR-196a-5p 的直接靶基因。miR-197-3p 和 miR-331-3p 被发现特异性地上调在 iPSC 衍生的糖尿病成纤维细胞中,而它们的靶基因 CAV1 和 CDKN3 则被抑制。CAV1 是伤口愈合的重要负调控因子,被证实是 miR-197-3p 的直接靶基因。总之,我们的研究结果表明,iPSC 重编程是一种有效的方法,可以消除糖尿病非愈合 miR 介导的表观遗传特征,并促进有利于愈合的细胞表型。