Cui Hui Song, Zheng Ya Xin, Cho Yoon Soo, Ro Yu Mi, Kwak In Suk, Joo So Young, Seo Cheong Hoon
Burn Institute, Department of Rehabilitation Medicine, Hangang Sacred Heart Hospital, College of Medicine, Hallym University, 94-200 Yeong-deungpo-Dong, Yeongdeungpo-Ku, Seoul 07247, Republic of Korea.
Department of Rehabilitation Medicine, Hangang Sacred Heart Hospital, College of Medicine, Hallym University, 94-200 Yeong-deungpo-Dong, Yeongdeungpo-Ku, Seoul 07247, Republic of Korea.
Int J Mol Sci. 2025 Jun 19;26(12):5876. doi: 10.3390/ijms26125876.
Methionine restriction (MetR) is a common adjuvant treatment for cancer. However, studies of MetR have paid little attention to its potential implications for fibrosis. Hypertrophic scarring (HTS) is an abnormal fibrotic response after burn trauma that results from the excessive activation of fibroblasts. Because of the absence of a fully effective pharmacological treatment, HTS frequently causes great annoyance in patients as a common sequela of burns. To date, the effects of MetR on hypertrophic scar fibroblasts (HTSFs) remain unclear. This study aimed to investigate the anti-fibrotic effects of MetR and explore the associated alterations in signaling pathways in HTSFs. We isolated HTSFs from post-burn HTS tissues and cultured them in a specially prepared MetR medium. Cell and immunocytochemical staining images were captured using light and fluorescence microscopes, respectively. Cell proliferation was evaluated using a CellTiter-Glo Luminescent Cell Viability Assay Kit. mRNA and protein expression levels were determined using quantitative reverse transcription polymerase chain reaction and Western blotting, respectively. In HTSFs, MetR reduced cellular inflammation; downregulated multiple signaling pathways, including the TGF-β-SMAD, STAT, and AKT/mTOR pathways; and upregulated MAPKs. Furthermore, MetR arrested the cell cycle, promoted apoptosis, suppressed cell proliferation and migration, and reduced extracellular matrix protein secretion, thereby exerting multifaceted inhibitory effects on HTS. Our results demonstrated that MetR can inhibit scars' formation and suggest that regulating methionine metabolism in the scar environment may help treat scars.
蛋氨酸限制(MetR)是一种常见的癌症辅助治疗方法。然而,关于MetR的研究很少关注其对纤维化的潜在影响。肥厚性瘢痕(HTS)是烧伤创伤后一种异常的纤维化反应,由成纤维细胞过度激活引起。由于缺乏完全有效的药物治疗,HTS作为烧伤的常见后遗症,经常给患者带来极大困扰。迄今为止,MetR对肥厚性瘢痕成纤维细胞(HTSFs)的影响仍不清楚。本研究旨在探讨MetR的抗纤维化作用,并探索HTSFs中信号通路的相关变化。我们从烧伤后HTS组织中分离出HTSFs,并在特制的MetR培养基中培养。分别使用光学显微镜和荧光显微镜拍摄细胞和免疫细胞化学染色图像。使用CellTiter-Glo发光细胞活力检测试剂盒评估细胞增殖。分别使用定量逆转录聚合酶链反应和蛋白质免疫印迹法测定mRNA和蛋白质表达水平。在HTSFs中,MetR减轻细胞炎症;下调多种信号通路,包括TGF-β-SMAD、STAT和AKT/mTOR通路;上调丝裂原活化蛋白激酶(MAPKs)。此外,MetR使细胞周期停滞,促进细胞凋亡,抑制细胞增殖和迁移,并减少细胞外基质蛋白分泌,从而对HTS发挥多方面的抑制作用。我们的结果表明,MetR可以抑制瘢痕形成,并提示调节瘢痕环境中的蛋氨酸代谢可能有助于治疗瘢痕。