Article
Biochemistry & Molecular Biology
Joon Seok Lee, Gyeong Hwa Kim, Jong Ho Lee, Jeong Yeop Ryu, Eun Jung Oh, Hyun Mi Kim, Suin Kwak, Keun Hur, Ho Yun Chung
Summary: In this study, miR-365a/b-3p was identified as a potential biomarker for hypertrophic scarring, suggesting its contribution to the formation of hypertrophic scars.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2022)
Article
Biotechnology & Applied Microbiology
Shuchen Gu, Xin Huang, Xiangwen Xu, Yunhan Liu, Yimin Khoong, Zewei Zhang, Haizhou Li, Yashan Gao, Tao Zan
Summary: The study confirmed the role of CSMD1 in hypertrophic scar and revealed that miR-190a-3p regulates fibroblast migration and FN1 secretion by targeting CSMD1. Furthermore, the knockdown of CSMD1 activated the JAK/STAT signaling pathway.
Article
Biochemistry & Molecular Biology
Hui Song Cui, So Young Joo, Seung Yeol Lee, Yoon Soo Cho, Dong Hyun Kim, Cheong Hoon Seo
Summary: It is unclear how scar fibroblasts (SFs) affect keratinocytes in hypertrophic scars (HTS) through cell-cell interaction. This study investigated the effects of HTS-derived exosomes on the proliferation and differentiation of normal human keratinocytes (NHKs) and compared them with normal fibroblasts (NFs).
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2023)
Article
Immunology
Hui Yu, Lei Qin, Yunzhi Peng, Wenhui Bai, Zhanli Wang
Summary: The study revealed that exosomes released from hypertrophic cardiomyocytes induced inflammatory responses in macrophages through miR-155, activating various signaling pathways, which may play a crucial role in the development of cardiac hypertrophy.
FRONTIERS IN IMMUNOLOGY
(2021)
Article
Medicine, Research & Experimental
Yun Li, Zhencheng Yu, Danyang Zhao, Dong Han
Summary: The study showed that corilagin has multiple effects on HSFs, including inhibition of collagen production, cell proliferation, cell migration, and suppression of HSF activation. Corilagin also significantly suppressed HS formation and collagen deposition in a rabbit ear scar model, as well as inhibited fibroblast proliferation and alpha-SMA expression in vivo. Additionally, western blot analysis revealed that corilagin downregulated the protein levels of TGF-beta 1 and TGF-beta receptor type I (TGF beta RI), thus affecting the levels of p-smad2/3, MMPs, and TIMP1.
Article
Biochemistry & Molecular Biology
Zun-jiang Zhao, De-jin Wu, Da-lun Lv, Bao-de Zhang, Lei Chen, Yin-qiao Sun
Summary: This study aimed to determine the role of ellagic acid (EA) in hypertrophic scar (HS) formation and its possible mechanism. In vitro experiments showed that EA inhibited the viability and migration of HS fibroblasts (HSFs), upregulated the expression of basic fibroblast growth factor (bFGF), and downregulated the expression of collagen-I (COL-I) and fibronectin 1 (FN1) in HSFs. Furthermore, EA prevented the activation of transforming growth factor (TGF)-beta/Smad signaling pathway in HSFs.
CHEMICAL BIOLOGY & DRUG DESIGN
(2023)
Article
Chemistry, Multidisciplinary
Sheng Meng, Qian Wei, Shengqiu Chen, Xi Liu, Shengnan Cui, Qilin Huang, Ziqiang Chu, Kui Ma, Wenhua Zhang, Wenzhi Hu, Shiyi Li, Zihao Wang, Lige Tian, Zhiliang Zhao, Haihong Li, Xiaobing Fu, Cuiping Zhang
Summary: This study provides a promising and effective exosome@DMNA-based miRNA delivery strategy for the treatment of hypertrophic scars. miR-141-3p is identified as an inhibitor of hypertrophic scar fibroblasts by targeting the TGF-beta 2/Smad pathway. The engineered exosomes encapsulating miR-141-3p show the same inhibitive effects and are delivered using dissolvable microneedle arrays for sustained release. This strategy effectively reduces the thickness of hypertrophic scars and improves tissue structure.
Article
Biochemistry & Molecular Biology
Hui Song Cui, Dong Hyun Kim, So Young Joo, Yoon Soo Cho, June-Bum Kim, Cheong Hoon Seo
Summary: In this study, it was found that exosomes derived from hypertrophic scar fibroblasts can change fibrosis-related signaling pathways in normal fibroblasts, leading to increased cell proliferation, migration, and epithelial-mesenchymal transition, as well as increased expression of fibronectin, type I collagen, and type III collagen.
ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS
(2022)
Article
Cell Biology
Yuhao Zhao, Lei Du, Jiali Sun, Xuelian Wang, Zhilei Cong, Shuyan Chen, Fei Wang, Zhen Li
Summary: Endothelial-to-mesenchymal transition (EndMT) plays a role in idiopathic pulmonary fibrosis, while exosomes derived from human umbilical cord mesenchymal stem cells (hucMSC-Exos) have shown potential as a treatment for organ fibrosis. This study found that intravenous administration of hucMSC-Exos alleviated pulmonary fibrosis and restored endothelial properties weakened by TGF-beta. The mechanism involves exosomal miR-218 inhibiting EndMT through the MeCP2/BMP2 pathway.
CELL BIOLOGY AND TOXICOLOGY
(2023)
Article
Biochemistry & Molecular Biology
Ya Gao, Yangdan Liu, Danning Zheng, Chiakang Ho, Dongsheng Wen, Jiaming Sun, Lu Huang, Yuxin Liu, Qingfeng Li, Yifan Zhang
Summary: This study reveals the overexpression of HDAC5 in hypertrophic scars and its depletion can inhibit scar formation. Knockdown of HDAC5 downregulates Smad2/3 phosphorylation in the TGF-8 signaling pathway and increases Smad7 expression. Moreover, HDAC5 interacts with MEF2A to suppress its binding to the Smad7 promoter region, resulting in repression of Smad7 promoter activity. Luciferase reporter assays and ChIP-qPCR assays confirmed this mechanism.
INTERNATIONAL JOURNAL OF BIOLOGICAL SCIENCES
(2022)
Article
Biochemistry & Molecular Biology
Sebastian P. Nischwitz, Julia Fink, Marlies Schellnegger, Hanna Luze, Vladimir Bubalo, Carolin Tetyczka, Eva Roblegg, Christian Holecek, Martin Zacharias, Lars-Peter Kamolz, Petra Kotzbeck
Summary: Persistent inflammation during wound healing is identified as a precipitating factor in the development of hypertrophic scars. However, lack of standardized models and limited evidence for therapeutic approaches hinder research progress. This study aimed to investigate scar formation mechanisms and develop a method for generating standardized hypertrophic scars through prolonged inflammation.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2023)
Article
Biochemistry & Molecular Biology
Jinling Zhang, Yong Wang
Summary: The study showed that TGF-beta 2 might alter the expression of miRNAs in EVs derived from HTMCs, potentially contributing to the pathogenesis of POAG. These findings could provide valuable information for the diagnosis and treatment of POAG.
DNA AND CELL BIOLOGY
(2021)
Article
Dermatology
Binyu Song, Yuhan Zhu, Ying Zhao, Kai Wang, Yixuan Peng, Lin Chen, Zhou Yu, Baoqiang Song
Summary: Our study identifies distinct fibroblast subpopulations in hypertrophic scars (HS) and establishes a diagnostic and predictive model using machine learning algorithms and deep learning. We have identified key genes associated with HS and demonstrated the role of THBS2 in its formation and development.
INTERNATIONAL WOUND JOURNAL
(2023)
Article
Chemistry, Medicinal
Qiannan Li, Chunming Lyu, Daqin Chen, Wanling Cai, Fang Kou, Qiang Li, Hai Wei, Huimin Zhang
Summary: This study investigates the potential efficacy and mechanism of gallic acid (GA) on hypertrophic scars (HS). GA ointments were applied to rabbit ear HS models for 28 days, and the results show that GA effectively suppresses HS formation and reduces fibroblast infiltration and scar thickness. Moreover, GA downregulates the expression of relevant signaling pathways, providing evidence for its efficacy in treating HS and revealing potential pharmacological mechanisms.
Article
Genetics & Heredity
Kakeru Hisakane, Masahiro Seike, Teppei Sugano, Kuniko Matsuda, Takeru Kashiwada, Shinji Nakamichi, Masaru Matsumoto, Akihiko Miyanaga, Rintaro Noro, Kaoru Kubota, Akihiko Gemma
Summary: The study found that serum-derived exosomal miR-125a-3p can predict the efficacy of anti-PD-1/PD-L1 monoclonal antibody treatment in NSCLC patients. High expression of miR-125a-3p is associated with reduced progression-free and overall survival. Cell experiments also demonstrated that this miRNA regulates PD-L1 expression by suppressing neuregulin 1 (NRG1).