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5. TLR8 aggravates skin inflammation and fibrosis by activating skin fibroblasts in systemic sclerosis.

Author

Kong, Xiangzhen, Jiang, Shuai, He, Qiuyu, Shi, Xiangguang, Pu, Weilin, Huang, Yan, Ma, Yanyun, Liu, Qingmei, Sun, Dayan, Huang, Delin, Wu, Fei, Li, Pengcheng, Tu, Wenzhen, Zhao, Yinhuan, Wang, Lei, Chen, Yuanyuan, Wu, Wenyu, Tang, Yulong, Zhao, Xiansheng, and Zhu, Qing

Subjects
RESEARCH funding, PLASMIDS, TOLL-like receptors, IN vivo studies, CELLULAR signal transduction, SKIN, FIBROSIS, FIBROBLASTS, GENE expression, MICE, SYSTEMIC scleroderma, ANIMAL experimentation, RECOMBINANT proteins, INFLAMMATION, INTERLEUKINS
Abstract

Objectives Innate immunity significantly contributes to SSc pathogenesis. TLR8 is an important innate immune mediator that is implicated in autoimmunity and fibrosis. However, the expression, mechanism of action, and pathogenic role of TLR8 in SSc remain unclear. The aim of this study was to explore the roles and underlying mechanisms of TLR8 in SSc. Methods The expression of TLR8 was analysed, based on a public dataset, and then verified in skin tissues and skin fibroblasts of SSc patients. The role of TLR8 in inflammation and fibrosis was investigated using a TLR8-overexpression vector, activator (VTX-2337), inhibitor (cu-cpt-8m), and TLR8 siRNA in skin fibroblasts. The pathogenic role of TLR8 in skin inflammation and fibrosis was further validated in a bleomycin (BLM)-induced mouse skin inflammation and fibrosis model. Results TLR8 levels were significantly elevated in SSc skin tissues and myofibroblasts, along with significant activation of the TLR8 pathway. In vitro studies showed that overexpression or activation of TLR8 by a recombinant plasmid or VTX-2337 upregulated IL-6, IL-1β, COL I, COL III and α-SMA in skin fibroblasts. Consistently, both TLR8-siRNA and cu-cpt-8m reversed the phenotypes observed in TLR8-activating fibroblasts. Mechanistically, TLR8 induces skin fibrosis and inflammation in a manner dependent on the MAPK, NF-κB and SMAD2/3 pathways. Subcutaneous injection of cu-cpt-8m significantly alleviated BLM-induced skin inflammation and fibrosis in vivo. Conclusion TLR8 might be a promising therapeutic target for improving the treatment strategy for skin inflammation and fibrosis in SSc. [ABSTRACT FROM AUTHOR]

Published
2024
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8. TLR8 aggravates skin inflammation and fibrosis by activating skin fibroblasts in systemic sclerosis

Author

Kong, Xiangzhen, primary, Jiang, Shuai, additional, He, Qiuyu, additional, Shi, Xiangguang, additional, Pu, Weilin, additional, Huang, Yan, additional, Ma, Yanyun, additional, Liu, Qingmei, additional, Sun, Dayan, additional, Huang, Delin, additional, Wu, Fei, additional, Li, Pengcheng, additional, Tu, Wenzhen, additional, Zhao, Yinhuan, additional, Wang, Lei, additional, Chen, Yuanyuan, additional, Wu, Wenyu, additional, Tang, Yulong, additional, Zhao, Xiansheng, additional, Zhu, Qing, additional, Gao, Jian, additional, Xu, Weihong, additional, Shui, Xiaochuan, additional, Qian, Feng, additional, and Wang, Jiucun, additional

Published
2023
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10. Enhancement of Zyxin Promotes Skin Fibrosis by Regulating FAK/PI3K/AKT and TGF-β Signaling Pathways via Integrins

Author

Huang, Yan, primary, Zhao, Han, additional, Zhang, Yuting, additional, Tang, Yulong, additional, Shi, Xiangguang, additional, Jiang, Shuai, additional, Pu, Weilin, additional, Liu, Jing, additional, Ma, Yanyun, additional, Lin, Juiming, additional, Lin, Jinran, additional, Wu, Wenyu, additional, Gong, Yiyi, additional, Wang, Jiucun, additional, and Liu, Qingmei, additional

Published
2023
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11. CTHRC1+ fibroblasts are stimulated by macrophage‐secreted SPP1 to induce excessive collagen deposition in keloids

Author

Liu, Jing, primary, Huang, Yan, additional, Gong, Yiyi, additional, Liu, Qingmei, additional, Lin, Jinran, additional, Liu, Jianlan, additional, Liu, Mengguo, additional, Huang, Jia, additional, Pu, Weilin, additional, Ma, Yanyun, additional, Zhang, Yuting, additional, Li, Haiyang, additional, Shi, Xiangguang, additional, Zhang, Yue, additional, Wang, Jian, additional, Zhu, Yifei, additional, Wang, Qin, additional, Wei, Kelu, additional, Wang, Jiayi, additional, Sha, Yu'ou, additional, Wang, Jiucun, additional, and Wu, Wenyu, additional

Published
2022
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12. Insights into male androgenetic alopecia using comparative transcriptome profiling: hypoxia-inducible factor-1 and Wnt/β-catenin signalling pathways

Author

Liu, Qingmei, primary, Tang, Yulong, additional, Huang, Yan, additional, Wang, Ji’an, additional, Yang, Kai, additional, Zhang, Yuting, additional, Pu, Weilin, additional, Liu, Jing, additional, Shi, Xiangguang, additional, Ma, Yanyun, additional, Ni, Chunya, additional, Zhang, Yue, additional, Zhu, Yifei, additional, Li, Haiyang, additional, Wang, Jiucun, additional, Lin, Jinran, additional, and Wu, Wenyu, additional

Published
2022
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13. Disrupted citric acid metabolism inhibits hair growth

Author

Shi, Xiangguang, primary, Chen, Yahui, additional, Yang, Kai, additional, Zhu, Yifei, additional, Ma, Yanyun, additional, Liu, Qingmei, additional, Wang, Ji'an, additional, Ni, Chunya, additional, Zhang, Yue, additional, Li, Haiyang, additional, Lin, Jinran, additional, Wang, Jiucun, additional, and Wu, Wenyu, additional

Published
2022
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15. LDLR dysfunction induces LDL accumulation and promotes pulmonary fibrosis

Author

Shi, Xiangguang, primary, Chen, Yahui, additional, Liu, Qingmei, additional, Mei, Xueqian, additional, Liu, Jing, additional, Tang, Yulong, additional, Luo, Ruoyu, additional, Sun, Dayan, additional, Ma, Yanyun, additional, Wu, Wenyu, additional, Tu, Wenzhen, additional, Zhao, Yinhuan, additional, Xu, Weihong, additional, Ke, Yuehai, additional, Jiang, Shuai, additional, Huang, Yan, additional, Zhang, Rui, additional, Wang, Lei, additional, Chen, Yuanyuan, additional, Xia, Jingjing, additional, Pu, Weilin, additional, Zhu, Honglin, additional, Zuo, Xiaoxia, additional, Li, Yisha, additional, Xu, Jinhua, additional, Gao, Fei, additional, Wei, Dong, additional, Chen, Jingyu, additional, Yin, Wenguang, additional, Wang, Qingwen, additional, Dai, Huaping, additional, Yang, Libing, additional, Guo, Gang, additional, Cui, Jimin, additional, Song, Nana, additional, Zou, Hejian, additional, Zhao, Shimin, additional, Distler, Jörg H.W., additional, Jin, Li, additional, and Wang, Jiucun, additional

Published
2022
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16. Hair Growth-Promoting Effect of Resveratrol in Mice, Human Hair Follicles and Dermal Papilla Cells

Author

Zhang, Yuting, primary, Ni, Chunya, additional, Huang, Yan, additional, Tang, Yulong, additional, Yang, Kai, additional, Shi, Xiangguang, additional, Zhang, Yue, additional, Li, Zheng, additional, Wang, Ji’an, additional, Zhu, Yifei, additional, Li, Haiyang, additional, Ma, Yanyun, additional, Lin, Jinran, additional, Wang, Jiucun, additional, Liu, Qingmei, additional, and Wu, Wenyu, additional

Published
2021
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17. Increased Expression of Zyxin and Its Potential Function in Androgenetic Alopecia

Author

Liu, Qingmei, primary, Shi, Xiangguang, additional, Zhang, Yue, additional, Huang, Yan, additional, Yang, Kai, additional, Tang, Yulong, additional, Ma, Yanyun, additional, Zhang, Yuting, additional, Wang, Ji'an, additional, Zhang, Li, additional, Zhang, Qi, additional, Liu, Xiao, additional, Lin, Jinran, additional, Wang, Jiucun, additional, and Wu, Wenyu, additional

Published
2021
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18. Hair Growth Promoting Effects of 650 nm Red Light Stimulation on Human Hair Follicles and Study of Its Mechanisms via RNA Sequencing Transcriptome Analysis

Author

Yang, Kai, primary, Tang, Yulong, additional, Ma, Yanyun, additional, Liu, Qingmei, additional, Huang, Yan, additional, Zhang, Yuting, additional, Shi, Xiangguang, additional, Zhang, Li, additional, Zhang, Yue, additional, Wang, Ji'an, additional, Zhu, Yifei, additional, Liu, Wei, additional, Tan, Yimei, additional, Lin, Jinran, additional, and Wu, Wenyu, additional

Published
2021
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19. Increased Expression of Zyxin and its Potential Function in Androgenetic Alopecia

Author

Liu, Qingmei, Shi, Xiangguang, Zhang, Yue, Huang, Yan, Yang, Kai, Tang, Yulong, Ma, Yanyun, Zhang, Yuting, Wang, Ji'an, Zhang, Li, Liu, Xiao, Lin, Jinran, Wang, Jiucun, and Wu, Wenyu

Subjects
body regions, integumentary system, Androgenetic alopecia, Zyxin, Hair follicle, Dermal papilla cell, RNA-seq, reproductive and urinary physiology
Abstract

Androgenetic alopecia (AGA) is the most common progressive form of hair loss, occurring in more than half of men aged > 50 years. Hair follicle (HF) miniaturization is the feature of AGA and dermal papillae (DP) play key roles in hair growth and regeneration by regulating follicular cell activity. Previous studies revealed that adhesion signal was an important factor in AGA development. As an actin-interacting protein, Zyxin (ZYX) is essential for cell adhesion and migration. Therefore, the aim of this research is to investigate the expression and potential role of ZYX in AGA. We observed that ZYX expression was elevated in AGA patients’ affected frontal HF compared to the unaffected occipital HF by real-time PCR. Moreover, increased Zyxin expression was also seen within the DP using the immunofluorescence staining. Our in vivo results revealed that ZYX knockout mice showed enhanced hair growth and anagen entry compared with the wild type mice. Within the ex vivo cultured HFs, we found that reduced ZYX expression by siRNA enhanced the hair shaft production, delayed hair follicle catagen entry, increased the proliferation of dermal papilla cell (DPC) and expression of stem cell related proteins. These results were further validated in the cultured DPCs in vitro. To further reveal the mechanism that how ZYX contributes to AGA, RNA-seq analysis was carried out to find the distinct gene signatures upon ZYX siRNA treatment in cultured hair follicle. Multiple pathways, including focal adhesion and HIF-1 signaling pathways, were found to be involved. Collectively, we discovered the elevated expression of ZYX in AGA patients’ affected frontal hair follicle and revealed the effects of ZYX downregulation on in vivo mouse, ex vivo hair follicle and in vitro DPC. These data suggested ZYX might play important roles in the pathogenesis of AGA and stem cell properties of DPC, and might be a potential therapeutic target in AGA.

Published
2020
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21. Salvianolic acid B attenuates experimental pulmonary inflammation by protecting endothelial cells against oxidative stress injury

Author

Liu, Qingmei, primary, Shi, Xiangguang, additional, Tang, Luyan, additional, Xu, Weihong, additional, Jiang, Shuai, additional, Ding, Weifeng, additional, Feng, Qian, additional, Chu, Haiyan, additional, Ma, Yanyun, additional, Li, Yuan, additional, Lu, Jiaying, additional, Pu, Weilin, additional, Zhou, Xiaodong, additional, Jin, Li, additional, Wang, Jiucun, additional, and Wu, Wenyu, additional

Published
2018
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22. MiR-3606-3p inhibits systemic sclerosis through targeting TGF-β type II receptor

Author

Shi, Xiangguang, primary, Liu, Qingmei, additional, Li, Na, additional, Tu, Wenzhen, additional, Luo, Ruoyu, additional, Mei, Xueqian, additional, Ma, Yanyun, additional, Xu, Weihong, additional, Chu, Haiyan, additional, Jiang, Shuai, additional, Du, Zhimin, additional, Zhao, Han, additional, Zhao, Liang, additional, Jin, Li, additional, Wu, Wenyu, additional, and Wang, Jiucun, additional

Published
2018
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23. Erratum: Increased expression of latent TGF-β-binding protein 4 affects the fibrotic process in scleroderma by TGF-β/SMAD signaling

Author

Lu, Jiaying, primary, Liu, Qingmei, additional, Wang, Lei, additional, Tu, Wenzhen, additional, Chu, Haiyan, additional, Ding, Weifeng, additional, Jiang, Shuai, additional, Ma, Yanyun, additional, Shi, Xiangguang, additional, Pu, Weilin, additional, Zhou, Xiaodong, additional, Jin, Li, additional, Wang, Jiucun, additional, and Wu, Wenyu, additional

Published
2017
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24. Treatment effects of the traditional Chinese medicine Shenks in bleomycin-induced lung fibrosis through regulation of TGF-beta/Smad3 signaling and oxidative stress

Author

Chu, Haiyan, primary, Shi, Ying, additional, Jiang, Shuai, additional, Zhong, Qicheng, additional, Zhao, Yongqiang, additional, Liu, Qingmei, additional, Ma, Yanyun, additional, Shi, Xiangguang, additional, Ding, Weifeng, additional, Zhou, Xiaodong, additional, Cui, Jimin, additional, Jin, Li, additional, Guo, Gang, additional, and Wang, Jiucun, additional

Published
2017
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27. ACKR1+ Endothelial Cells Mediate Leukocyte Infiltration and Synergize with SFRP2/ASPN+ Fibroblasts to Promote Skin Fibrosis in Systemic Sclerosis.

Author

Huang Y, Pu W, Wang L, Ma Q, Ma Y, Liu Q, Jiang S, Zhao X, Zhang Y, He Q, Tang Y, Liu J, Lin JM, Shi X, Tu W, Chen Y, Lin J, Gong Y, Wu W, and Wang J

Abstract

Background: Skin fibrosis is the most typical pathological manifestation of systemic sclerosis (SSc) and localized scleroderma (LS) with unclear etiology and few effective treatments. Though excessive collagen secretion by fibroblasts is the primary cause of skin fibrosis, many lines of evidence suggested that vascular damage was the initiating event and various cell types along with fibroblasts worked together to contribute to the pathogenesis of skin fibrosis., Objectives: We sought to explore the relationships between vascular endothelial cell lesions and immune cell infiltration, along with the cell-cell interactions among various cell types within the fibrotic skin ecosystem., Methods: Single-cell RNA-seq (10x Genomics) was performed on skin biopsies of 3 healthy donors and 7 SSc patients in Chinese. The additional 3 localized scleroderma patients' data from NCBI database (GSE160536) were integrated by Harmony. CellChat package (v1.5.0) was applied to analyze cell communication network. Transwell assay and subcutaneous bleomycin (BLM) injection in mice were used to explore the role of ACKR1 on immune cell infiltration. Milo single-cell western blot was applied to show the activation of fibroblast subclusters., Results: A total of 62,295 cells were obtained and subpopulations of stromal and immune cells were identified. Interaction network analysis revealed that multiple chemokines secreted by macrophages, pericytes, and pro-inflammatory fibroblasts could bind with Duffy antigen/receptor for chemokines (ACKR1), which is highly expressed on ACKR1+ endothelial cells of lesion skin. Transwell assay revealed that over-expressed ACKR1 in HUVEC facilitated leukocyte infiltration under the treatment of IL8. The BLM mice showed enhanced ACKR1 expression, massive immune cell infiltration, and fibrosis in skin, which could be attenuated by ACKR1 inhibition. Furthermore, infiltrated macrophages with TGFB1 or PDGFB high production could activate SFRP2/ASPN+ fibroblasts to contribute to excessive accumulation of extracellular matrix (ECM), and the SOX4-ASPN axis plays an important role in the TGF-β signaling cascade and the etiology of skin fibrosis., Conclusions: Our results reveal that highly expressed ACKR1 in endothelial cells of fibrotic skin tissue promotes immune cell infiltration, and SFRP2/ASPN+ fibroblasts synergize to exacerbate skin fibrosis., (© The Author(s) 2024. Published by Oxford University Press on behalf of British Association of Dermatologists. All rights reserved. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact journals.permissions@oup.com.)

Published
2024
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28. Glycolytic reprogramming in cancer cells: PKM2 dimer predominance induced by pulsatile PFK-1 activity.

Author

Shi X, You L, and Luo RY

Subjects
Carrier Proteins metabolism, Cellular Reprogramming, HeLa Cells, Humans, Membrane Proteins metabolism, Phosphofructokinase-1, Muscle Type metabolism, Thyroid Hormones metabolism, Thyroid Hormone-Binding Proteins, Carrier Proteins genetics, Fructosediphosphates metabolism, Glycolysis, Membrane Proteins genetics, Phosphofructokinase-1, Muscle Type genetics, Thyroid Hormones genetics
Abstract

The glycolytic enzyme pyruvate kinase M2 (PKM2) exists in both catalytically inactive dimeric and active tetrameric forms. In cancer cells, PKM2 dimer predominance contributes to tumor growth by triggering glycolytic reprogramming. However, the mechanism that promotes PKM2 dimer predominance over tetramer in cancer cells remains elusive. Here, we show that pulsatile phosphofructokinase (PFK-1) activity results in PKM2 dimer predominance. Mathematical simulations predict that pulsatile PFK-1 activity prevents the formation of PKM2 tetramer even under high levels of fructose-1,6-bisphosphate (FBP), a PKM2 tetramer-promoting metabolite produced by PFK-1. We experimentally confirm these predictions at the single-molecule level by providing evidence for pulsatile PFK-1 activity-induced synchronized dissociation of PKM2 tetramers and the subsequent accumulation of PKM2 dimers under high levels of FBP in HeLa cells. Moreover, we show that pulsatile PFK-1 activity-induced PKM2 dimer predominance also controls cell proliferation. Thus, our study reveals the significance of pulsatile PFK-1 activity in cancer cell metabolism.

Published
2019
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