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Journal articles on the topic 'Fibroblast activation'

Author: Grafiati

Published: 4 June 2021

Last updated: 26 July 2025

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1

Caporarello, Nunzia, Jeffrey A. Meridew, Dakota L. Jones та ін. "PGC1α repression in IPF fibroblasts drives a pathologic metabolic, secretory and fibrogenic state". Thorax 74, № 8 (2019): 749–60. http://dx.doi.org/10.1136/thoraxjnl-2019-213064.

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Idiopathic pulmonary fibrosis (IPF) is a fatal ageing-related disease linked to mitochondrial dysfunction. The present study aimed to determine whether peroxisome proliferator activated receptor gamma co-activator 1-alpha (PPARGC1A, encoding PGC1α), a master regulator of mitochondrial biogenesis, is diminished in IPF and controls pathologic fibroblast activation. Primary human IPF, control lung fibroblasts and fibroblasts sorted from bleomycin-injured mice were used to evaluate the expression and function of PGC1α. In vitro PGC1α manipulation was performed by small interfering RNA knockdown or

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Cai, Zhou, Hua Guo, Jing Qian та ін. "Effects of bone morphogenetic protein 4 on TGF-β1-induced cell proliferation, apoptosis, activation and differentiation in mouse lung fibroblasts via ERK/p38 MAPK signaling pathway". PeerJ 10 (27 липня 2022): e13775. http://dx.doi.org/10.7717/peerj.13775.

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Fibroblasts, in particular myofibroblasts, are the critical effector cells in idiopathic pulmonary fibrosis (IPF), a deadly lung disease characterized by abnormal lung remodeling and the formation of “fibroblastic foci”. Aberrant activation of TGF-β1 is frequently encountered and promotes fibroblast proliferation, activation, and differentiation in pulmonary fibrosis. Hence, the inhibition of TGF-β1-induced lung fibroblast activation holds promise as a therapeutic strategy for IPF. The present study aimed to investigate the potential effect and underlying mechanisms of bone morphogenetic prote

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Xin, Yanguo, Wenchao Wu, Jing Qu, et al. "Inhibition of Mitofusin-2 Promotes Cardiac Fibroblast Activation via the PERK/ATF4 Pathway and Reactive Oxygen Species." Oxidative Medicine and Cellular Longevity 2019 (April 16, 2019): 1–16. http://dx.doi.org/10.1155/2019/3649808.

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Mitofusin-2 (Mfn2) is a key outer mitochondrial membrane protein, which maintains normal mitochondrial dynamics and function. However, its role in cardiac fibroblast activation remains poorly understood. In the present study, a rat model of transverse aortic constriction (TAC) was established to observe the cardiac fibroblast activation in vivo. TGF-β1 treatment for 24 hours was used to induce cardiac fibroblast activation in vitro. As a result, the expression of Mfn2 decreased in the hypertrophic heart tissues and cardiac fibroblasts treated with TGF-β1. siMfn2 and adenovirus were applied to

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Liu, Fei, David Lagares, Kyoung Moo Choi, et al. "Mechanosignaling through YAP and TAZ drives fibroblast activation and fibrosis." American Journal of Physiology-Lung Cellular and Molecular Physiology 308, no. 4 (2015): L344—L357. http://dx.doi.org/10.1152/ajplung.00300.2014.

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Pathological fibrosis is driven by a feedback loop in which the fibrotic extracellular matrix is both a cause and consequence of fibroblast activation. However, the molecular mechanisms underlying this process remain poorly understood. Here we identify yes-associated protein (YAP) (homolog of drosophila Yki) and transcriptional coactivator with PDZ-binding motif (TAZ) (also known as Wwtr1), transcriptional effectors of the Hippo pathway, as key matrix stiffness-regulated coordinators of fibroblast activation and matrix synthesis. YAP and TAZ are prominently expressed in fibrotic but not health

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Heng, Madalene. "Phosphorylase Kinase Inhibition Therapy in Burns and Scalds." BioDiscovery 20 (February 24, 2017): e11207. https://doi.org/10.3897/biodiscovery.20.e11207.

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Severe burns and scalds almost always result in unsightly hypertrophic scarring. Among the important processes involved in scarring are fibroblast formation and transformation of fibroblasts into myofibroblasts. Myofibroblasts contain α-smooth muscle actin which has contractile properties and can lead to wound contraction and hypertrophic scarring. Phosphorylase kinase (PhK), expressed within 5 mins of injury, is among the earliest enzymes released after tissue damage. It is responsible for activation of NF-kB, which in turn activates over 200 different genes related to inflammation, fibroblas

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Aravamudhan, Aja, Andrew J. Haak, Kyoung Moo Choi, et al. "TBK1 regulates YAP/TAZ and fibrogenic fibroblast activation." American Journal of Physiology-Lung Cellular and Molecular Physiology 318, no. 5 (2020): L852—L863. http://dx.doi.org/10.1152/ajplung.00324.2019.

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Idiopathic pulmonary fibrosis (IPF) results in scarring of the lungs by excessive extracellular matrix (ECM) production. Resident fibroblasts are the major cell type involved in ECM deposition. The biochemical pathways that facilitate pathological fibroblast activation leading to aberrant ECM deposition are not fully understood. Tank binding protein kinase-1 (TBK1) is a kinase that regulates multiple signaling pathways and was recently identified as a candidate regulator of fibroblast activation in a large-scale small-interfering RNA (siRNA) screen. To determine the effect of TBK1 on fibroblas

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Tang, Rui, Yung-Chun Wang, Xiaohan Mei, et al. "LncRNA GAS5 attenuates fibroblast activation through inhibiting Smad3 signaling." American Journal of Physiology-Cell Physiology 319, no. 1 (2020): C105—C115. http://dx.doi.org/10.1152/ajpcell.00059.2020.

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Transforming growth factor-β (TGF-β)-induced fibroblast activation is a key pathological event during tissue fibrosis. Long noncoding RNA (lncRNA) is a class of versatile gene regulators participating in various cellular and molecular processes. However, the function of lncRNA in fibroblast activation is still poorly understood. In this study, we identified growth arrest-specific transcript 5 (GAS5) as a novel regulator for TGF-β-induced fibroblast activation. GAS5 expression was downregulated in cultured fibroblasts by TGF-β and in resident fibroblasts from bleomycin-treated skin tissues. Ove

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Stauffer, Winston T., Erik A. Blackwood, Khalid Azizi, Randal J. Kaufman, and Christopher C. Glembotski. "The ER Unfolded Protein Response Effector, ATF6, Reduces Cardiac Fibrosis and Decreases Activation of Cardiac Fibroblasts." International Journal of Molecular Sciences 21, no. 4 (2020): 1373. http://dx.doi.org/10.3390/ijms21041373.

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Activating transcription factor-6 α (ATF6) is one of the three main sensors and effectors of the endoplasmic reticulum (ER) stress response and, as such, it is critical for protecting the heart and other tissues from a variety of environmental insults and disease states. In the heart, ATF6 has been shown to protect cardiac myocytes. However, its roles in other cell types in the heart are unknown. Here we show that ATF6 decreases the activation of cardiac fibroblasts in response to the cytokine, transforming growth factor β (TGFβ), which can induce fibroblast trans-differentiation into a myofib

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Margulis, Alexander, Karl H. Nocka, Nancy L. Wood, Stanley F. Wolf, Samuel J. Goldman, and Marion T. Kasaian. "MMP dependence of fibroblast contraction and collagen production induced by human mast cell activation in a three-dimensional collagen lattice." American Journal of Physiology-Lung Cellular and Molecular Physiology 296, no. 2 (2009): L236—L247. http://dx.doi.org/10.1152/ajplung.90462.2008.

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Mast cell-fibroblast interactions may contribute to fibrosis in asthma and other disease states. Fibroblast contraction is known to be stimulated by coculture with the human mast cell line, HMC-1, or by mast cell-derived agents. Matrix metalloproteinases (MMPs) can also mediate contraction, but the MMP-dependence of mast cell-induced fibroblast contractility is not established, and the consequences of mast cell activation within the coculture system have not been fully explored. We demonstrate that activation of primary human mast cells (pHMC) with IgE receptor cross-linking, or activation of

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Cheng, Maye F., Faizah S. Abdullah, and Matthew B. Buechler. "Essential growth factor receptors for fibroblast homeostasis and activation." F1000Research 13 (February 19, 2024): 120. http://dx.doi.org/10.12688/f1000research.143514.1.

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Fibroblasts are cells of mesenchymal origin that are found throughout the body. While these cells have several functions, their integral roles include maintaining tissue architecture through the production of key extracellular matrix components, and participation in wound healing after injury. Fibroblasts are also key mediators in disease progression during fibrosis, cancer, and other inflammatory diseases. Under these perturbed states, fibroblasts can activate into inflammatory fibroblasts or contractile myofibroblasts. Fibroblasts require various growth factors and mitogenic molecules for su

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11

Ye, Chen, Hui Tang, Zheng Zhao, et al. "MDM2 mediates fibroblast activation and renal tubulointerstitial fibrosis via a p53-independent pathway." American Journal of Physiology-Renal Physiology 312, no. 4 (2017): F760—F768. http://dx.doi.org/10.1152/ajprenal.00528.2016.

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It is well recognized that murine double minute gene 2 (MDM2) plays a critical role in cell proliferation and inflammatory processes during tumorigenesis. It is also reported that MDM2 is expressed in glomeruli and involved in podocyte injury. However, whether MDM2 is implicated in renal fibrosis remains unclear. Here we investigated the role of MDM2 in tubulointerstitial fibrosis (TIF). By immunohistochemical staining and Western blotting we confirmed that MDM2 is upregulated in the tubulointerstitial compartment in patients with TIF and unilateral urethral obstruction (UUO) mice, which mainl

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Dorbala, Sharmila. "Fibroblast Activation." JACC: Cardiovascular Imaging 15, no. 11 (2022): 1971–73. http://dx.doi.org/10.1016/j.jcmg.2022.08.019.

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Woodley, Joe P., Daniel W. Lambert, and Ilida Ortega Asencio. "Reduced Fibroblast Activation on Electrospun Polycaprolactone Scaffolds." Bioengineering 10, no. 3 (2023): 348. http://dx.doi.org/10.3390/bioengineering10030348.

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In vivo, quiescent fibroblasts reside in three-dimensional connective tissues and are activated in response to tissue injury before proliferating rapidly and becoming migratory and contractile myofibroblasts. When deregulated, chronic activation drives fibrotic disease. Fibroblasts cultured on stiff 2D surfaces display a partially activated phenotype, whilst many 3D environments limit fibroblast activation. Cell mechanotransduction, spreading, polarity, and integrin expression are controlled by material mechanical properties and micro-architecture. Between 3D culture systems, these features ar

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Wei, Juan, Junhui Zhan, Hui Ji, et al. "Fibroblast Upregulation of Vitamin D Receptor Represents a Self-Protective Response to Limit Fibroblast Proliferation and Activation during Pulmonary Fibrosis." Antioxidants 12, no. 8 (2023): 1634. http://dx.doi.org/10.3390/antiox12081634.

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Dysregulation of vitamin D receptor (VDR) is implicated in chronic obstructive pulmonary disease. However, whether VDR dysregulation contributes to the development of pulmonary fibrosis remains largely unknown. Analysis of bulk and single-cell RNA profiling datasets revealed VDR upregulation in lung fibroblasts from patients with pulmonary fibrosis or fibrotic mice, which was validated in lung fibroblasts from bleomycin-exposed mice and bleomycin-treated fibroblasts. Stable VDR knockdown promoted, whereas the VDR agonist paricalcitol suppressed lung fibroblast proliferation and activation. Gen

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Wang, S., H. Zhang, and X. Zhao. "DOP90 Amphiregulin promotes colitis-associated intestinal fibrosis through activation of PI3K/AKT signaling in Intestinal fibroblasts." Journal of Crohn's and Colitis 18, Supplement_1 (2024): i243. http://dx.doi.org/10.1093/ecco-jcc/jjad212.0130.

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Abstract Background Intestinal fibrosis is one of the most threatening complications of Crohn’s disease (CD). Amphiregulin (AREG) expression is increased in patients with CD with fibrosis. Methods The role of AREG in activating intestinal fibroblasts and driving fibrogenesis is largely unexplored. In this study, fibrotic and nonfibrotic tissues were obtained from CD patients undergoing surgical resection while normal intestinal tissues were obtained from patients with diverticulum of small intestine. Fibrosis index score for fibrosis were assessed by Masson staining. AREG, collagen Ⅰ and α-SMA

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Alam, Perwez, Sara M. Stiens, Hunter J. Bowles, Hieu Bui та Douglas K. Bowles. "Yoda1 Inhibits TGFβ-Induced Cardiac Fibroblast Activation via a BRD4-Dependent Pathway". Cells 14, № 13 (2025): 1028. https://doi.org/10.3390/cells14131028.

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Fibrosis represents a pivotal pathological process in numerous diseases, characterized by excessive deposition of extracellular matrix (ECM) that disrupts normal tissue architecture and function. In the heart, cardiac fibrosis significantly impairs both structural integrity and functional capacity, contributing to the progression of heart failure. Central to this process are cardiac fibroblasts (CFs), which, upon activation, differentiate into contractile myofibroblasts, driving pathological ECM accumulation. Transforming growth factor-beta (TGFβ) is a well-established regulator of fibroblast

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Pang, Maoyin, Jagan Kothapally, Haiping Mao, et al. "Inhibition of histone deacetylase activity attenuates renal fibroblast activation and interstitial fibrosis in obstructive nephropathy." American Journal of Physiology-Renal Physiology 297, no. 4 (2009): F996—F1005. http://dx.doi.org/10.1152/ajprenal.00282.2009.

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Activation of renal interstitial fibroblasts is critically involved in the development of tubulointerstitial fibrosis in chronic kidney diseases. In this study, we investigated the effect of trichostatin A (TSA), a specific histone deacetylase (HDAC) inhibitor, on the activation of renal interstitial fibroblasts in a rat renal interstitial fibroblast line (NRK-49F) and the development of renal fibrosis in a murine model of unilateral ureteral obstruction (UUO) . α-Smooth muscle actin (α-SMA) and fibronectin, two hallmarks of fibroblast activation, were highly expressed in cultured NRK-49F cell

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Researcher. "FIBROBLAST ACTIVATION AND EXTRACELLULAR MATRIX DEPOSITION IN THE PATHOGENESIS OF INTESTINAL FIBROSIS IN CROHN'S DISEASE AND EMERGING ANTIFIBROTIC THERAPIES." International Journal of Medical Gastroenterology (IJMG) 3, no. 1 (2025): 1–7. https://doi.org/10.5281/zenodo.14792135.

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Intestinal fibrosis is a severe complication of Crohn’s Disease (CD), characterized by excessive deposition of the extracellular matrix (ECM) and fibroblast activation. Persistent inflammation in CD leads to the activation of fibroblasts, which contribute to ECM deposition and tissue stiffening, eventually causing intestinal strictures. Despite extensive research, effective antifibrotic therapies remain elusive. However, recent advances in molecular understanding and targeted therapies have shown promise in modulating fibroblast activity and ECM deposition. This paper explores the role o

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Eguchi, Akito, Ryan Coleman, Kenneth Gresham, et al. "GRK5 is a regulator of fibroblast activation and cardiac fibrosis." Proceedings of the National Academy of Sciences 118, no. 5 (2021): e2012854118. http://dx.doi.org/10.1073/pnas.2012854118.

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Pathological remodeling of the heart is a hallmark of chronic heart failure (HF) and these structural changes further perpetuate the disease. Cardiac fibroblasts are the critical cell type that is responsible for maintaining the structural integrity of the heart. Stress conditions, such as a myocardial infarction (MI), can activate quiescent fibroblasts into synthetic and contractile myofibroblasts. G protein-coupled receptor kinase 5 (GRK5) is an important mediator of cardiovascular homeostasis through dampening of GPCR signaling, and is expressed in the heart and up-regulated in human HF. Of

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Matilla, Lara, Vanessa Arrieta, Eva Jover, et al. "Soluble St2 Induces Cardiac Fibroblast Activation and Collagen Synthesis via Neuropilin-1." Cells 9, no. 7 (2020): 1667. http://dx.doi.org/10.3390/cells9071667.

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Circulating levels of soluble interleukin 1 receptor-like 1 (sST2) are increased in heart failure and associated with poor outcome, likely because of the activation of inflammation and fibrosis. We investigated the pathogenic role of sST2 as an inductor of cardiac fibroblasts activation and collagen synthesis. The effects of sST2 on human cardiac fibroblasts was assessed using proteomics and immunodetection approaches to evidence the upregulation of neuropilin-1 (NRP-1), a regulator of the profibrotic transforming growth factor (TGF)-β1. In parallel, sST2 increased fibroblast activation, colla

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Jiao, Baihai, Changlong An, Hao Du, et al. "STAT6 Deficiency Attenuates Myeloid Fibroblast Activation and Macrophage Polarization in Experimental Folic Acid Nephropathy." Cells 10, no. 11 (2021): 3057. http://dx.doi.org/10.3390/cells10113057.

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Renal fibrosis is a pathologic feature of chronic kidney disease, which can lead to end-stage kidney disease. Myeloid fibroblasts play a central role in the pathogenesis of renal fibrosis. However, the molecular mechanisms pertaining to myeloid fibroblast activation remain to be elucidated. In the present study, we examine the role of signal transducer and activator of transcription 6 (STAT6) in myeloid fibroblast activation, macrophage polarization, and renal fibrosis development in a mouse model of folic acid nephropathy. STAT6 is activated in the kidney with folic acid nephropathy. Compared

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Rauber, S., H. Mohammadian, M. G. Raimondo, et al. "POS0040 SILENCING OF JOINT FIBROBLAST TO PROTECT FROM JOINT DAMAGE." Annals of the Rheumatic Diseases 82, Suppl 1 (2023): 229.2–229. http://dx.doi.org/10.1136/annrheumdis-2023-eular.6425.

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BackgroundDespite significant progress in the development of targeted biologic therapies for the treatment of chronic inflammatory joint diseases such as rheumatoid arthritis or psoriatic arthritis, more than 40% of patients still record gradual loss of joint function, mostly because of failure to archive complete remission. Herein, persistent joint fibroblast activity leads to continuous destruction of the joint, whereas its inhibition/silencing prevents joint damage despite presence of a residual inflammation[1]. Persistent activation of the joint fibroblasts leads to destruction of the join

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Li, Ningning, Zhan Wang, Tao Sun, Yanfei Lei, Xianghua Liu, and Zhenzhen Li. "Apigenin Alleviates Renal Fibroblast Activation through AMPK and ERK Signaling Pathways In Vitro." Current Pharmaceutical Biotechnology 21, no. 11 (2020): 1107–18. http://dx.doi.org/10.2174/1389201021666200320140908.

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Objective: Renal fibrosis is a common pathway leading to the progression of chronic kidney disease. Activated fibroblasts contribute remarkably to the development of renal fibrosis. Although apigenin has been demonstrated to play a protective role from fibrotic diseases, its pharmacological effect on renal fibroblast activation remains largely unknown. Materials and Methods: Here, we examined the functional role of apigenin in the activation of renal fibroblasts response to transforming growth factor (TGF)-β1 and its potential mechanisms. Cultured renal fibroblasts (NRK-49F) were exposed to ap

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Shen, Yan, Lei Jiang, Ping Wen, et al. "Tubule-derived lactate is required for fibroblast activation in acute kidney injury." American Journal of Physiology-Renal Physiology 318, no. 3 (2020): F689—F701. http://dx.doi.org/10.1152/ajprenal.00229.2019.

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Acute kidney injury (AKI) is a highly prevalent medical syndrome associated with high mortality and morbidity. Several types of cells, including epithelial cells, vascular endothelial cells, pericytes, and macrophages, participate in the development of AKI. Recently, renal fibroblasts were found to play an important role in the regulation of tubular injury, repair, and recovery after AKI. However, the mechanisms underlying fibroblast activation and proliferation during the progression of AKI remain unclear. In the present study, we found many activated myofibroblasts located in the renal inter

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Kim, Jihee, Bomi Kim, Soo Kim, et al. "Hypoxia-Induced Epithelial-To-Mesenchymal Transition Mediates Fibroblast Abnormalities via ERK Activation in Cutaneous Wound Healing." International Journal of Molecular Sciences 20, no. 10 (2019): 2546. http://dx.doi.org/10.3390/ijms20102546.

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Previous studies described the involvement of extracellular signal-related kinase (ERK) in systemic fibrotic diseases, but the role of ERK in cutaneous scarring is unknown. Although hypoxia drives tissue fibrosis by activating hypoxia-inducible factor-1α (HIF-1α), the specific roles of hypoxia and associated ERK phosphorylation in abnormal fibroblast activity during cutaneous scarring are unclear. Here, we investigated whether pathologic myofibroblast-like keloid fibroblast activity is promoted by hypoxia-induced epithelial–mesenchymal transition mediated by ERK activation. ERK phosphorylation

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Rinne, Andreas, and Florentina Pluteanu. "Ca2+ Signaling in Cardiovascular Fibroblasts." Biomolecules 14, no. 11 (2024): 1365. http://dx.doi.org/10.3390/biom14111365.

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Fibrogenesis is a physiological process required for wound healing and tissue repair. It is induced by activation of quiescent fibroblasts, which first proliferate and then change their phenotype into migratory, contractile myofibroblasts. Myofibroblasts secrete extracellular matrix proteins, such as collagen, to form a scar. Once the healing process is terminated, most myofibroblasts undergo apoptosis. However, in some tissues, such as the heart, myofibroblasts remain active and sensitive to neurohumoral factors and inflammatory mediators, which lead eventually to excessive organ fibrosis. Ma

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Ivey, Malina J., Jill T. Kuwabara, Kara L. Riggsbee та Michelle D. Tallquist. "Platelet-derived growth factor receptor-α is essential for cardiac fibroblast survival". American Journal of Physiology-Heart and Circulatory Physiology 317, № 2 (2019): H330—H344. http://dx.doi.org/10.1152/ajpheart.00054.2019.

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Platelet-derived growth factor receptor α (PDGFRα), a receptor tyrosine kinase required for cardiac fibroblast development, is uniquely expressed by fibroblasts in the adult heart. Despite the consensus that PDGFRα is expressed in adult cardiac fibroblasts, we know little about its function when these cells are at rest. Here, we demonstrate that loss of PDGFRα in cardiac fibroblasts resulted in a rapid reduction of resident fibroblasts. Furthermore, we observe that phosphatidylinositol 3-kinase signaling was required for PDGFRα-dependent fibroblast maintenance. Interestingly, this reduced numb

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Liu, Rui, Hui Li, Liang Liu, Jinpu Yu, and Xiubao Ren. "Fibroblast activation protein." Cancer Biology & Therapy 13, no. 3 (2012): 123–29. http://dx.doi.org/10.4161/cbt.13.3.18696.

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Pablos, José L., Patricia E. Carreira, Lourdes Serrano, Pedro Del Castillo, and Juan J. Gomez-Reino. "Apoptosis and Proliferation of Fibroblasts During Postnatal Skin Development and Scleroderma in the Tight-skin Mouse." Journal of Histochemistry & Cytochemistry 45, no. 5 (1997): 711–19. http://dx.doi.org/10.1177/002215549704500509.

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Tight-skin (Tsk) is a dominant gene mutation that causes a fibrotic skin disease in mice, similar to human scleroderma. Both conditions are characterized by increased numbers of dermal fibroblasts containing high levels of procollagen mRNA. Whether this fibroblast population arises from fibroblast growth or fibroblast transcriptional activation is debated. Proliferation and apoptosis of fibroblasts of normal and Tsk mice were studied in skin sections before, at onset, and in established fibrosis. Tissue sections were immunostained with proliferating cell nuclear antigen (PCNA) as proliferation

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Chu, Han, Wei Wang, Wei Luo, et al. "CircHECTD1 mediates pulmonary fibroblast activation via HECTD1." Therapeutic Advances in Chronic Disease 10 (January 2019): 204062231989155. http://dx.doi.org/10.1177/2040622319891558.

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Background: Circular RNA (circRNA), a new class of noncoding RNA, has been shown to be important in silicosis due to its unique role as a transcription regulator or as a sponge of small RNA regulators. Here, the mechanisms underlying circHECTD1/HECTD1 in fibroblast activation and subsequent fibrosis induced by SiO2 were investigated. Methods: Primary human pulmonary fibroblasts (HPF-a) were utilized, combined with quantitative real-time PCR (qRT-PCR) and fluorescence in situ hybridization (FISH) assays. LC3B-LV-RFP lentivirus was used to evaluate the role of autophagy. The CRISPR/Cas9 system w

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Zhang, Yun, Lichong Shen, Honglin Zhu та ін. "PGC-1α regulates autophagy to promote fibroblast activation and tissue fibrosis". Annals of the Rheumatic Diseases 79, № 9 (2020): 1227–33. http://dx.doi.org/10.1136/annrheumdis-2020-216963.

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ObjectivesCoactivators are a heterogeneous family of transcriptional regulators that are essential for modulation of transcriptional outcomes and fine-tune numerous cellular processes. The aim of the present study was to evaluate the role of the coactivator peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α) in the pathogenesis of systemic sclerosis (SSc).MethodsExpression of PGC-1α was analysed by real-time PCR, western blot and immunofluorescence. Modulation of autophagy was analysed by reporter studies by expression of autophagy-related genes. The effects of PGC-1α knoc

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Zhou, X., T. Trinh-Minh, C. Tran Manh, et al. "AB0130 DEREGULATION OF TFAM EXPRESSION PROMOTES MITOCHONDRIAL DAMAGE AND FIBROBLAST ACTIVATION IN SYSTEMIC SCLEROSIS." Annals of the Rheumatic Diseases 81, Suppl 1 (2022): 1195.1–1195. http://dx.doi.org/10.1136/annrheumdis-2022-eular.2085.

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BackgroundTranscription factor A, mitochondrial (TFAM) is a transcription factor with essential function in the mitochondrial homeostasis, such as mitochondria biogenesis and mtDNA replication. Deregulation of TFAM expression has been linked to mitochondrial dysfunction. However, its role in the pathogenesis of rheumatic diseases has not been studied so far.ObjectivesWe aimed to study the role of TFAM in the pathological fibroblast activation in SSc.MethodsThe expression of TFAM in SSc skin fibroblast and skin biopsies was analyzed by immunofluorescence and Western blot. The role of TFAM in fi

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Kalekar, Lokesh A., Jarish N. Cohen, Nicolas Prevel, et al. "Regulatory T cells in skin are uniquely poised to suppress profibrotic immune responses." Science Immunology 4, no. 39 (2019): eaaw2910. http://dx.doi.org/10.1126/sciimmunol.aaw2910.

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At the center of fibrosing diseases is the aberrant activation of tissue fibroblasts. The cellular and molecular mechanisms of how the immune system augments fibroblast activation have been described; however, little is known about how the immune system controls fibroblast function in tissues. Here, we identify regulatory T cells (Tregs) as important regulators of fibroblast activation in skin. Bulk cell and single-cell analysis of Tregs in murine skin and lungs revealed that Tregs in skin are transcriptionally distinct and skewed toward T helper 2 (TH2) differentiation. When compared with Tre

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Heinzelmann, Katharina, Mareike Lehmann, Michael Gerckens, et al. "Cell-surface phenotyping identifies CD36 and CD97 as novel markers of fibroblast quiescence in lung fibrosis." American Journal of Physiology-Lung Cellular and Molecular Physiology 315, no. 5 (2018): L682—L696. http://dx.doi.org/10.1152/ajplung.00439.2017.

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Fibroblasts play an important role in lung homeostasis and disease. In lung fibrosis, fibroblasts adopt a proliferative and migratory phenotype, with increased expression of α-smooth muscle actin (αSMA) and enhanced secretion of extracellular matrix components. Comprehensive profiling of fibroblast heterogeneity is limited because of a lack of specific cell-surface markers. We have previously profiled the surface proteome of primary human lung fibroblasts. Here, we sought to define and quantify a panel of cluster of differentiation (CD) markers in primary human lung fibroblasts and idiopathic

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Liang, M., and J. H. W. Distler. "POS0477 ATTENUATION OF FIBROBLAST ACTIVATION AND FIBROSIS BY ADROPIN IN A HEDGEHOG-DEPENDENT MANNER." Annals of the Rheumatic Diseases 81, Suppl 1 (2022): 493.1–493. http://dx.doi.org/10.1136/annrheumdis-2022-eular.2061.

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BackgroundAdropin is a secretory protein encoded by the energy homeostasis-associated (ENHO) gene. Emerging evidence indicate its role in metabolism and energy homeostasis, which is known to be deregulated in SSc. However, adropin/ENHO has not been linked to the pathogenesis of fibrosis, tissue remodeling or fibroblast activation so far.ObjectivesThe aim of the current study was to investigate the role of adropin/ENHO in the pathogenesis of fibroblast activation and fibrosis in SSc.MethodsMachine learning and bioinformatics models were used to identify candidate genes regulating fibroblast act

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Huang, Steven, Scott H. Wettlaufer, Cory Hogaboam, David M. Aronoff, and Marc Peters-Golden. "Prostaglandin E2 inhibits collagen expression and proliferation in patient-derived normal lung fibroblasts via E prostanoid 2 receptor and cAMP signaling." American Journal of Physiology-Lung Cellular and Molecular Physiology 292, no. 2 (2007): L405—L413. http://dx.doi.org/10.1152/ajplung.00232.2006.

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Uncontrolled fibroblast activation is one of the hallmarks of fibrotic lung disease. Prostaglandin E2 (PGE2) has been shown to inhibit fibroblast migration, proliferation, collagen deposition, and myofibroblast differentiation in the lung. Understanding the mechanisms for these effects may provide insight into the pathogenesis of fibrotic lung disease. Previous work has focused on commercially available fibroblast cell lines derived from tissue whose precise origin and histopathology are often unknown. Here, we sought to define the mechanism of PGE2 inhibition in patient-derived fibroblasts fr

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Tang, Ri, Yang Zhou, Shuya Mei, et al. "Fibrotic extracellular vesicles contribute to mechanical ventilation-induced pulmonary fibrosis development by activating lung fibroblasts via JNK signalling pathway: an experimental study." BMJ Open Respiratory Research 10, no. 1 (2023): e001753. http://dx.doi.org/10.1136/bmjresp-2023-001753.

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AbstractRecent research has revealed that mechanical ventilation (MV) could initiate ventilator-induced lung injury along with the initiation of the process of pulmonary fibrosis (PF), leading to MV-induced PF (MVPF). However, the underlying mechanism remains unclear. This study aimed to explore the role of MV-induced extracellular vesicles (MV-EVs) and the c-Jun N-terminal kinase (JNK) signalling pathway in the pathogenesis of MVPF in vivo and in vitro. The process of MV is accompanied by the secretion of MV-EVs, which could induce lung fibroblast activation. Furthermore, single-cell RNA-sequ

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Marinković, Aleksandar, Justin D. Mih, Jin-Ah Park, Fei Liu та Daniel J. Tschumperlin. "Improved throughput traction microscopy reveals pivotal role for matrix stiffness in fibroblast contractility and TGF-β responsiveness". American Journal of Physiology-Lung Cellular and Molecular Physiology 303, № 3 (2012): L169—L180. http://dx.doi.org/10.1152/ajplung.00108.2012.

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Lung fibroblast functions such as matrix remodeling and activation of latent transforming growth factor-β1 (TGF-β1) are associated with expression of the myofibroblast phenotype and are directly linked to fibroblast capacity to generate force and deform the extracellular matrix. However, the study of fibroblast force-generating capacities through methods such as traction force microscopy is hindered by low throughput and time-consuming procedures. In this study, we improved at the detail level methods for higher-throughput traction measurements on polyacrylamide hydrogels using gel-surface-bou

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Chen, Po-Yuan, Neng-Lang Shih, Wen-Rui Hao, Chun-Chao Chen, Ju-Chi Liu, and Li-Chin Sung. "Inhibitory Effects of Momordicine I on High-Glucose-Induced Cell Proliferation and Collagen Synthesis in Rat Cardiac Fibroblasts." Oxidative Medicine and Cellular Longevity 2018 (October 8, 2018): 1–11. http://dx.doi.org/10.1155/2018/3939714.

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Diabetes-associated cardiac fibrosis is a severe cardiovascular complication. Momordicine I, a bioactive triterpenoid isolated from bitter melon, has been demonstrated to have antidiabetic properties. This study investigated the effects of momordicine I on high-glucose-induced cardiac fibroblast activation. Rat cardiac fibroblasts were cultured in a high-glucose (25 mM) medium in the absence or presence of momordicine I, and the changes in collagen synthesis, transforming growth factor-β1 (TGF-β1) production, and related signaling molecules were assessed. Increased oxidative stress plays a cri

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Ishii, Kenichiro, Izumi Matsuoka, Takeshi Sasaki, et al. "Loss of Fibroblast-Dependent Androgen Receptor Activation in Prostate Cancer Cells is Involved in the Mechanism of Acquired Resistance to Castration." Journal of Clinical Medicine 8, no. 9 (2019): 1379. http://dx.doi.org/10.3390/jcm8091379.

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Loss of androgen receptor (AR) dependency in prostate cancer (PCa) cells is associated with progression to castration-resistant prostate cancer (CRPC). The tumor stroma is enriched in fibroblasts that secrete AR-activating factors. To investigate the roles of fibroblasts in AR activation under androgen deprivation, we used three sublines of androgen-sensitive LNCaP cells (E9 and F10 cells: low androgen sensitivity; and AIDL cells: androgen insensitivity) and original fibroblasts derived from patients with PCa. We performed in vivo experiments using three sublines of LNCaP cells and original fi

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Akers, Ian A., Maddy Parsons, Michael R. Hill, et al. "Mast cell tryptase stimulates human lung fibroblast proliferation via protease-activated receptor-2." American Journal of Physiology-Lung Cellular and Molecular Physiology 278, no. 1 (2000): L193—L201. http://dx.doi.org/10.1152/ajplung.2000.278.1.l193.

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Mast cells play a potentially important role in fibroproliferative diseases, releasing mediators including tryptase that are capable of stimulating fibroblast proliferation and procollagen synthesis. The mechanism by which tryptase stimulates fibroblast proliferation is unclear, although recent studies suggest it can activate protease-activated receptor (PAR)-2. We therefore investigated the role of PAR-2 in tryptase-induced proliferation of human fetal lung and adult lung parenchymal and airway fibroblasts and, for comparative purposes, adult dermal fibroblasts. Tryptase (0.7–70 mU/ml) induce

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Jara, Paul, Jazmin Calyeca, Yair Romero, et al. "Matrix metalloproteinase (MMP)-19-deficient fibroblasts display a profibrotic phenotype." American Journal of Physiology-Lung Cellular and Molecular Physiology 308, no. 6 (2015): L511—L522. http://dx.doi.org/10.1152/ajplung.00043.2014.

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Idiopathic pulmonary fibrosis (IPF) is a progressive and usually lethal interstitial lung disease of unknown etiology characterized by aberrant activation of epithelial cells that induce the migration, proliferation and activation of fibroblasts. The resulting distinctive fibroblastic/myofibroblastic foci are responsible for the excessive extracellular matrix (ECM) production and abnormal lung remodeling. We have recently found that matrix metalloproteinase 19 (MMP-19)-deficient ( Mmp19−/−) mice develop an exaggerated bleomycin-induced lung fibrosis, but the mechanisms are unclear. In this stu

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Zhu, Yu, Chao Yu, and Shougang Zhuang. "Protein arginine methyltransferase 1 mediates renal fibroblast activation and fibrogenesis through activation of Smad3 signaling." American Journal of Physiology-Renal Physiology 318, no. 2 (2020): F375—F387. http://dx.doi.org/10.1152/ajprenal.00487.2019.

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Protein arginine methyltransferase 1 (PRMT1), which primarily causes asymmetric arginine methylation of histone and nonhistone proteins, has been found to activate gene expression and mediate multiple pathological processes. Its role in renal fibrosis, however, remains unclear. In the present study, we observed that PRMT1 and its specific epigenetic marker, asymmetric di-methylated histone 4 arginine 3 (H4R3Me2a), were highly expressed in cultured renal interstitial fibroblasts. Treatment of PRMT1 with AMI-1, a selective inhibitor of PRMT1, or silencing PRMT1 with siRNA inhibited serum-induced

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Huang, Yingying, Sufang Zhou, Yong Huang, et al. "Isolation of Fibroblast-Activation Protein-Specific Cancer-Associated Fibroblasts." BioMed Research International 2017 (2017): 1–8. http://dx.doi.org/10.1155/2017/4825108.

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The current study is to develop a gentle and efficient method for purification of fibroblast-activation protein positive (FAP+) cancer-associated fibroblasts (CAFs) from tumor tissues. Fresh tissues were isolated from BALB/c-Nude mice bearing human liver cancer cell line (HepG2), fully minced and separated into three parts, and digested with trypsin digestion and then treated with collagenase type IV once, twice, or thrice, respectively. Finally, the cells were purified by using FAP magnetic beads. The isolated CAFs were grown in culture medium and detected for the surface expression of fibrob

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Bergmann, Christina, Amelie Brandt, Benita Merlevede, et al. "The histone demethylase Jumonji domain-containing protein 3 (JMJD3) regulates fibroblast activation in systemic sclerosis." Annals of the Rheumatic Diseases 77, no. 1 (2017): 150–58. http://dx.doi.org/10.1136/annrheumdis-2017-211501.

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ObjectivesSystemic sclerosis (SSc) fibroblasts remain activated even in the absence of exogenous stimuli. Epigenetic alterations are thought to play a role for this endogenous activation. Trimethylation of histone H3 on lysine 27 (H3K27me3) is regulated by Jumonji domain-containing protein 3 (JMJD3) and ubiquitously transcribed tetratricopeptide repeat on chromosome X (UTX) in a therapeutically targetable manner. The aim of this study was to explore H3K27me3 demethylases as potential targets for the treatment of fibrosis.MethodsJMJD3 was inactivated by small interfering RNA-mediated knockdown

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Owen, Jasmine S., Aled Clayton, and Helen B. Pearson. "Cancer-Associated Fibroblast Heterogeneity, Activation and Function: Implications for Prostate Cancer." Biomolecules 13, no. 1 (2022): 67. http://dx.doi.org/10.3390/biom13010067.

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The continuous remodeling of the tumor microenvironment (TME) during prostate tumorigenesis is emerging as a critical event that facilitates cancer growth, progression and drug-resistance. Recent advances have identified extensive communication networks that enable tumor–stroma cross-talk, and emphasized the functional importance of diverse, heterogeneous stromal fibroblast populations during malignant growth. Cancer-associated fibroblasts (CAFs) are a vital components of the TME, which mediate key oncogenic events including angiogenesis, immunosuppression, metastatic progression and therapeut

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Qian, W., Y. Li, and W. Zhu. "P055 Exosomal miR-103a-3p from Crohn’s creeping fat-derived ASCs contributes to intestinal fibrosis by targeting TGFBR3 and activating fibroblasts." Journal of Crohn's and Colitis 17, Supplement_1 (2023): i222. http://dx.doi.org/10.1093/ecco-jcc/jjac190.0185.

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Abstract Background Mesenteric adipose tissue hypertrophy is a hallmark of Crohn’s disease (CD), and creeping fat (CF) is unique to CD. Adipose-derived stem cells (ASCs) from inflammatory status exhibited altered biological functions. The role of ASCs isolated from CF in intestinal fibrosis and the potential mechanism remains unclear. Methods ASCs were isolated from CF (CF-ASCs) and disease unaffected mesenteric adipose tissue (Ctrl-ASCs) of patients with CD. A series of in vitro and in vivo experiments were conducted to study the effects of exosomes from CF-ASCs (CF-Exos) on intestinal fibros

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Nemeth, Julia, Wioletta Skronska-Wasek, Sophie Keppler, et al. "Adiponectin suppresses stiffness-dependent, pro-fibrotic activation of lung fibroblasts." American Journal of Physiology-Lung Cellular and Molecular Physiology, August 6, 2024. http://dx.doi.org/10.1152/ajplung.00037.2024.

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Idiopathic pulmonary fibrosis (IPF) is a progressive, irreversible respiratory disease with limited therapeutic options. A hallmark of IPF is excessive fibroblast activation and extracellular matrix (ECM) deposition. The resulting increase in tissue stiffness amplifies fibroblast activation and drives disease progression. Dampening stiffness-dependent activation of fibroblasts could slow disease progression. We performed an unbiased, next generation sequencing (NGS) screen to identify signaling pathways involved in stiffness-dependent lung fibroblast activation. Adipocytokine signaling was dow

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Tuleta, Izabela, Anis Hanna, Claudio Humeres та ін. "Fibroblast-specific TGF-β signaling mediates cardiac dysfunction, fibrosis, and hypertrophy in obese diabetic mice". Cardiovascular Research, 7 жовтня 2024. http://dx.doi.org/10.1093/cvr/cvae210.

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Abstract Aims Transforming growth factor (TGF)-β is up-regulated in the diabetic myocardium and may mediate fibroblast activation. We aimed at examining the role of TGF-β-induced fibroblast activation in the pathogenesis of diabetic cardiomyopathy. Methods and results We generated lean and obese db/db mice with fibroblast-specific loss of TbR2, the Type 2 receptor-mediating signaling through all three TGF-β isoforms, and mice with fibroblast-specific Smad3 disruption. Systolic and diastolic function, myocardial fibrosis, and hypertrophy were assessed. Transcriptomic studies and in vitro experi

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Lee, Ye-Ji, Minsuk Kim, Hee-Sun Kim, and Jihee Lee Kang. "Administration of Gas6 attenuates lung fibrosis via inhibition of the epithelial-mesenchymal transition and fibroblast activation." Cell Biology and Toxicology 40, no. 1 (2024). http://dx.doi.org/10.1007/s10565-024-09858-5.

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AbstractThe epithelial-mesenchymal transition (EMT) and fibroblast activation are major events in idiopathic pulmonary fibrosis pathogenesis. Here, we investigated whether growth arrest-specific protein 6 (Gas6) plays a protective role in lung fibrosis via suppression of the EMT and fibroblast activation. rGas6 administration inhibited the EMT in isolated mouse ATII cells 14 days post-BLM treatment based on morphologic cellular alterations, changes in mRNA and protein expression profiles of EMT markers, and induction of EMT-activating transcription factors. BLM-induced increases in gene expres

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