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https://www.readbyqxmd.com/read/28804544/sirt3-attenuates-angii-induced-cardiac-fibrosis-by-inhibiting-myofibroblasts-transdifferentiation-via-stat3-nfatc2-pathway
#1
Xiaobin Guo, Fangying Yan, Jingyuan Li, Chunmei Zhang, Peili Bu
Cardiac fibrosis is a maladaptive response to various stresses, characterized by increased interstitial collagen deposition and progressive cardiac dysfunction. The transdifferentiation of fibroblasts into myofibroblasts is an essential process in the pathogenesis of cardiac fibrosis. SIRT3, as a mitochondrial NAD(+)-dependent histone deacetylase, has been demonstrated beneficial in many cardiovascular diseases. However, the specific mechanism of its protective role in cardiac fibrosis needs to be elucidated further...
2017: American Journal of Translational Research
https://www.readbyqxmd.com/read/28801610/creb3l2-mediated-expression-of-sec23a-sec24d-is-involved-in-hepatic-stellate-cell-activation-through-er-golgi-transport
#2
Shotaro Tomoishi, Shinichi Fukushima, Kentaro Shinohara, Toshiaki Katada, Kota Saito
Hepatic fibrosis is caused by exaggerated wound healing response to chronic injury, which eventually leads to hepatic cirrhosis. Differentiation of hepatic stellate cells (HSCs) to myofibroblast-like cells by inflammatory cytokines is the critical step in fibrosis. This step is accompanied by enlargement of the endoplasmic reticulum (ER) and Golgi apparatus, suggesting that protein synthesis and secretion are augmented in the activated HSCs. However, the process of rearrangement of secretory organelles and their functions remain to be fully elucidated...
August 11, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28801346/pan-ppar-agonist-iva337-is-effective-in-experimental-lung-fibrosis-and-pulmonary-hypertension
#3
Jerome Avouac, Irena Konstantinova, Christophe Guignabert, Sonia Pezet, Jeremy Sadoine, Thomas Guilbert, Anne Cauvet, Ly Tu, Jean-Michel Luccarini, Jean-Louis Junien, Pierre Broqua, Yannick Allanore
OBJECTIVE: To evaluate the antifibrotic effects of the pan-peroxisome proliferator-activated receptor (PPAR) agonist IVA337 in preclinical mouse models of pulmonary fibrosis and related pulmonary hypertension (PH). METHODS: IVA337 has been evaluated in the mouse model of bleomycin-induced pulmonary fibrosis and in Fra-2 transgenic mice, this latter being characterised by non-specific interstitial pneumonia and severe vascular remodelling of pulmonary arteries leading to PH...
August 11, 2017: Annals of the Rheumatic Diseases
https://www.readbyqxmd.com/read/28800587/highly-efficient-gene-inactivation-by-adenoviral-crispr-cas9-in-human-primary-cells
#4
Olaf Voets, Frans Tielen, Edo Elstak, Julian Benschop, Max Grimbergen, Jan Stallen, Richard Janssen, Andre van Marle, Christian Essrich
Phenotypic assays using human primary cells are highly valuable tools for target discovery and validation in drug discovery. Expression knockdown (KD) of such targets in these assays allows the investigation of their role in models of disease processes. Therefore, efficient and fast modes of protein KD in phenotypic assays are required. The CRISPR/Cas9 system has been shown to be a versatile and efficient means of gene inactivation in immortalized cell lines. Here we describe the use of adenoviral (AdV) CRISPR/Cas9 vectors for efficient gene inactivation in two human primary cell types, normal human lung fibroblasts and human bronchial epithelial cells...
2017: PloS One
https://www.readbyqxmd.com/read/28800024/the-roles-of-dermal-white-adipose-tissue-loss-in-scleroderma-skin-fibrosis
#5
Roberta G Marangoni, Theresa T Lu
PURPOSE OF REVIEW: Dermal white adipose tissue (DWAT) is distinct from subcutaneous white adipose tissue and is lost in scleroderma skin fibrosis. The roles of DWAT loss in scleroderma skin fibrosis have not been well understood, and here we discuss recent findings that begin to provide insight into the multiple mechanisms involved. RECENT FINDINGS: The DWAT loss in part reflects the direct contribution of DWAT cells to the fibrotic tissue, with the reprogramming of adipocytes to myofibroblasts...
August 10, 2017: Current Opinion in Rheumatology
https://www.readbyqxmd.com/read/28799781/microrna-29c-prevents-pulmonary-fibrosis-by-regulating-epithelial-cell-renewal-and-apoptosis
#6
Ting Xie, Jiurong Liang, Yan Geng, Ningshan Liu, Adrianne Kurkciyan, Vrishika Kulur, Dong Leng, Nan Deng, Zhenqiu Liu, Jianbo Song, Peter Chen, Paul W Noble, Dianhua Jiang
Successful repair and renewal of alveolar epithelial cells are critical in prohibiting the accumulation of myofibroblasts in pulmonary fibrogenesis. MicroRNAs (miRNAs) are multi-focal regulators involved in lung injury and repair. But the contribution of miRNAs to AEC2 renewal and apoptosis is incompletely understood. We report that microRNA-29c (MiR-29c) expression is lower in AEC2s of individuals with idiopathic pulmonary fibrosis (IPF) than healthy lungs. Epithelial cells overexpressing miR-29c show higher proliferative rate and viability...
August 11, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28798253/cyp2e1-regulates-the-development-of-radiation-induced-pulmonary-fibrosis-via-er-stress-and-ros-dependent-mechanisms
#7
Beomseok Son, TaeWoo Kwon, Sungmin Lee, IkJoon Han, Wanyeon Kim, HyeSook Youn, BuHyun Youn
Radiation-induced pulmonary fibrosis (RIPF) is one of the most common side effects of lung cancer radiotherapy. This study was conducted to identify the molecular mechanism responsible for RIPF. We revealed that the transcriptional level of cytochrome P450 2E1 (CYP2E1) was elevated by examining expression profile analysis of RIPF mouse models. We also confirmed that CYP2E1 regulated levels of endoplasmic reticulum (ER) stress and reactive oxygen species (ROS) in alveolar epithelial type II (AE2) cells and lung fibroblasts...
August 10, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28797711/identification-of-a-myofibroblast-specific-expression-signature-in-skin-wounds
#8
Vera Bergmeier, Julia Etich, Lena Pitzler, Christian Frie, Manuel Koch, Matthias Fischer, Gunter Rappl, Hinrich Abken, James J Tomasek, Bent Brachvogel
After skin injury fibroblasts migrate into the wound and transform into contractile, extracellular matrix-producing myofibroblasts to promote skin repair. Persistent activation of myofibroblasts can cause excessive fibrotic reactions, but the underlying mechanisms are not fully understood. We used SMA-GFP transgenic mice to study myofibroblast recruitment and activation in skin wounds. Myofibroblasts were initially recruited to wounds three days post injury, their number reached a maximum after seven days and subsequently declined...
August 7, 2017: Matrix Biology: Journal of the International Society for Matrix Biology
https://www.readbyqxmd.com/read/28783377/extracellular-mitochondrial-dna-is-generated-by-fibroblasts-and-predicts-death-in-idiopathic-pulmonary-fibrosis
#9
Changwan Ryu, Huanxing Sun, Mridu Gulati, Jose D Herazo-Maya, Yonglin Chen, Awo Osafo-Addo, Caitlin Brandsdorfer, Julia Winkler, Christina Blaul, Jaden Faunce, Hongyi Pan, Tony Woolard, Argyrios Tzouvelekis, Danielle E Antin-Ozerkis, Jonathan T Puchalski, Martin Slade, Anjelica L Gonzalez, Daniel F Bogenhagen, Varvara Kirillov, Carol Feghali-Bostwick, Kevin Gibson, Kathleen Lindell, Raimund I Herzog, Charles S Dela Cruz, Wajahat Mehal, Naftali Kaminski, Erica Herzog, Glenda Trujillo
RATIONALE: Idiopathic pulmonary fibrosis (IPF) involves the accumulation of alpha smooth muscle actin (αSMA) expressing myofibroblasts arising from interactions with soluble mediators such as transforming growth factor beta-1 (TGFβ1), and mechanical influences such as local tissue stiffness. While IPF fibroblasts are enriched for aerobic glycolysis and innate immune receptor activation, innate immune ligands related to mitochondrial injury, such as extracellular mitochondrial DNA (mtDNA) have not been identified in IPF...
August 7, 2017: American Journal of Respiratory and Critical Care Medicine
https://www.readbyqxmd.com/read/28782074/a-cell-culture-technique-for-human-epiretinal-membranes-to-describe-cell-behavior-and-membrane-contraction-in-vitro
#10
Christian Wertheimer, Kirsten H Eibl-Lindner, Denise Compera, Alexander Kueres, Armin Wolf, Denitsa Docheva, Siegfried G Priglinger, Claudia Priglinger, Ricarda G Schumann
PURPOSE: To introduce a human cell culture technique for investigating in-vitro behavior of primary epiretinal cells and membrane contraction of fibrocellular tissue surgically removed from eyes with idiopathic macular pucker. METHODS: Human epiretinal membranes were harvested from ten eyes with idiopathic macular pucker during standard vitrectomy. Specimens were fixed on cell culture plastic using small entomological pins to apply horizontal stress to the tissue, and then transferred to standard cell culture conditions...
August 7, 2017: Graefe's Archive for Clinical and Experimental Ophthalmology
https://www.readbyqxmd.com/read/28777943/mesenchymal-stem-cells-in-fibrotic-disease
#11
REVIEW
Elie El Agha, Rafael Kramann, Rebekka K Schneider, Xiaokun Li, Werner Seeger, Benjamin D Humphreys, Saverio Bellusci
Fibrosis is associated with organ failure and high mortality and is commonly characterized by aberrant myofibroblast accumulation. Investigating the cellular origin of myofibroblasts in various diseases is thus a promising strategy for developing targeted anti-fibrotic treatments. Recent studies using genetic lineage tracing technology have implicated diverse organ-resident perivascular mesenchymal stem cell (MSC)-like cells and bone marrow-MSCs in myofibroblast generation during fibrosis development. In this Review, we give an overview of the emerging role of MSCs and MSC-like cells in myofibroblast-mediated fibrotic disease in the kidney, lung, heart, liver, skin, and bone marrow...
August 3, 2017: Cell Stem Cell
https://www.readbyqxmd.com/read/28777747/breast-fibroadenoma-with-pseudoangiomatous-pash-like-stroma
#12
Josko Bezic, Jelena Srbljin
Pseudoangiomatous stromal hyperplasia (PASH) is a breast stromal change, histologically characterized by anastomosing, slit-like spaces lined by slender myofibroblasts and surrounded by dense collagenous stroma. Mass forming cases clinically and radiologically simulate fibroadenoma. A middle aged women presented with unpalpable breast nodule discovered on ultrasound examination. The ultrasound characteristics were typical for fibroadenoma, while fine-needle aspiration cytology was inconclusive. The histological examination of the lumpectomy specimen showed fibroadenoma with peculiar stromal alteration consistent with pseudoangiomatous stromal hyperplasia...
August 2, 2017: Breast Disease
https://www.readbyqxmd.com/read/28776666/potential-role-of-the-jagged1-notch1-signaling-pathway-in-the-endothelial-myofibroblast-transition-during-blm-induced-pulmonary-fibrosis
#13
Qian Yin, Weihua Wang, Guangbin Cui, Linfeng Yan, Song Zhang
Endothelial cell myofibroblast transition (EndoMT) is found during the process of bleomycin (BLM)-induced pulmonary fibrosis in rats, and plays a very important role in sustaining inflammation and collagen secretion. Moreover, some studies have suggested that the Notch1 signaling pathway may be involved in the expression of Î ± -smooth muscle actin (Î ± -SMA) in pulmonary microvascular endothelial cells (PMVECs), a protein marker of EndoMT. Therefore, we aimed to investigate the expression level of Î ± -SMA and Notch1-related signaling molecules in PMVECs from BLM-induced rats and determine the relationship between the Notch1 signaling pathway and the expression of Î ± -SMA in PMVECs...
August 4, 2017: Journal of Cellular Physiology
https://www.readbyqxmd.com/read/28776353/autotransplantation-of-the-heart-for-recurrent-inflammatory-myofibroblastic-tumor
#14
Hyun Oh Park, Jun Ho Yang, Sung Hwan Kim, Seong Ho Moon, Joung Hun Byun, Jun Young Choi, Chung Eun Lee, Jung Wook Yang, Jong Woo Kim
We report a rare case of dyspnea caused by a cardiac tumor in a 53-year-old woman. The patient had undergone a cardiac tumor (inflammatory myofibroblastic tumor, 6.2 × 4.2 × 3.3 cm) resection at our institute 13 months earlier. We performed preoperative evaluations which revealed a cardiac tumor originating from the posterior wall of the left atrium. Cardiac autotransplantation surgery (cardiac explantation, ex vivo tumor resection, cardiac reconstruction, and cardiac reimplantation) was successfully performed for the complete resection of the recurrent tumor without major postoperative complications...
September 2017: Journal of Korean Medical Science
https://www.readbyqxmd.com/read/28775125/smad3-stat3-signaling-mediates-%C3%AE-cell-epithelial-mesenchymal-transition-in-chronic-pancreatitis-related-diabetes
#15
Xiangwei Xiao, Shane Fischbach, Tina Zhang, Congde Chen, Qingfeng Sheng, Ray Zimmerman, Sneha Patnaik, Joseph Fusco, Yungching Ming, Ping Guo, Chiyo Shiota, Krishna Prasadan, Nupur Gangopadhyay, Sohail Z Husain, Henry Dong, George K Gittes
Many patients with chronic pancreatitis develop diabetes (chronic pancreatitis-related diabetes; CPRD) through an undetermined mechanism. Here, we used long-term partial pancreatic duct ligation (PDL) as a model to study CPRD. We found that long-term PDL induced significant β-cell dedifferentiation, followed by a time-dependent decrease in functional β-cell mass, all specifically in the ligated tail portion of the pancreas (PDL-tail). High levels of transforming growth factor β1 (TGFβ1) were detected in the PDL-tail, mainly produced by M2 macrophages at the early stage, and by activated myofibroblasts at the later stage...
August 3, 2017: Diabetes
https://www.readbyqxmd.com/read/28775097/platelet-derived-growth-factor-receptor-alpha-pdgfr%C3%AE-and-ras-related-c3-botulinum-toxin-substrate-1-rac1-regulate-mechano-responsiveness-of-lung-fibroblasts
#16
Stephen E McGowan, Diann M McCoy
Platelet-derived growth factor (PDGF)-A, which only signals through PDGF-receptor-alpha (PDGFRα) is required for secondary alveolar septal formation. Although PDGFRα distinguishes mesenchymal progenitor cells during the saccular stage, PDGFRα-expressing alveolar cells persist through adulthood. PDGF-A sustains proliferation, limits apoptosis, and maintains alpha-smooth muscle actin (αSMA) containing alveolar cells, which congregate at the alveolar entry ring at postnatal day (P)12. PDGFRα-expressing, αSMA-containing, alveolar cells re-distribute in the elongating septum, suggesting that they migrate to the alveolar entry rings where mechanical tension is higher...
August 3, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28775095/transglutaminase-2-in-pulmonary-and-cardiac-tissue-remodeling-in-experimental-pulmonary-hypertension
#17
Krishna C Penumatsa, Deniz Toksoz, Rod R Warburton, Mousa Kharnaf, Ioana R Preston, Navin Kumar Kapur, Chaitan Khosla, Nicholas S Hill, Barry L Fanburg
Tissue matrix remodeling and fibrosis leading to loss of pulmonary arterial and right ventricular compliance are important features of both experimental and clinical pulmonary hypertension (PH). We have previously reported that transglutaminase 2 (TG2) is involved in PH development while others have shown it to be a crosslinking enzyme that participates in remodeling of extracellular matrix in fibrotic diseases in general. In the present studies, we used a mouse model of experimental PH (Sugen 5416 and hypoxia; SuHypoxia) and cultured primary human cardiac and pulmonary artery adventitial fibroblasts to evaluate the relationship of TG2 to the processes of fibrosis, protein crosslinking, extracellular matrix collagen accumulation and fibroblast to myofibroblast transformation...
August 3, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28771711/tannic-acid-attenuates-tgf-%C3%AE-1-induced-epithelial-to-mesenchymal-transition-by-effectively-intervening-tgf-%C3%AE-signaling-in-lung-epithelial-cells
#18
Dhamotharan Pattarayan, Ayyanar Sivanantham, Venkateshwaran Krishnaswami, Lakshmanan Loganathan, Rajaguru Palanichamy, Subramanian Natesan, Karthikeyan Muthusamy, Subbiah Rajasekaran
Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive and an irreversible lung disorder characterized by the accumulation of fibroblasts and myofibroblasts in the extracellular matrix. The transforming growth factor-β1 (TGF-β1)-induced epithelial-to-mesenchymal transition (EMT) is thought to be one of the possible sources for a substantial increase in the number of fibroblasts/myofibroblasts in IPF lungs. Tannic acid (TA), a natural dietary polyphenolic compound has been shown to possess diverse pharmacological effects...
August 3, 2017: Journal of Cellular Physiology
https://www.readbyqxmd.com/read/28771607/il-25-induced-activation-of-nasal-fibroblast-and-its-association-with-the-remodeling-of-chronic-rhinosinusitis-with-nasal-polyposis
#19
Soo-Kyoung Park, Yong-De Jin, Yeong-Kyu Park, Sun-Hee Yeon, Jun Xu, Rui-Ning Han, Ki-Sang Rha, Yong-Min Kim
BACKGROUND AND OBJECTIVE: Interleukin (IL)-25 has been shown to play an important role in the pathogenesis of chronic rhinosinusitis with nasal polyps. Nasal polyps are associated with chronic inflammation of the mucous membranes in the paranasal sinuses and are involved in extracellular matrix (ECM) accumulation. The aim of this study is to evaluate the effects of IL-25 on myofibroblast differentiation, ECM production and the expression of matrix metalloproteinases in nasal polyp derived fibroblasts (NPDFs) and to determine the molecular mechanism underlying these processes...
2017: PloS One
https://www.readbyqxmd.com/read/28771545/augmented-sphingosine-1-phosphate-receptor-1-signaling-in-cardiac-fibroblasts-induces-cardiac-hypertrophy-and-fibrosis-through-angiotensin-ii-and-interleukin-6
#20
Sei-Ichiro Ohkura, Soichiro Usui, Shin-Ichiro Takashima, Noriko Takuwa, Kazuaki Yoshioka, Yasuo Okamoto, Yutaka Inagaki, Naotoshi Sugimoto, Teppei Kitano, Masayuki Takamura, Takashi Wada, Shuichi Kaneko, Yoh Takuwa
Cardiac fibroblasts, together with cardiomyocytes, occupy the majority of cells in the myocardium and are involved in myocardial remodeling. The lysophospholipid mediator sphigosine-1-phosphate (S1P) regulates functions of cardiovascular cells through multiple receptors including S1PR1-S1PR3. S1PR1 but not other S1P receptors was upregulated in angiotensin II-induced hypertrophic hearts. Therefore, we investigated a role of S1PR1 in fibroblasts for cardiac remodeling by employing transgenic mice that overexpressed S1PR1 under the control of α-smooth muscle actin promoter...
2017: PloS One
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