نتایج جستجو برای: myofibroblast

تعداد نتایج: 2555  

Journal: :Journal of cellular physiology 2008
Ya-Rong Liu Wen-Lei Ye Xi-Min Zeng Wen-Hua Ren Yu-Qiu Zhang Yan-Ai Mei

Our previous studies have indicated that TGF-beta1 exerts its effect on the expression of A-type potassium channels (I(A)) in rat vascular myofibroblasts by activation of protein kinase C during the phenotypic transformation of vascular fibroblasts to myofibroblasts. In the present study, patch-clamp whole-cell recording and transwell-migration assays were used to examine the effects of TGF-bet...

Journal: :The Journal of Cell Biology 2007
Pierre-Jean Wipff Daniel B. Rifkin Jean-Jacques Meister Boris Hinz

The conjunctive presence of mechanical stress and active transforming growth factor beta1 (TGF-beta1) is essential to convert fibroblasts into contractile myofibroblasts, which cause tissue contractures in fibrotic diseases. Using cultured myofibroblasts and conditions that permit tension modulation on the extracellular matrix (ECM), we establish that myofibroblast contraction functions as a me...

2014
Matthew Rozycki Monika Lodyga Jessica Lam Maria Zena Miranda Károly Fátyol Pam Speight András Kapus

Myofibroblasts, the culprit of organ fibrosis, can originate from mesenchymal and epithelial precursors through fibroblast-myofibroblast and epithelial-myofibroblast transition (EMyT). Because certain ciliopathies are associated with fibrogenesis, we sought to explore the fate and potential role of the primary cilium during myofibroblast formation. Here we show that myofibroblast transition fro...

Journal: :Arteriosclerosis, thrombosis, and vascular biology 2011
Cindy Y Y Yip Mark C Blaser Zahra Mirzaei Xiao Zhong Craig A Simmons

OBJECTIVE Calcific aortic valve disease is associated with the differentiation of valvular interstitial cells (VICs) to myofibroblast and osteoblast-like cells, particularly in the fibrosa layer of the valve. Previous studies suggested that C-type natriuretic peptide (CNP) protects against calcific aortic valve disease to maintain homeostasis. We aimed to determine whether CNP inhibits VIC path...

2016
Nahoko Sato Naoki Takasaka Masahiro Yoshida Kazuya Tsubouchi Shunsuke Minagawa Jun Araya Nayuta Saito Yu Fujita Yusuke Kurita Kenji Kobayashi Saburo Ito Hiromichi Hara Tsukasa Kadota Haruhiko Yanagisawa Mitsuo Hashimoto Hirofumi Utsumi Hiroshi Wakui Jun Kojima Takanori Numata Yumi Kaneko Makoto Odaka Toshiaki Morikawa Katsutoshi Nakayama Hirotsugu Kohrogi Kazuyoshi Kuwano

BACKGROUND Accumulation of profibrotic myofibroblasts in fibroblastic foci (FF) is a crucial process for development of fibrosis during idiopathic pulmonary fibrosis (IPF) pathogenesis, and transforming growth factor (TGF)-β plays a key regulatory role in myofibroblast differentiation. Reactive oxygen species (ROS) has been proposed to be involved in the mechanism for TGF-β-induced myofibroblas...

Journal: :The Journal of biological chemistry 2016
Matthew Rozycki Janne Folke Bialik Pam Speight Qinghong Dan Teresa E T Knudsen Stephen G Szeto Darren A Yuen Katalin Szászi Stine F Pedersen András Kapus

TGFβ-induced expression of the NADPH oxidase Nox4 is essential for fibroblast-myofibroblast transition. Rho has been implicated in Nox4 regulation, but the underlying mechanisms are largely unknown. Myocardin-related transcription factor (MRTF), a Rho/actin polymerization-controlled coactivator of serum response factor, drives myofibroblast transition from various precursors. We have shown that...

Journal: :American journal of physiology. Heart and circulatory physiology 2007
Vanja Drobic Ryan H Cunnington Kristen M Bedosky Joshua E Raizman Vinit V Elimban Sunil G Rattan Ian M C Dixon

Myofibroblasts respond to an array of signals from mitogens and cytokines during the course of wound healing following a myocardial infarction (MI), and these signals may coordinate ventricular myofibroblast proliferation. Furthermore, myofibroblasts are contractile and contribute to wound contraction by imparting mechanical tension on surrounding extracellular matrix. Although TGF-beta(1), CT-...

2016
José A. Rodríguez-Nieves Susan C. Patalano Diego Almanza Mehrnaz Gharaee-Kermani Jill A. Macoska

Benign prostate hyperplasia (BPH), an enlargement of the prostate common in aging in men, is associated with urinary voiding dysfunction manifest as Lower Urinary Tract Symptoms (LUTS). Although inflammation and abnormal smooth muscle contractions are known to play key roles in the development of LUTS, tissue fibrosis may also be an important and previously unrecognized contributing factor. Tis...

2014
Monique Bernard Mélanie Dieudé Bing Yang Katia Hamelin Katy Underwood Marie-Josée Hébert

Recent evidence suggests that autophagy may favor fibrosis through enhanced differentiation of fibroblasts in myofibroblasts. Here, we sought to characterize the mediators and signaling pathways implicated in autophagy-induced myofibroblast differentiation. Fibroblasts, serum starved for up to 4 d, showed increased LC3-II/-I ratios and decreased SQSTM1/p62 levels. Autophagy was associated with ...

Journal: :American journal of respiratory cell and molecular biology 2012
Xiangwei Huang Naiheng Yang Vincent F Fiore Thomas H Barker Yi Sun Stephan W Morris Qiang Ding Victor J Thannickal Yong Zhou

The mechanical properties of the extracellular matrix have recently been shown to promote myofibroblast differentiation and lung fibrosis. Mechanisms by which matrix stiffness regulates myofibroblast differentiation are not fully understood. The goal of this study was to determine the intrinsic mechanisms of mechanotransduction in the regulation of matrix stiffness-induced myofibroblast differe...

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