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Smad AND Ang 2

Sudhir Singh, Scott R Manson, Heedoo Lee, Yeawon Kim, Tuoen Liu, Qiusha Guo, Julio J Geminiani, Paul F Austin, Ying Maggie Chen
Emerging evidence has highlighted the pivotal role of microvasculature injury in the development and progression of renal fibrosis. Angiopoietin-1 (Ang-1) is a secreted vascular growth factor that binds to the endothelial-specific Tie2 receptor. Ang-1/Tie2 signaling is critical for regulating blood vessel development and modulating vascular response after injury, but is dispensable in mature, quiescent vessels. Although dysregulation of vascular endothelial growth factor (VEGF) signaling has been well studied in renal pathologies, much less is known about the role of the Ang-1/Tie2 pathway in renal interstitial fibrosis...
2016: PloS One
Y Zhang, L Wang, H Zhang, Y T Ma, Y N Yang, B D Chen, M M Ma, X L Zhu
OBJECTIVE: To observe the effect of β3 adrenergic receptor (β3-AR) on fibrosis in cardiac fibroblasts(CFBs) and explore the related mechanisms. METHODS: Neonatal CFBs were divided into negative control group (N-CFC): CFBs without any intervention; group treated with β3 adrenergic receptor agonist (AngⅡ-CFC-β3-AR BRL): CFBs treated with 10(-6) mol/L angiotensin Ⅱ(AngⅡ), 1 hour later treated with 10(-5) mol/L β3 adrenergic receptor agonist (β3-AR BRL37344); group treated with β3 adrenergic receptor antagonist (AngⅡ-CFC-β3-AR SR): CFBs treated with 10(-6) mol/L AngⅡ, 1 hour later treated with 10(-5) mol/L β3 adrenergic receptor antagonist (β3-AR SR59230A); and positive control group (AngⅡ-CFC): CFBs treated with 10(-6) mol/L AngⅡonly...
June 24, 2016: Zhonghua Xin Xue Guan Bing za Zhi
Lin Cui, Youping Wang, Rui Yu, Bin Li, Shiyang Xie, Yuan Gao, Xiaoxiao Wang, Mingjun Zhu
Jia-Shen decoction (JSD) is a traditional Chinese medicine, which is used widely to treat chronic heart failure. However, the underlying mechanism remains to be elucidated. The present study aimed to investigate the mechanism underlying the effects of JSD on cardiac fibroblast (CF) proliferation and differentiation. The CFs were obtained from the hearts of neonatal (1‑3‑day old) Sprague‑Dawley rats and treated with JSD-medicated serum (JSDS) with or without angiotensin II (Ang II). Cell proliferation was assessed using Cell Counting Kit‑8 reagent...
August 2016: Molecular Medicine Reports
Shuang-Ming Cai, Ren-Qiang Yang, Yang Li, Zuo-Wei Ning, Li-Li Zhang, Gao-Su Zhou, Wei Luo, Da-Huan Li, Yan Chen, Miao-Xia Pan, Xu Li
AIMS: Angiotensin II (Ang II) aggravates hepatic fibrosis by inducing NADPH oxidase (NOX)-dependent oxidative stress. Angiotensin-(1-7) [Ang-(1-7)], which counter-regulates Ang II, has been evidenced to protect against hepatic fibrosis. The NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome, being activated by reactive oxygen species (ROS), is identified as a novel mechanism of liver fibrosis. However, whether the NLRP3 inflammasome involves in regulation of Ang II-induced hepatic fibrosis remains unclear...
May 10, 2016: Antioxidants & Redox Signaling
Chang Seong Kim, In Jin Kim, Eun Hui Bae, Seong Kwon Ma, JongUn Lee, Soo Wan Kim
BACKGROUND: Angiotensin-(1-7) [Ang-(1-7)] counteracts many actions of the renin-angiotensin-aldosterone system. Despite its renoprotective effects, extensive controversy exists regarding the role of Ang-(1-7) in obstructive nephropathy, which is characterized by renal tubulointerstitial fibrosis and apoptosis. METHODS: To examine the effects of Ang-(1-7) in unilateral ureteral obstruction (UUO), male Sprague-Dawley rats were divided into three groups: control, UUO, and Ang-(1-7)-treated UUO rats...
2015: PloS One
Jingying Hou, Ping Yan, Tianzhu Guo, Yue Xing, Shaoxin Zheng, Changqing Zhou, Hui Huang, Huibao Long, Tingting Zhong, Quanhua Wu, Jingfeng Wang, Tong Wang
BACKGROUND: In this study, we hypothesized that CSCs mediated the expression of Cx43 after transplantation post MI via the ANG II/AT1R/TGF-beta1 signaling pathway. METHODS: Myocardial infarction (MI) was induced in twenty male Sprague-Dawley rats. The rats were randomized into two groups and were then received the injection of 5 × 10(6) CSCs labeled with PKH26 in phosphate buffer solution (PBS) or equal PBS alone into the infarct anterior ventricular free wall two weeks after MI...
December 2015: Experimental and Molecular Pathology
Haipeng Guo, Xin Zhang, Yuqian Cui, Heng Zhou, Dachun Xu, Tichao Shan, Fan Zhang, Yuan Guo, Yuguo Chen, Dawei Wu
Cardiac hypertrophy is a key pathophysiological component to biomechanical stress, which has been considered to be an independent and predictive risk factor for adverse cardiovascular events. Taxifolin (TAX) is a typical plant flavonoid, which has long been used clinically for treatment of cardiovascular and cerebrovascular diseases. However, very little is known about whether TAX can influence the development of cardiac hypertrophy. In vitro studies, we found that TAX concentration-dependently inhibited angiotensin II (Ang II) induced hypertrophy and protein synthesis in cardiac myocytes...
September 1, 2015: Toxicology and Applied Pharmacology
Hui Sun, Yong Zhao, Xiuping Bi, Shaohua Li, Guohai Su, Ya Miao, Xiao Ma, Yun Zhang, Wei Zhang, Ming Zhong
BACKGROUND: Angiotensin II (Ang II) and transforming growth factor β (TGFβ) are closely involved in the pathogenesis of diabetic complications. We aimed to determine whether an aberrant thrombospondin 1 (TSP1)-mediated TGFβ1/Smads signaling pathway specifically affects vascular fibrosis in diabetic rats and whether valsartan, an Ang II subtype 1 receptor blocker, has an anti-fibrotic effect. METHODS: Age-matched male Wistar rats were randomly divided into 3 groups: control (n = 8), diabetes (n = 16) and valsartan (30 mg/kg/day) (n = 16)...
2015: Diagnostic Pathology
Catalina Cofre, María José Acuña, Osvaldo Contreras, María Gabriela Morales, Cecilia Riquelme, Claudio Cabello-Verrugio, Enrique Brandan
Duchenne muscular dystrophy is a genetic disorder characterized by myofiber degeneration, muscle weakness, and increased fibrosis. Transforming growth factor type-β (TGF-β), a central mediator of fibrosis, is upregulated in fibrotic diseases. Angiotensin-(1-7) [Ang-(1-7)] is a peptide with actions that oppose those of angiotensin-II (Ang II). Ang-(1-7) effects are mediated by the Mas receptor. Treatment with Ang-(1-7) produce positive effects in the mdx mouse, normalizing skeletal muscle architecture, decreasing local fibrosis, and fibroblasts, and improving muscle function...
March 2015: BioFactors
Cheng-Chih Chung, Rung-Chieh Hsu, Yu-Hsun Kao, Jing-Ping Liou, Yen-Yu Lu, Yi-Jen Chen
BACKGROUND: Androgen deficiency produces heart failure, which can be ameliorated by testosterone supplementation. Cardiac fibrosis plays a critical role in the pathophysiology of heart failure. This study aimed to evaluate whether testosterone can attenuate cardiac fibroblast activity through modulating transforming growth factor (TGF)-β and angiotensin (Ang) II signaling. METHODS: Migration, proliferation, myofibroblast differentiation, collagen production, and transcription signaling were evaluated in adult male rat (weighing 300-350 g) cardiac fibroblasts with and without incubation with testosterone (10nM) and co-administration of TGF-β1 (10 ng/ml) or Ang II (100 nM) by cell migration analysis, proliferation assay, soluble collagen measurement, zymographic analysis, immunofluorescence microscopy, real-time PCR and Western blot...
September 20, 2014: International Journal of Cardiology
Kyle A Carver, Thomas L Smith, Patricia E Gallagher, E Ann Tallant
OBJECTIVE: The effect of the heptapeptide hormone Ang-(1-7) on microvascular fibrosis in rats with Ang II-induced hypertension was investigated, since vascular fibrosis/remodeling plays a prominent role in hypertension-induced end-organ damage and Ang-(1-7) inhibits vascular growth and fibrosis. METHODS: Fibrosis of cremaster microvessels was studied in male Lewis rats infused with Ang II and/or Ang-(1-7). RESULTS: Ang II elevated systolic blood pressure by approximately 40 mmHg, while blood pressure was not changed by Ang-(1-7)...
January 2015: Microcirculation: the Official Journal of the Microcirculatory Society, Inc
María Gabriela Morales, Johanna Abrigo, Carla Meneses, Felipe Simon, Franco Cisternas, Juan Carlos Rivera, Yaneisi Vazquez, Claudio Cabello-Verrugio
AngII (angiotensin II) induces pathological conditions such as fibrosis in skeletal muscle. In this process, AngII increases ROS (reactive oxygen species) and induces a biphasic phosphorylation of p38 MAPK (mitogen-activated protein kinase). In addition, AngII stimulates the expression and production of TGF (transforming growth factor)-β1 via a mechanism dependent on ROS production mediated by NADPH oxidase (NOX) and p38 MAPK activation. In the present study, we investigated whether Ang-(1-7) [angiotensin-(1-7)], through the Mas-1 receptor, can counteract the signalling induced by AngII in mouse skeletal muscle and cause a decrease in the expression and further activity of TGF-β1 in skeletal muscle cells...
August 2014: Clinical Science (1979-)
José Pablo Vázquez-Medina, José G Soñanez-Organis, Ruben Rodriguez, Jose A Viscarra, Akira Nishiyama, Daniel E Crocker, Rudy M Ortiz
Elephant seals naturally experience prolonged periods of absolute food and water deprivation (fasting). In humans, rats and mice, prolonged food deprivation activates the renin-angiotensin system (RAS) and increases oxidative damage. In elephant seals, prolonged fasting activates RAS without increasing oxidative damage likely due to an increase in antioxidant defenses. The mechanism leading to the upregulation of antioxidant defenses during prolonged fasting remains elusive. Therefore, we investigated whether prolonged fasting activates the redox-sensitive transcription factor Nrf2, which controls the expression of antioxidant genes, and if such activation is potentially mediated by systemic increases in RAS...
August 1, 2013: Journal of Experimental Biology
Paula Painemal, María José Acuña, Cecilia Riquelme, Enrique Brandan, Claudio Cabello-Verrugio
Excessive deposition of extracellular matrix (ECM) proteins, a condition known as fibrosis, is a hallmark of Duchenne muscular dystrophy. Among the factors that trigger muscle fibrosis are transforming growth factor beta (TGF-β) and angiotensin II (Ang-II). Ang-II belongs to the renin-angiotensin system, and its biological effects are exerted by Ang-II receptors type 1 and type 2 (AT-1 and AT-2, respectively). This study aims to determine the effect of TGF-β1 on the expression of AT-1 and AT-2 receptor in skeletal muscle...
July 2013: BioFactors
Jun Gu, Xu Liu, Quan-xing Wang, Hong-wei Tan, Meng Guo, Wei-feng Jiang, Li Zhou
The activation of transforming growth factor-β1(TGF-β1)/Smad signaling pathway and increased expression of connective tissue growth factor (CTGF) induced by angiotensin II (AngII) have been proposed as a mechanism for atrial fibrosis. However, whether TGFβ1/non-Smad signaling pathways involved in AngII-induced fibrogenetic factor expression remained unknown. Recently tumor necrosis factor receptor associated factor 6 (TRAF6)/TGFβ-associated kinase 1 (TAK1) has been shown to be crucial for the activation of TGF-β1/non-Smad signaling pathways...
October 1, 2012: Experimental Cell Research
Feifei Ma, Yulin Li, Lixin Jia, Yalei Han, Jizhong Cheng, Huihua Li, Yongfen Qi, Jie Du
Interleukin-6 (IL-6) is an important cytokine participating in multiple biologic activities in immune regulation and inflammation. IL-6 has been associated with cardiovascular remodeling. However, the mechanism of IL-6 in hypertensive cardiac fibrosis is still unclear. Angiotensin II (Ang II) infusion in mice increased IL-6 expression in the heart. IL-6 knockout (IL-6-/-) reduced Ang II-induced cardiac fibrosis: 1) Masson trichrome staining showed that Ang II infusion significantly increased fibrotic areas of the wild-type mouse heart, which was greatly suppressed in IL-6-/- mice and 2) immunohistochemistry staining showed decreased expression of α-smooth muscle actin (α-SMA), transforming growth factor β1 (TGF-β1) and collagen I in IL-6-/- mouse heart...
2012: PloS One
Zhen Liu, Xiao Ru Huang, Hai-Yong Chen, Josef M Penninger, Hui Yao Lan
It is known that angiotensin (Ang)-converting enzyme (ACE) 2 catalyzes Ang II to Ang 1-7 to prevent the detrimental effect of Ang II on blood pressure, renal fibrosis, and inflammation. However, mechanisms of renoprotective role of Ace2 remain largely unclear. The present study tested the hypothesis that deficiency of Ace2 may accelerate intrarenal Ang II-mediated fibrosis and inflammation independent of blood pressure in a model of unilateral ureteral obstructive (UUO) nephropathy induced in Ace2(+/y) and Ace2(-/y) mice...
May 2012: Laboratory Investigation; a Journal of Technical Methods and Pathology
Sarah J Watkins, Gillian M Borthwick, Rachael Oakenfull, Andrew Robson, Helen M Arthur
Cardiac hypertrophy occurs as an adaptation to hypertension but a sustained hypertrophic response can ultimately lead to heart failure. Angiotensin-II (Ang II) is released following hemodynamic overload and stimulates a cardiac hypertrophic response. AngII also increases expression of the regulatory cytokine, transforming growth factor-β1 (TGFβ1), which is also implicated in the cardiac hypertrophic response and can stimulate activation of Smad2/3 as well as TGFβ-activated kinase 1 (TAK1) signaling mediators...
April 2012: Hypertension Research: Official Journal of the Japanese Society of Hypertension
Monika Jeub, Michael Emrich, Bruno Pradier, Omneya Taha, Valerie Gailus-Durner, Helmut Fuchs, Martin Hrabe de Angelis, Danny Huylebroeck, Andreas Zimmer, Heinz Beck, Ildiko Racz
The perception of pain is initiated by the transduction of noxious stimuli through specialized ion channels and receptors expressed by primary nociceptive neurons. The molecular mechanisms that orchestrate the expression and function of ion channels relevant for pain processing are poorly understood. We demonstrate here a central role of the transcription factor Smad-interacting protein 1 (Sip1/Zfhx1b/Zeb2), a 2-handed zinc finger DNA-binding protein with essential functions in neural crest and forebrain development, in controlling nociceptive neuron excitability and pain sensitivity...
October 2011: Pain
M S Rye, S P Wiertsema, E S H Scaman, J Oommen, W Sun, R W Francis, W Ang, C E Pennell, D Burgner, P Richmond, S Vijayasekaran, H L Coates, S D Brown, J M Blackwell, S E Jamieson
Otitis media (OM) is a common childhood disease characterised by middle ear inflammation following infection. Susceptibility to recurrent acute OM (rAOM) and chronic OM with effusion (COME) is highly heritable. Two murine mutants, Junbo and Jeff, spontaneously develop severe OM with similar phenotypes to human disease. Fine-mapping of these mutants identified two genes (Evi1 and Fbxo11) that interact with the transforming growth factor β (TGFβ) signalling pathway. We investigated these genes, as well as four Sma- and Mad-related (SMAD) genes of the TGFβ pathway, as candidate rAOM/COME susceptibility genes in two predominantly Caucasian populations...
July 2011: Genes and Immunity
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