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Angiotensin II stimulates endothelin transcription

Renna Luo, Weiru Zhang, Cheng Zhao, Yujin Zhang, Hongyu Wu, Jianping Jin, Wenzheng Zhang, Almut Grenz, Holger K Eltzschig, Lijian Tao, Rodney E Kellems, Yang Xia
Hypertensive chronic kidney disease is one of the most prevalent medical conditions with high morbidity and mortality in the United States and worldwide. However, early events initiating the progression to hypertensive chronic kidney disease are poorly understood. We hypothesized that elevated endothelial hypoxia-inducible factor-1α (HIF-1α) is a common early insult triggering initial glomerular injury leading to hypertensive chronic kidney disease. To test our hypothesis, we used an angiotensin II infusion model of hypertensive chronic kidney disease to determine the specific cell type and mechanisms responsible for elevation of HIF-1α and its role in the progression of hypertensive chronic kidney disease...
July 2015: Hypertension
Liming Yu, Guang Yang, Xinyu Weng, Peng Liang, Luyang Li, Jianfei Li, Zhiwen Fan, Wenfang Tian, Xiaoyan Wu, Huihui Xu, Minming Fang, Yong Ji, Yuehua Li, Qi Chen, Yong Xu
OBJECTIVE: Endothelin-1 is a potent vasoconstrictor derived from vascular endothelium. Elevated endothelin-1 levels are observed in a host of cardiovascular pathologies including cardiomyopathy. The epigenetic mechanism responsible for endothelin-1 induction in these pathological processes remains elusive. APPROACH AND RESULTS: We report here that induction of endothelin-1 expression in endothelial cells by angiotensin II (Ang II) was accompanied by the accumulation of histone H3K4 trimethylation, a preeminent histone modification for transcriptional activation, on the endothelin-1 promoter...
May 2015: Arteriosclerosis, Thrombosis, and Vascular Biology
Xinyu Weng, Liming Yu, Peng Liang, Luyang Li, Xin Dai, Bisheng Zhou, Xiaoyan Wu, Huihui Xu, Mingming Fang, Qi Chen, Yong Xu
Angiotensin II (Ang II) induces cardiac hypertrophy and fibrosis in part by stimulating endothelin (ET-1) transcription. The involvement of the epigenetic machinery in this process is largely undefined. In the present study, we examined the epigenetic maneuvering underlying cardiac hypertrophy and fibrosis following ET-1 transactivation by Ang II. In response to Ang II stimulation, core components of the mammalian chromatin remodeling complex (Brahma-related gene 1, or Brg1, and Brahma or Brm) and histone H3K4 methylation complex (Ash2, absent, small, or homeotic discs 2, or Ash2 and WD domain repeat 5, or Wdr5) were recruited to the ET-1 promoter region in endothelial cells...
May 2015: Journal of Molecular and Cellular Cardiology
Xinyu Weng, Liming Yu, Peng Liang, Dewei Chen, Xian Cheng, Yuyu Yang, Luyang Li, Ting Zhang, Bisheng Zhou, Xiaoyan Wu, Huihui Xu, Mingming Fang, Yuqi Gao, Qi Chen, Yong Xu
Angiotensin II (Ang II) stimulates endothelin (ET-1) transcription, which contributes to cardiac hypertrophy and fibrosis. We have previously reported that myocardin related transcription factor A (MRTF-A) is indispensable for ET-1 transcription in vascular endothelial cells under hypoxic conditions, indicating that MRTF-A might mediate Ang II-induced pathological hypertrophy. Here we report that Ang II augmented the expression of MRTF-A in cultured endothelial cells and in the lungs of mice with cardiac hypertrophy...
March 2015: Journal of Molecular and Cellular Cardiology
Yuanjie Mao, Jialin Su, Lei Lei, Lei Meng, Yongfen Qi, Yong Huo, Chaoshu Tang
BACKGROUND: The activation of Gq-protein-coupled receptors induces proliferation of vascular smooth muscle cells (VSMCs) proliferation and is involved in vascular remodeling. The regulator of G protein signaling 2 (RGS2), which accelerates the termination of Gq protein signaling, may play a role in vascular remodeling. However, this role remains unclear. METHODS: Aortic balloon injury or sham operation was produced in male Wistar rats. Histological examination and gene expression analysis were performed after surgery...
July 2014: Journal of Cardiovascular Medicine
Estelle R Simo Cheyou, Ali Bouallegue, Ashok K Srivastava
Vasoactive peptides such as angiotensin II and endothelin-1 as well as growth factors regulate vascular homeostasis through signaling pathways that are triggered in both normal and disease states. These vasoactive peptides and growth factors also increase the cellular levels of calcium which, through calcium binding effector systems initiating the downstream signaling and physiological responses in target cells. A multifunctional calcium-calmodulin-dependent protein kinase II (CaMKII) has emerged as an important transducer of vasoactive peptide-induced responses in vascular smooth muscle cells (VSMC)...
March 2014: Current Vascular Pharmacology
Krishna P Subedi, Omkar Paudel, James S K Sham
Intracellular calcium (Ca(2+)) plays pivotal roles in distinct cellular functions through global and local signaling in various subcellular compartments, and subcellular Ca(2+) signal is the key factor for independent regulation of different cellular functions. In vascular smooth muscle cells, subsarcolemmal Ca(2+) is an important regulator of excitation-contraction coupling, and nucleoplasmic Ca(2+) is crucial for excitation-transcription coupling. However, information on Ca(2+) signals in these subcellular compartments is limited...
April 1, 2014: American Journal of Physiology. Cell Physiology
María V Correa, Mariela B Nolly, Claudia I Caldiz, Gladys E Chiappe de Cingolani, Horacio E Cingolani, Irene L Ennis
Emerging evidence supports a key role for endothelin-1 (ET-1) and the transactivation of the epidermal growth factor receptor (EGFR) in angiotensin II (Ang II) action. We aim to determine the potential role played by endogenous ET-1, EGFR transactivation and redox-dependent sodium hydrogen exchanger-1 (NHE-1) activation in the hypertrophic response to Ang II of cardiac myocytes. Electrically paced adult cat cardiomyocytes were placed in culture and stimulated with 1 nmol l(-1) Ang II or 5 nmol l(-1) ET-1...
September 2014: Pflügers Archiv: European Journal of Physiology
Charis Putinski, Mohammad Abdul-Ghani, Rebecca Stiles, Steve Brunette, Sarah A Dick, Pasan Fernando, Lynn A Megeney
Cardiomyocyte hypertrophy is the cellular response that mediates pathologic enlargement of the heart. This maladaptation is also characterized by cell behaviors that are typically associated with apoptosis, including cytoskeletal reorganization and disassembly, altered nuclear morphology, and enhanced protein synthesis/translation. Here, we investigated the requirement of apoptotic caspase pathways in mediating cardiomyocyte hypertrophy. Cardiomyocytes treated with hypertrophy agonists displayed rapid and transient activation of the intrinsic-mediated cell death pathway, characterized by elevated levels of caspase 9, followed by caspase 3 protease activity...
October 22, 2013: Proceedings of the National Academy of Sciences of the United States of America
Akira Funayama, Tetsuro Shishido, Shunsuke Netsu, Taro Narumi, Shinpei Kadowaki, Hiroki Takahashi, Takuya Miyamoto, Tetsu Watanabe, Chang-Hoon Woo, Jun-ichi Abe, Koichiro Kuwahara, Kazuwa Nakao, Yasuchika Takeishi, Isao Kubota
AIMS: High mobility group box 1 (HMGB1) is an abundant and ubiquitous nuclear DNA-binding protein that has multiple functions dependent on its cellular location. HMGB1 binds to DNA, facilitating numerous nuclear functions including maintenance of genome stability, transcription, and repair. However, little is known about the effects of nuclear HMGB1 on cardiac hypertrophy and heart failure. The aim of this study was to examine whether nuclear HMGB1 plays a role in the development of cardiac hypertrophy induced by pressure overload...
September 1, 2013: Cardiovascular Research
Jerzy Bełtowski, Anna Jazmroz-Wiśniewska
Many experimental and clinical studies have demonstrated that elevated leptin concentration in patients with obesity/metabolic syndrome contributes to the pathogenesis of cardiovascular disorders including arterial hypertension, atherosclerosis, restenosis after coronary angioplasty and myocardial hypertrophy. Receptor tyrosine kinases belonging to the ErbB family, especially ErbB1 (epidermal growth factor receptor) and ErbB2 are abundantly expressed in the blood vessels and the heart. EGFR is activated not only by its multiple peptide ligands but also by many other factors including angiotensin II, endothelin-1, norepinephrine, thrombin and prorenin; the phenomenon referred to as "transactivation"...
2014: Current Pharmaceutical Design
Weiru Zhang, Yujin Zhang, Wei Wang, Yingbo Dai, Chen Ning, Renna Luo, Kaiqi Sun, Louise Glover, Almut Grenz, Hong Sun, Lijian Tao, Wenzheng Zhang, Sean P Colgan, Michael R Blackburn, Holger K Eltzschig, Rodney E Kellems, Yang Xia
RATIONALE: Hypertension is the most prevalent life-threatening disease worldwide and is frequently associated with chronic kidney disease (CKD). However, the molecular basis underlying hypertensive CKD is not fully understood. OBJECTIVE: We sought to identify specific factors and signaling pathways that contribute to hypertensive CKD and thereby exacerbate disease progression. METHODS AND RESULTS: Using high-throughput quantitative reverse-transcription polymerase chain reaction profiling, we discovered that the expression level of 5'-ectonucleotidase (CD73), a key enzyme that produces extracellular adenosine, was significantly increased in the kidneys of angiotensin II-infused mice, an animal model of hypertensive nephropathy...
May 24, 2013: Circulation Research
Jessica I Gold, Jeffrey S Martini, Jonathan Hullmann, Erhe Gao, J Kurt Chuprun, Linda Lee, Douglas G Tilley, Joseph E Rabinowitz, Julie Bossuyt, Donald M Bers, Walter J Koch
G protein-Coupled Receptors (GPCRs) kinases (GRKs) play a crucial role in regulating cardiac hypertrophy. Recent data from our lab has shown that, following ventricular pressure overload, GRK5, a primary cardiac GRK, facilitates maladaptive myocyte growth via novel nuclear localization. In the nucleus, GRK5's newly discovered kinase activity on histone deacetylase 5 induces hypertrophic gene transcription. The mechanisms governing the nuclear targeting of GRK5 are unknown. We report here that GRK5 nuclear accumulation is dependent on Ca(2+)/calmodulin (CaM) binding to a specific site within the amino terminus of GRK5 and this interaction occurs after selective activation of hypertrophic Gq-coupled receptors...
2013: PloS One
Ravi Kumar Chilukoti, Jörg Mostertz, Alicja Bukowska, Christoph Aderkast, Stephan B Felix, Matthias Busch, Uwe Völker, Andreas Goette, Carmen Wolke, Georg Homuth, Uwe Lendeckel
BACKGROUND: Atrial fibrillation (AF) is characterized by electrical and structural remodeling of the atria with atrial fibrosis being one hallmark. Angiotensin II (AngII) is a major contributing factor and blockage of its type I receptor (AT1R) prevents remodeling to some extent. Here we explored the effects of the AT1R antagonist irbesartan on global gene expression and profibrotic signaling pathways after induction of rapid atrial pacing (RAP) in vivo in pigs. METHODS AND RESULTS: Microarray-based RNA profiling was used to screen left atrial (LA) tissue specimens for differences in atrial gene expression in a model of acute RAP...
October 3, 2013: International Journal of Cardiology
Linda R Klei, D Yesica Garciafigueroa, Aaron Barchowsky
Dysfunctional lipid and glucose metabolism contribute to metabolic syndrome-a major public health concern that enhances cardiovascular disease risk. Arsenic (As(III)) exposure may increase metabolic syndrome and cardiovascular disease risk by impairing adipose tissue differentiation, function, and insulin sensitivity through pathogenic mechanisms that remain unclear. We hypothesized that As(III) signals through the Pertussis toxin (Ptx) sensitive, Gi protein-coupled receptor (GPCR) to impair adipogenesis, as previously demonstrated for its stimulation of vascular oxidant generation, angiogenesis, and remodeling...
February 2013: Toxicological Sciences: An Official Journal of the Society of Toxicology
Renée S Suen, Sarah N Rampersad, Duncan J Stewart, David W Courtman
Because both endothelin-1 (ET-1) and angiotensin II (AngII) are independent mediators of arterial remodeling, we sought to determine the role of ET receptor inhibition in AngII-accelerated atherosclerosis and aortic aneurysm formation. We administered saline or AngII and/or bosentan, an endothelin receptor antagonist (ERA) for 7, 14, or 28 days to 6-week- and 6-month-old apolipoprotein E-knockout mice. AngII treatment increased aortic atherosclerosis, which was reduced by ERA. ET-1 immunostaining was localized to macrophage-rich regions in aneurysmal vessels...
September 2011: American Journal of Pathology
Yessica-Haydee Gomez Sandoval, Yuan Li, Madhu B Anand-Srivastava
We earlier showed that the increased expression of Gi proteins exhibited by vascular smooth muscle cells (VSMC) from spontaneously hypertensive rats (SHR) was attributed to the enhanced levels of endogenous endothelin. Since the levels of angiotensin II (Ang II) are also enhanced in VSMC from SHR, the present study was undertaken to examine the role of enhanced levels of endogenous Ang II in the overexpression of Giα proteins in VSMC from SHR and to further explore the underlying mechanisms responsible for this increase...
November 2011: Cellular Signalling
Liming Wang, Jae-Hyung Chang, Seung-Yeol Paik, Yuping Tang, William Eisner, Robert F Spurney
To determine the role of Gq signaling and calcineurin (CN) activation in promoting apoptosis of glomerular podocytes, constitutively active Gq [Gq(+)] or CN [CN(+)] proteins were introduced into cultured podocytes using protein transduction by tagging the proteins with the transactivator of transcription peptide. To investigate the role of CN in promoting podocyte apoptosis in vivo, a genetic model of type 1 diabetes mellitus (Akita mice) was treated with the CN inhibitor FK506. In cultured podocytes, Gq(+) stimulated nuclear translocation of nuclear factor of activated T cells (NFAT) family members, activated an NFAT reporter construct, and enhanced podocyte apoptosis in a CN-dependent fashion...
August 2011: Molecular Endocrinology
Andreas Rinne, Lothar A Blatter
The Ca(2+)-sensitive nuclear factor of activated T cell (NFAT) transcription factors are implicated in cardiac development and cellular remodeling associated with cardiac disease. In adult myocytes it is not resolved what specific Ca(2+) signals control the activity of different NFAT isoforms in an environment that undergoes large changes of intracellular Ca(2+) concentration with every heart beat. Cardiac myocytes possess the complete inositol 1,4,5-trisphosphate (IP(3))/Ca(2+)-signaling cassette; however, its physiological and pathological significance has been a matter of ongoing debate...
November 2010: American Journal of Physiology. Heart and Circulatory Physiology
Songcang Chen, Christopher S Law, Christopher L Grigsby, Keith Olsen, David G Gardner
We have explored the mechanism(s) underlying 1,25 dihydroxyvitamin D's (1,25(OH)(2)D) suppression of agonist-induced vascular smooth muscle cell (VSMC) proliferation. Quiescent cultured adult rat VSMC were treated with 1,25(OH)(2)D for 48h and endothelin (ET) or angiotensin II (AII) for the final 24h. We show that VSMC responded to 1,25(OH)(2)D or its less hypercalcemic analogue RO 25-6760 with ∼70% inhibition of ET-dependent (3)H-thymidine incorporation. The inhibition was linked to a comparable reduction in ET-stimulated cyclin-dependent kinase 2 (Cdk2) activity and suppression of an ET-induced Cdk2 activator, cell division cycle 25 homolog A (Cdc25A)...
November 2010: Journal of Steroid Biochemistry and Molecular Biology
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