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Sirt3 AND angiotensin

Lirong Guo, Ankang Yin, Qi Zhang, Tiecheng Zhong, Stephen T O'Rourke, Chengwen Sun
The objectives of the current study were to investigate the effect of Ang-(1-7) on the development of cardiac hypertrophy, and to identify the intracellular mechanism underlying this action of Ang-(1-7). Blood pressure and heart rate were recorded using radiotelemetry before and after chronic subcutaneous infusion of control (PBS), Ang II, Ang-(1-7), or Ang II+Ang-(1-7) for 4 weeks in normotensive rats. Chronic administration of Ang-(1-7) did not affect either basal blood pressure or the Ang II-induced elevation in blood pressure...
April 14, 2017: American Journal of Physiology. Heart and Circulatory Physiology
Xiao-Hui Guan, Xuan Hong, Ning Zhao, Xiao-Hong Liu, Yun-Fei Xiao, Ting-Tao Chen, Li-Bin Deng, Xiao-Lei Wang, Jian-Bin Wang, Guang-Ju Ji, Mingui Fu, Ke-Yu Deng, Hong-Bo Xin
Cardiac hypertrophy is an early hallmark during the clinical course of heart failure and regulated by various signalling pathways. Recently, we observed that mouse embryonic fibroblasts from CD38 knockout mice were significantly resistant to oxidative stress such as H2 O2 -induced injury and hypoxia/reoxygenation-induced injury. In addition, we also found that CD38 knockout mice protected heart from ischaemia reperfusion injury through activating SIRT1/FOXOs-mediated antioxidative stress pathway. However, the role of CD38 in cardiac hypertrophy is not explored...
March 12, 2017: Journal of Cellular and Molecular Medicine
Sujana Katta, Santosh Karnewar, Devayani Panuganti, Mahesh Kumar Jerald, Sastry B K, Srigiridhar Kotamraju
In this study, we explored the microRNAs responsible for the regulation of PAI-1 during LPS-stimulated inflammation in human aortic endothelial cells, subsequently studied the effect of a newly synthesized mitochondria-targeted esculetin (Mito-Esc) that was shown for its anti-atherosclerotic potential in modulating PAI-1 levels and its targeted miRs during angiotensin-II-induced atherosclerosis in ApoE(-/-) mice. LPS-stimulated PAI-1 was accompanied with an upregulation of miR-19b and down-regulation of miR-30c...
February 18, 2017: Journal of Cellular Physiology
Jingyuan Li, Tongshuai Chen, Ming Xiao, Na Li, Shujian Wang, Hongyan Su, Xiaobin Guo, Hui Liu, Fangying Yan, Yi Yang, Yun Zhang, Peili Bu
Sirt3, a mitochondrial NAD+-dependent histone deacetylase, is the only member proven to promote longevity in mammalian Sirtuin family. The processed short form of Sirt3 has been demonstrated to target many mediators of energy metabolism and mitochondrial stress adaptive program. Autophagy serves as a dynamic recycling mechanism and provides energy or metabolic substrates. Among the mechanisms triggered by cardiac stress, opinions vary as to whether autophagy is a protective or detrimental response. Here, by inducing the Sirt3-knockout mice to myocardial hypertrophy with chronic angiotensin II infusion for four weeks, we determined the role of Sirt3 in myocardial hypertrophy and autophagy...
December 27, 2016: Oncotarget
Yu-Xuan Luo, Xiaoqiang Tang, Xi-Zhou An, Xue-Min Xie, Xiao-Feng Chen, Xiang Zhao, De-Long Hao, Hou-Zao Chen, De-Pei Liu
AIMS: Oxidative stress contributes to the development of cardiac hypertrophy and heart failure. One of the mitochondrial sirtuins, Sirt4, is highly expressed in the heart, but its function remains unknown. The aim of the present study was to investigate the role of Sirt4 in the pathogenesis of pathological cardiac hypertrophy and the molecular mechanism by which Sirt4 regulates mitochondrial oxidative stress. METHODS AND RESULTS: Male C57BL/6 Sirt4 knockout mice, transgenic (Tg) mice exhibiting cardiac-specific overexpression of Sirt4 (Sirt4-Tg) and their respective controls were treated with angiotensin II (Ang II, 1...
April 20, 2016: European Heart Journal
Santosh Karnewar, Sathish Babu Vasamsetti, Raja Gopoju, Anantha Koteswararao Kanugula, Sai Krishna Ganji, Sripadi Prabhakar, Nandini Rangaraj, Nitin Tupperwar, Jerald Mahesh Kumar, Srigiridhar Kotamraju
Mitochondria-targeted compounds are emerging as a new class of drugs that can potentially alter the pathophysiology of those diseases where mitochondrial dysfunction plays a critical role. We have synthesized a novel mitochondria-targeted esculetin (Mito-Esc) with an aim to investigate its effect during oxidative stress-induced endothelial cell death and angiotensin (Ang)-II-induced atherosclerosis in ApoE(-/-) mice. Mito-Esc but not natural esculetin treatment significantly inhibited H2O2- and Ang-II-induced cell death in human aortic endothelial cells by enhancing NO production via AMPK-mediated eNOS phosphorylation...
April 11, 2016: Scientific Reports
Sabzali Javadov, Nelson Escobales
Cardiac ischemia-reperfusion stimulates the renin-angiotensin system (RAS) associated with elevated levels of circulating angiotensin II. Numerous studies demonstrate that the antagonist for the angiotensin II type 1 receptor, losartan improves cardiac function in animal models of ischemia-reperfusion. Molecular mechanisms of the cardioprotective effects of RAS inhibitors on cardiac ischemia-reperfusion remain poorly understood, and are not associated with the anti-hypertensive action of these drugs. This Commentary focuses on the study published in the Journal of Pharmacy and Pharmaceutical Sciences, 2015, 18:112-123, that elucidates the role of SIRT3 in the cardioprotective action of losartan against ischemic-reperfusion injury...
2015: Journal of Pharmacy & Pharmaceutical Sciences: a Publication of the Canadian Society for Pharmaceutical Sciences
Hui Liu, Tongshuai Chen, Na Li, Shujian Wang, Peili Bu
BACKGROUND: SIRT3, a member of the sirtuin family of NAD(+)-dependent deacetylases, resides primarily in the mitochondria and has been shown to deacetylate several metabolic and respiratory enzymes that regulate important mitochondrial functions. Previous researches show an important role of SIRT3 in regulating the production of reactive oxygen species (ROS), and highlight the ability of SIRT3 to protect cells from oxidative damage. A key substance of renin-angiotensin-aldosterone system (RAAS), Angiotensin II (AngII) can induce cells dysfunction by increasing the production of ROS...
2015: BMC Cardiovascular Disorders
Eirini Pantazi, Mohamed Bejaoui, Mohamed Amine Zaouali, Emma Folch-Puy, Anabela Pinto Rolo, Arnau Panisello, Carlos Marques Palmeira, Joan Roselló-Catafau
AIM: To investigate a possible association between losartan and sirtuin 1 (SIRT1) in reduced-size orthotopic liver transplantation (ROLT) in rats. METHODS: Livers of male Sprague-Dawley rats (200-250 g) were preserved in University of Wisconsin preservation solution for 1 h at 4 °C prior to ROLT. In an additional group, an antagonist of angiotensin II type 1 receptor (AT1R), losartan, was orally administered (5 mg/kg) 24 h and 1 h before the surgical procedure to both the donors and the recipients...
July 14, 2015: World Journal of Gastroenterology: WJG
Mohsen Sharifi Klishadi, Farideh Zarei, Seyyed Hassan Hejazian, Ali Moradi, Mahdieh Hemati, Fatemeh Safari
PURPOSE: Sirtuin-3 (SIRT3) deacetylase protects the heart against oxidative stress via survival factors upregulation. Clinical and experimental studies have demonstrated that activation of systemic and local renin-angiotensin system (RAS) is implicated in ischemia-induced cardiac injury. However, the relation between RAS and SIRT3 in pathophysiology of myocardial ischemia reperfusion is unknown. In this study, the cardiac transcription and expression of SIRT3 levels was examined in response to ischemia reperfusion in untreated and losartan treated rats...
2015: Journal of Pharmacy & Pharmaceutical Sciences: a Publication of the Canadian Society for Pharmaceutical Sciences
Yao-Ping Lin, Wen-Chung Yu, Meng-Erh Hsu, Hsiao-Chien Tsai, Chen-Chung Liao, Chao-Hsiung Lin
BACKGROUND: Chronic kidney disease (CKD) is associated with cardiac hypertrophy that leads to increased cardiovascular morbidity and mortality. To date, use of the renin-angiotensin-aldosterone system blockade has been the main treatment modality. However, renin-angiotensin-aldosterone system blockade by the angiotensin converting enzyme inhibitors (ACEi) can only partially reverse the cardiac hypertrophy without having a significant impact on all-cause mortality as evidenced by meta-analyses from clinical trials...
April 2015: Journal of the Chinese Medical Association: JCMA
Yong Li, Guangsi Shen, Chen Yu, Guangfei Li, Junkang Shen, Jianping Gong, Youjia Xu
Previous report showed that angiotensin II accelerates osteoporosis, and recent clinical studies suggest that several antihypertensive drugs, especially angiotensin-converting enzyme inhibitors, reduced bone fractures. However, the underling mechanism by which angiotensin II induces bone dysfunction is largely unknown. Here in this study, we show that angiotensin II induces mitochondrial oxidative stress and mitochondrial DNA (mtDNA) damage. We find that the protein and RNA levels of mitochondrial catalase and manganese superoxide dismutase (MnSOD) are decreased in osteoblasts in the presence of angiotensin II...
December 5, 2014: Biochemical and Biophysical Research Communications
Takeshi Shiraishi, Yoshifuru Tamura, Kei Taniguchi, Masato Higaki, Shuko Ueda, Tomoko Shima, Michito Nagura, Takahiko Nakagawa, Richard J Johnson, Shunya Uchida
An inhibition in the renin-angiotensin system (RAS) is one of the most widely used therapies to treat chronic kidney disease. However, its effect is occasionally not sufficient and additional treatments may be required. Recently, we reported that nicorandil exhibited renoprotective effects in a mouse model of diabetic nephropathy. Here we examined if nicorandil can provide an additive protection on enalapril in chronic kidney disease. Single treatment with either enalapril or nicorandil significantly ameliorated glomerular and tubulointerstitial injury in the rat remnant kidney while the combination of these two compounds provided additive effects...
December 15, 2014: American Journal of Physiology. Renal Physiology
Munehiro Kitada, Shinji Kume, Daisuke Koya
PURPOSE OF REVIEW: Accumulating evidence indicates the beneficial effects of sirtuins (SIRTs), including SIRT1 and SIRT3, which are NAD-dependent deacetylases, in age-related diseases such as diabetes, neuron disease, cardiovascular disease and kidney disease. RECENT FINDINGS: SIRT1 deacetylates many targets, such as transcriptional factors and proteins, and exhibits renoprotection through reduction of fibrosis, antiapoptotic and anti-inflammatory effects and induction of autophagy in renal cells...
January 2014: Current Opinion in Nephrology and Hypertension
Xinning Wu, Peili Bu, Junni Liu, Lixing Zhao, Xi Wang, Na Li
OBJECTIVE: To detect the expression of Sirtuin3 (Sirt3) in mice vascular smooth muscle cells (VSMCs) and explore the effect of Sirt3 on VSMCs proliferation induced by angiotensin II (AngII). METHODS: The mRNA and protein expressions of Sirt3 in wild C57 mice VSMCs were assessed by RT-PCR and Western blotting, respectively. After the cells were exposed to various concentrations of AngII (10(-7);, 10(-6);, 10(-5); mol/L), the mRNA and protein expressions of Sirt3 were assessed again in the same way...
March 2013: Xi Bao Yu Fen Zi Mian Yi Xue za Zhi, Chinese Journal of Cellular and Molecular Immunology
Jun Mori, Osama Abo Alrob, Cory S Wagg, Robert A Harris, Gary D Lopaschuk, Gavin Y Oudit
The renin-angiotensin system (RAS) may alter cardiac energy metabolism in heart failure. Angiotensin II (ANG II), the main effector of the RAS in heart failure, has emerged as an important regulator of cardiac hypertrophy and energy metabolism. We studied the metabolic perturbations and insulin response in an ANG II-induced hypertrophy model. Ex vivo heart perfusion showed that hearts from ANG II-treated mice had a lower response to insulin with significantly reduced rates of glucose oxidation in association with increased pyruvate dehydrogenase kinase 4 (PDK4) levels...
April 15, 2013: American Journal of Physiology. Heart and Circulatory Physiology
Luciano S A Capettini, Fabrizio Montecucco, Francois Mach, Nikos Stergiopulos, Robson A S Santos, Rafaela F da Silva
Recent data support the idea that the effects of RAS are not restricted to the cardiovascular and renal systems. Importantly, RAS modulates free radical production and the cellular synthesis of several molecules such as cytokines, chemokines and transcription factors. These functions reflect directly the RAS ability to modulate the cell growth, senescence and migration. Activation of the classic RAS, ACE/Ang II/AT1R, has been strictly related to down regulation of pro-survival genes (Nampt and Sirt3), increase in ROS production and pro-inflammatory cytokines and chemokines release, leading to cell senescence, inflammation and development of autoimmune dysfunctions...
2012: Current Pharmaceutical Design
Ariela Benigni, Daniela Corna, Carla Zoja, Aurelio Sonzogni, Roberto Latini, Monica Salio, Sara Conti, Daniela Rottoli, Lorena Longaretti, Paola Cassis, Marina Morigi, Thomas M Coffman, Giuseppe Remuzzi
The renin-angiotensin system plays a role in the etiology of hypertension and the pathophysiology of cardiac and renal diseases in humans. Ang II is the central product of this system and is involved in regulating immune responses, inflammation, cell growth, and proliferation by acting through Ang II type 1 receptors (AT1 and AT2). Here, we show that targeted disruption of the Agtr1a gene that encodes AT1A results in marked prolongation of life span in mice. Agtr1a-/- mice developed less cardiac and vascular injury, and multiple organs from these mice displayed less oxidative damage than wild-type mice...
March 2009: Journal of Clinical Investigation
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