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Condition: Hypertension

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Total 587 results found since Jan 2013.

Rho‐kinase inhibitor fasudil reduces allergic airway inflammation and mucus hypersecretion by regulating STAT6 and NFκB
Conclusions and Clinical RelevanceThese findings indicate that the Rho‐A/Rho kinase inhibitor, fasudil, plays a negative regulatory role in allergen‐induced mucus secretion and MUC5AC expression by regulating STAT6 and NFκB.
Source: Clinical and Experimental Allergy - November 19, 2015 Category: Allergy & Immunology Authors: T. Xie, GY. Luo, Y. Zhang, X. Wang, XY. Wang, M. Wu, GP. Li Tags: Original Article Source Type: research

Raf/ERK drives the proliferative and invasive phenotype of BMPR2-silenced pulmonary artery endothelial cells.
This study examined the non-canonical signaling consequences of BMPR2 silencing in human pulmonary artery endothelial cells to identify potential therapeutic targets. BMPR2 siRNA silencing resulted in a proliferative, pro-migratory pulmonary artery endothelial cell phenotype and disruption of cytoskeletal architecture. Expression profiling closely reflected these phenotypic changes. Gene set enrichment and promoter analyses, as well as the differential expression of pathway components identified Ras/Raf/ERK signaling as an important consequence of BMPR2 silencing. Raf family members and ERK1/2 were constitutively activated...
Source: Am J Physiol Lung Ce... - November 20, 2015 Category: Respiratory Medicine Authors: Awad KS, Elinoff JM, Wang S, Gairhe S, Ferreyra GA, Cai R, Sun J, Solomon MA, Danner RL Tags: Am J Physiol Lung Cell Mol Physiol Source Type: research

Threonine532 phosphorylation in ClC‐3 channels is required for angiotensin II‐induced Cl− current and migration in cultured vascular smooth muscle cells
Conclusions And ImplicationsClC‐3 protein phosphorylation at Thr532 by ROCK2 is required for AngII‐induced Cl− current and VSMC migration that are involved in AngII‐induced vascular remodelling in hypertension.
Source: British Journal of Pharmacology - January 15, 2016 Category: Drugs & Pharmacology Authors: Ming‐Ming Ma, Cai‐Xia Lin, Can‐Zhao Liu, Min Gao, Lu Sun, Yong‐Bo Tang, Jia‐Guo Zhou, Guan‐Lei Wang, Yong‐Yuan Guan Tags: RESEARCH PAPER Source Type: research

Raf/ERK drives the proliferative and invasive phenotype of BMPR2-silenced pulmonary artery endothelial cells
This study examined the noncanonical signaling consequences of BMPR2 silencing in human pulmonary artery endothelial cells to identify potential therapeutic targets. BMPR2 siRNA silencing resulted in a proliferative, promigratory pulmonary artery endothelial cell phenotype and disruption of cytoskeletal architecture. Expression profiling closely reflected these phenotypic changes. Gene set enrichment and promoter analyses, as well as the differential expression of pathway components identified Ras/Raf/ERK signaling as an important consequence of BMPR2 silencing. Raf family members and ERK1/2 were constitutively activated a...
Source: AJP: Lung Cellular and Molecular Physiology - January 15, 2016 Category: Respiratory Medicine Authors: Awad, K. S., Elinoff, J. M., Wang, S., Gairhe, S., Ferreyra, G. A., Cai, R., Sun, J., Solomon, M. A., Danner, R. L. Tags: ARTICLES Source Type: research

NLRP3 Deletion Protects against Renal Fibrosis and Attenuates Mitochondrial Abnormality in Mouse with 5/6 Nephrectomy.
Abstract Progressive fibrosis in chronic kidney disease (CKD) is the well-recognized cause leading to the progressive loss of renal function. Emerging evidence indicated a pathogenic role of NLRP3 inflammasome in mediating kidney injury. However, the role of NLRP3 in remnant kidney disease model is still undefined. The present study is undertaken to evaluate the function of NLRP3 in modulating renal fibrosis in a CKD model of 5/6 nephrectomy (5/6 Nx) and the potential involvement of mitochondrial dysfunction in the pathogenesis. Employing NLRP3+/+ and NLRP3-/- mice with or without 5/6 Nx, we examined renal fibroti...
Source: Am J Physiol Renal P... - February 17, 2016 Category: Urology & Nephrology Authors: Gong W, Mao S, Yu J, Song J, Jia Z, Huang S, Zhang A Tags: Am J Physiol Renal Physiol Source Type: research

MiR-590-5p-Meidated LOX-1 Upregulation Promotes Angiotensin II-Induced Endothelial Cell Apoptosis.
CONCLUSION: Our data demonstrated that miR-590-5p downregulation promoted Ang II-induced endothelial cell apoptosis by elevating LOX-1 expression and consequently increasing ROS generation. Thus, restoration of miR-590-5p or block of LOX-1 could be therapeutically exploited to alleviate endothelial cell apoptosis. PMID: 26906623 [PubMed - as supplied by publisher]
Source: Biochemical and Biophysical Research communications - February 20, 2016 Category: Biochemistry Authors: Luo P, Zhang WF, Qian ZX, Xiao LF, Wang H, Zhu TT, Li F, Hu CP, Zhang Z Tags: Biochem Biophys Res Commun Source Type: research

Modulators of right ventricular apoptosis and contractility in a rat model of pulmonary hypertension
Conclusion These results suggest that RV decompensation is associated with the death of cardiomyocytes, resulting in fibrosis. However, the remaining myocytes are capable of sustaining RV contractility through the mechanism that involves CSQ2.
Source: Cardiovascular Research - March 18, 2016 Category: Cardiology Authors: Zungu-Edmondson, M., Shults, N. V., Wong, C.-M., Suzuki, Y. J. Tags: Integrative physiology and pathophysiology Source Type: research

Loss of Akt increases soluble endoglin release from endothelial cells but not placenta
Conclusion This study confirms that the PI3K/Akt cell protection pathway is down regulated in preeclampsia, but demonstrates that this dysregulation is unlikely to be responsible for the excessive placental soluble endoglin release characteristic of preeclampsia.
Source: Pregnancy Hypertension: An International Journal of Womens Cardiovascular Health - March 28, 2016 Category: OBGYN Source Type: research

In Pulmonary Arterial Hypertension, Reduced BMPR2 Promotes Endothelial-to-Mesenchymal Transition via HMGA1 and its Target Slug.
CONCLUSIONS: -Increased HMGA1 in PAECs resulting from dysfunctional BMPR2 signaling can transition endothelium to SM-like cells associated with PAH. PMID: 27045138 [PubMed - as supplied by publisher]
Source: Circulation - April 3, 2016 Category: Cardiology Authors: Hopper RK, Moonen JA, Diebold I, Cao A, Rhodes CJ, Tojais NF, Hennigs JK, Gu M, Wang L, Rabinovitch M Tags: Circulation Source Type: research

Inhibition of Fatty Acid Synthase is Protective in Pulmonary Hypertension
ConclusionsOur results demonstrate that FAS activity gets modulated in PH and its inhibition may serve as a new therapeutic approach to treat PH.
Source: British Journal of Pharmacology - April 6, 2016 Category: Drugs & Pharmacology Authors: Neetu Singh, Amit Manhas, Gurpreet Kaur, Kumaravelu Jagavelu, Kashif Hanif Tags: RESEARCH PAPER Source Type: research

Calpain-2 Activates Akt via TGFβ1-mTORC2 Pathway in Pulmonary Artery Smooth Muscle Cells.
Abstract Calpain is a family of calcium-dependent nonlysosomal neutral cysteine endopeptidases. Akt is a serine/threonine kinase that belongs to AGC kinases and plays important roles in cell survival, growth, proliferation, angiogenesis, and cell metabolism. Both calpain and Akt are the downstream signaling molecules of platelet-derived growth factor (PDGF) and mediate PDGF-induced collagen synthesis and proliferation of pulmonary artery smooth muscle cells (PASMCs) in pulmonary vascular remodeling. We found that inhibitions of calpain-2 by using calpain inhibitor MDL28170 and calpain-2 siRNA attenuated Akt phosph...
Source: Am J Physiol Cell Ph... - April 19, 2016 Category: Cytology Authors: Abeyrathna P, Kovacs L, Han W, Su Y Tags: Am J Physiol Cell Physiol Source Type: research

Lipopolysaccharide potentiates endothelin-1-induced proliferation of pulmonary arterial smooth muscle cells by upregulating TRPC channels
Publication date: August 2016 Source:Biomedicine & Pharmacotherapy, Volume 82 Author(s): Hong-Ni Jiang, Bo Zeng, Gui-Lan Chen, Bin Lai, Shao-Hua Lu, Jie-Ming Qu Lipopolysaccharide (LPS) and endothelin-1 (ET-1) are critical pathogenic factors in sepsis-induced pulmonary hypertension; however it is unknown whether they have a coordinated action in the pathogenesis of this disease. Here we found that although LPS did not change the contractility of rat pulmonary arterial smooth muscle cells (PASMCs) in response to ET-1, it significantly promoted ET-1-induced PASMC proliferation. Measurement of ET-1-evoked Ca2+...
Source: Biomedicine and Pharmacotherapy - May 3, 2016 Category: Drugs & Pharmacology Source Type: research

Resveratrol via activation of LKB1-AMPK signaling suppresses oxidative stress to prevent endothelial dysfunction in diabetic mice.
CONCLUSIONS: We conclude that AMPK activation is required for resveratrol to improve endothelial function in diabetic mice. PMID: 27149559 [PubMed - as supplied by publisher]
Source: Clinical and Experimental Hypertension - May 4, 2016 Category: Cardiology Authors: Hu M, Liu B Tags: Clin Exp Hypertens Source Type: research

High salt medium activates RhoA/ROCK and downregulates eNOS expression via the upregulation of ADMA.
Authors: Cao Y, Fang Y, Mu J, Liu X Abstract Endothelial dysfunction has an important role in the development and progression of salt-sensitive hypertension. Asymmetric dimethylarginine (ADMA), which is an endogenous inhibitor of nitric oxide synthase (NOS), has been demonstrated to be involved in the pathophysiological processes of endothelial dysfunction and salt‑sensitive hypertension. However, it is currently unclear how high salt intake may induce these processes. The present study investigated the effects of high salt medium on ADMA, endothelial NOS (eNOS) and the Ras homolog gene family, member A (RhoA)/R...
Source: Molecular Medicine Reports - May 15, 2016 Category: Molecular Biology Tags: Mol Med Rep Source Type: research

Osmotic induction of placental growth factor in retinal pigment epithelial cells in vitro: contribution of NFAT5 activity.
Abstract One risk factor of neovascular age-related macular degeneration is systemic hypertension; hypertension is mainly caused by extracellular hyperosmolarity after consumption of dietary salt. In retinal pigment epithelial (RPE) cells, high extracellular osmolarity induces vascular endothelial growth factor (VEGF)-A (Hollborn et al. in Mol Vis 21:360-377, 2015). The aim of the present study was to determine whether extracellular hyperosmolarity and chemical hypoxia trigger the expression of further VEGF family members including placental growth factor (PlGF) in human RPE cells. Hyperosmotic media were made up ...
Source: Molecular Biology Reports - May 25, 2016 Category: Molecular Biology Authors: Hollborn M, Reichmuth K, Prager P, Wiedemann P, Bringmann A, Kohen L Tags: Mol Biol Rep Source Type: research