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rho kinase and endoplasmic reticulum stress

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https://www.readbyqxmd.com/read/27701635/the-role-of-ire-xbp1-pathway-in-regulation-of-retinal-pigment-epithelium-tight-junctions
#1
Jacey H Ma, Joshua J Wang, Junhua Li, Bruce A Pfeffer, Yiming Zhong, Sarah X Zhang
Purpose: The retinal pigment epithelium (RPE) tight junctions play a pivotal role in maintaining the homeostatic environment of the neural retina. Herein, we investigated the role of X-box binding protein 1 (XBP1), an endoplasmic reticulum (ER) stress-responsive transcription factor, in regulation of RPE tight junctions. Methods: Human RPE cell line (ARPE-19) and primary primate RPE cells were used for in vitro experiments and RPE-specific XBP1 knockout (KO) mice were used for in vivo study...
October 1, 2016: Investigative Ophthalmology & Visual Science
https://www.readbyqxmd.com/read/25964548/combining-cal-101-with-celecoxib-enhances-apoptosis-of-ebv-transformed-b-cells-through-mapk-induced-er-stress
#2
Ga Bin Park, Dae Young Hur, Daejin Kim
BACKGROUND: Phosphoinositide-3 kinase (PI3K) inhibition attenuates proliferation and survival in B-cell malignancies. Celecoxib induces endoplasmic reticulum (ER) stress-induced apoptosis via a cyclo-oxgenase-2 (COX2)-independent manner in certain types of cancer cells. In the present study, we assessed the effects of combinations of drugs with a p110δ-specific inhibitor, CAL-101, and celecoxib to induce apoptosis in Epstein-Barr virus (EBV)-transformed B-cells and non-Hodgkin's lymphoma (NHL) cells...
May 2015: Anticancer Research
https://www.readbyqxmd.com/read/24553922/proteomic-survey-reveals-altered-energetic-patterns-and-metabolic-failure-prior-to-retinal-degeneration
#3
Ana Griciuc, Michel J Roux, Juliane Merl, Angela Giangrande, Stefanie M Hauck, Liviu Aron, Marius Ueffing
Inherited mutations that lead to misfolding of the visual pigment rhodopsin (Rho) are a prominent cause of photoreceptor neuron (PN) degeneration and blindness. How Rho proteotoxic stress progressively impairs PN viability remains unknown. To identify the pathways that mediate Rho toxicity in PNs, we performed a comprehensive proteomic profiling of retinas from Drosophila transgenics expressing Rh1(P37H), the equivalent of mammalian Rho(P23H), the most common Rho mutation linked to blindness in humans. Profiling of young Rh1(P37H) retinas revealed a coordinated upregulation of energy-producing pathways and attenuation of energy-consuming pathways involving target of rapamycin (TOR) signaling, which was reversed in older retinas at the onset of PN degeneration...
February 19, 2014: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/23928855/tdag51-deficiency-promotes-oxidative-stress-induced-apoptosis-through-the-generation-of-reactive-oxygen-species-in-mouse-embryonic-fibroblasts
#4
Eui-Soon Park, Juhyeok Kim, Tae-uk Ha, Jong-Soon Choi, Kwan Soo Hong, Jaerang Rho
Apoptosis has an important role in maintaining tissue homeostasis in cellular stress responses such as inflammation, endoplasmic reticulum stress, and oxidative stress. T-cell death-associated gene 51 (TDAG51) is a member of the pleckstrin homology-like domain family and was first identified as a pro-apoptotic gene in T-cell receptor-mediated cell death. However, its pro-apoptotic function remains controversial. In this study, we investigated the role of TDAG51 in oxidative stress-induced apoptotic cell death in mouse embryonic fibroblasts (MEFs)...
2013: Experimental & Molecular Medicine
https://www.readbyqxmd.com/read/23665024/fasudil-inhibits-er-stress-induced-vcam-1-expression-by-modulating-unfolded-protein-response-in-endothelial-cells
#5
Daiji Kawanami, Keiichiro Matoba, Rina Okada, Masami Tsukamoto, Jun Kinoshita, Sho Ishizawa, Yasushi Kanazawa, Tamotsu Yokota, Kazunori Utsunomiya
The process of atherosclerosis is affected by interactions among numerous biological pathways. Accumulating evidence shows that endoplasmic reticulum (ER) stress plays a crucial role in the development of atherosclerosis. Rho-kinase is an effector of small GTP-binding protein Rho, and has been implicated as an atherogenic factor. Previous studies demonstrated that fasudil, a specific Rho-kinase inhibitor, exerts a cardioprotective effect by downregulating ER stress signaling. However, the molecular link between ER stress and Rho-kinase in endothelial cells has not been elucidated...
May 31, 2013: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/23118936/fasudil-protects-the-heart-against-ischemia-reperfusion-injury-by-attenuating-endoplasmic-reticulum-stress-and-modulating-serca-activity-the-differential-role-for-pi3k-akt-and-jak2-stat3-signaling-pathways
#6
Yapeng Li, Wei Zhu, Jianping Tao, Ping Xin, Mingya Liu, Jingbo Li, Meng Wei
Disordered calcium homeostasis can lead to endoplasmic reticulum (ER) stress. Our previous data showed that time course activation of ER stress contributes to time-related increase in ischemia-reperfusion (I/R) injury. However, it has not been tested whether PI3K/Akt and JAK2/STAT3 pathways play differential roles in reducing ER stress to protect the heart. In the present study, using fasudil which is a specific inhibitor of ROCK, we aimed to investigate whether improved SERCA expression and activity accounts for reduced ER stress by ROCK inhibition, specifically whether PI3K/Akt and JAK2/STAT3 pathways are differentially involved in modulating SERCA activity to reduce ER stress and hence I/R injury...
2012: PloS One
https://www.readbyqxmd.com/read/23024816/neurokinin-1-receptor-mediates-membrane-blebbing-and-sheer-stress-induced-microparticle-formation-in-hek293-cells
#7
Panpan Chen, Steven D Douglas, John Meshki, Florin Tuluc
Cell-derived microparticles participate in intercellular communication similar to the classical messenger systems of small and macro-molecules that bind to specialized membrane receptors. Microparticles have been implicated in the regulation of a variety of complex physiopathologic processes, such as thrombosis, the control of innate and adaptive immunity, and cancer. The neurokinin 1 receptor (NK1R) is a Gq-coupled receptor present on the membrane of a variety of tissues, including neurons in the central and peripheral nervous system, immune cells, endocrine and exocrine glands, and smooth muscle...
2012: PloS One
https://www.readbyqxmd.com/read/22989520/lapatinib-and-obatoclax-kill-breast-cancer-cells-through-reactive-oxygen-species-dependent-endoplasmic-reticulum-stress
#8
Nichola Cruickshanks, Yong Tang, Laurence Booth, Hossein Hamed, Steven Grant, Paul Dent
Previous studies showed that lapatinib and obatoclax interact in a greater-than-additive fashion to cause cell death and do so through a toxic form of autophagy. The present studies sought to extend our analyses. Lapatinib and obatoclax killed multiple tumor cell types, and cells lacking phosphatase and tensin homolog (PTEN) function were relatively resistant to drug combination lethality; expression of PTEN in PTEN-null breast cancer cells restored drug sensitivity. Coadministration of lapatinib with obatoclax elicited autophagic cell death that was attributable to the actions of mitochondrial reactive oxygen species...
December 2012: Molecular Pharmacology
https://www.readbyqxmd.com/read/22432009/er-stress-in-retinal-degeneration-in-s334ter-rho-rats
#9
Vishal M Shinde, Olga S Sizova, Jonathan H Lin, Matthew M LaVail, Marina S Gorbatyuk
The S334ter rhodopsin (Rho) rat (line 4) bears the rhodopsin gene with an early termination codon at residue 334 that is a model for several such mutations found in human patients with autosomal dominant retinitis pigmentosa (ADRP). The Unfolded Protein Response (UPR) is implicated in the pathophysiology of several retinal disorders including ADRP in P23H Rho rats. The aim of this study was to examine the onset of UPR gene expression in S334ter Rho retinas to determine if UPR is activated in ADRP animal models and to investigate how the activation of UPR molecules leads to the final demise of S334ter Rho photoreceptors...
2012: PloS One
https://www.readbyqxmd.com/read/22194610/group-via-pla2-ipla2%C3%AE-is-activated-upstream-of-p38-mitogen-activated-protein-kinase-mapk-in-pancreatic-islet-%C3%AE-cell-signaling
#10
Haowei Song, Mary Wohltmann, Min Tan, Shunzhong Bao, Jack H Ladenson, John Turk
Group VIA phospholipase A(2) (iPLA(2)β) in pancreatic islet β-cells participates in glucose-stimulated insulin secretion and sarco(endo)plasmic reticulum ATPase (SERCA) inhibitor-induced apoptosis, and both are attenuated by pharmacologic or genetic reductions in iPLA(2)β activity and amplified by iPLA(2)β overexpression. While exploring signaling events that occur downstream of iPLA(2)β activation, we found that p38 MAPK is activated by phosphorylation in INS-1 insulinoma cells and mouse pancreatic islets, that this increases with iPLA(2)β expression level, and that it is stimulated by the iPLA(2)β reaction product arachidonic acid...
February 17, 2012: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/19137259/transient-and-constitutive-repression-of-cytoplasmic-translation-signaling-in-cells-with-mtdna-mutation
#11
G M C Janssen, P Schwertman, T A T Wanga, R S Jahangir Tafrechi, P J A van den Broek, A K Raap
Cytoplasmic translation is under sophisticated control but how cells adapt its rate to constitutive loss of mitochondrial oxidative phosphorylation is unknown. Here we show that translation is repressed in cells with the pathogenic A3243G mtDNA mutation or in mtDNA-less rho(0) cells by at least two distinct pathways, one transiently targeting elongation factor eEF-2 and the other initiation factor eIF-2alpha constitutively. Under conditions of exponential cell growth and mammalian target of rapamycin (mTOR) activation, eEF-2 becomes transiently phosphorylated by an AMP-activated protein kinase (AMPK)-dependent pathway, especially high in mutant cells...
February 2009: Cellular and Molecular Life Sciences: CMLS
https://www.readbyqxmd.com/read/16775602/meeting-report-isn-forefronts-in-nephrology-on-endothelial-biology-and-renal-disease-from-bench-to-prevention
#12
M S Goligorsky, T Rabelink
This ISN-sponsored Forefront in Nephrology meeting, which has brought together 120 scientists from 21 countries, has been concerned with various aspects of endothelial function and dysfunction and their contribution to progression of chronic kidney disease and/or its cardiovascular complications. The following themes were discussed in great depth: (1) phenotypical changes in the vascular endothelium - permeability, senescence, and apoptosis; (2) regulation of endothelial nitric oxide (NO) synthase function - caveolar and shear stress mechanisms, epigenetic regulation, S-nitrosylation, and Rho-kinase regulation; (3) oxidative stress and hypoxia-induced changes; (4) organellar dysfunction - lysosomes, mitochondria, and endoplasmic reticulum; (5) NO-independent mechanisms of vasomotion - epoxides, heme oxygenase-1 and carbon monoxide, thromboxane, tumor necrosis factor-alpha, and uric acid; (6) endothelial crosstalk with podocytes, monocytes, smooth muscle cells, and platelets; (7) candidate clinical biomarkers of endothelial dysfunction - functional testing of macro- and micro-vascular functions, surrogate markers, circulating detached endothelial cells, and endothelial precursor cells; and culminated in Round Table discussion on the diagnosis of endothelial dysfunction and its treatment options...
July 2006: Kidney International
https://www.readbyqxmd.com/read/16115036/reactive-oxygen-species-as-mediators-of-calcium-signaling-by-angiotensin-ii-implications-in-vascular-physiology-and-pathophysiology
#13
REVIEW
Rhian M Touyz
Reactive oxygen species (ROS), including superoxide anion, hydrogen peroxide, and hydroxyl radical, and reactive nitrogen species, such as nitric oxide and peroxynitrite, are biologically relevant O2 derivatives increasingly being recognized as important in vascular biology through their oxidation/reduction (redox) potential. All vascular cell types produce ROS primarily via membrane-associated NAD(P)H oxidase. ROS influence vascular function by modulating contraction/dilation, cell growth, apoptosis/anoikis, migration, inflammation, and fibrosis...
September 2005: Antioxidants & Redox Signaling
https://www.readbyqxmd.com/read/12775580/rho-rock-limk-cofilin-pathway-regulates-shear-stress-activation-of-sterol-regulatory-element-binding-proteins
#14
Tong Lin, Lingfang Zeng, Yi Liu, Kathryn DeFea, Martin A Schwartz, Shu Chien, John Y-J Shyy
Previous studies have shown that integrin activation and fluid shear stress can modulate the activity of sterol regulatory element binding proteins (SREBPs) in vascular endothelial cells. We investigated the role of small GTPase Rho-mediated signal transduction pathway in this mode of SREBP activation. Fluid shear stress activates the Rho downstream effectors ROCK, LIM kinase (LIMK), and cofilin. The various negative mutants of RhoA, ROCK, LIMK, and cofilin can block the shear stress activation of SREBPs. The shear stress-activated SREBP depends on S2P proteases but not caspase-3...
June 27, 2003: Circulation Research
https://www.readbyqxmd.com/read/11956649/interaction-of-the-small-gtpase-rac3-with-nrbp-a-protein-with-a-kinase-homology-domain
#15
Stijn De Langhe, Leena Haataja, Dinithi Senadheera, John Groffen, Nora Heisterkamp
The family of Rac small GTPases including Rac1, Rac2 and Rac3 regulate numerous cellular processes. Since the cellular functions of Rac3 have not been defined, constitutively active V12Rac3 was used to identify targets that transduce its signals. We here identify human NRBP as a Rac family-interacting protein. NRBP formed a complex with activated Rac3. NRBP contains a kinase-homology domain and exhibits an associated kinase activity. NRBP represents a novel family of evolutionarily conserved proteins with homologs in C...
May 2002: International Journal of Molecular Medicine
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