Curator of an Investigator Initiated Study: Aviva Lev-Ari, PhD, RN
Inhibition of ET-1, ETA and ETA-ETB, Induction of NO production, stimulation of eNOS and Treatment Regime with PPAR-gamma agonists (TZD): cEPCs Endogenous Augmentation for Cardiovascular Risk Reduction – A Bibliography
Alonso D, Radomski MW, (2003). Nitric oxide, platelet function, myocardial infarction and reperfusion therapies. Heart Fail Rev., 8:47–54.
Anthony MS, Clarkson TB, Williams JK, (1998). Effects of soy isoflavones on atherosclerosis: potential mechanisms. Am J Clin Nutr., 68(6 Suppl):1390S–1393S.
Benowitz, NL., (2004). Antihypertensive Agents. Chapter 11 in Katzung, BG., Basic & Clinical Pharmacology. McGraw-Hill, 9th Edition, pp. 160-183.
Bisoendial RJ, et al. (2003). Restoration of endothelial function by increasing high-density lipoprotein in subjects with isolated low high-density lipoprotein. Circulation, 107:2944–2948.
Blair A, Shaul PW, Yuhanna IS, Conrad PA, Smart EJ., (1999). Oxidized low density lipoprotein displaces endothelial nitric-oxide synthase (eNOS) from plasmalemmal caveolae and impairs eNOS activation. J. Biol. Chem., 274:32512–32519.
Brixius K, Song Q, Malick A, Boelck B, Addicks K, Bloch W, Mehlhorn U, Schwinger R, (2006). eNOS is not activated by nebivolol in human failing myocardium. Life Sci., 2006 Apr 25
Broeders MAW, Doevendans PA, Bekkers BCAM, Bronsaer R, van Gorsel E, Heemskerk JWM. oude Egbrink MGA, van Breda E, Reneman RS, van der Zee R, (2000). Nebivolol: A Third-Generation ß-Blocker That Augments Vascular Nitric Oxide Release, Endothelial ß2-Adrenergic Receptor–Mediated Nitric Oxide Production.Circulation,102:677.
Brown BG, et al. Simvastatin and niacin, antioxidant vitamins, or the combination for the prevention of coronary disease. N. Engl. J. Med., 345:1583–1592.
Brugada P, Brugada J, Brugada R, (2001). Dealing with biological variation in the Brugada syndrome. Eur. Heart J., 22(24): 2231 – 2232.
Caulin-Glaser T, Garcia-Cardena G, Sarrel P, Sessa WC, Bender JR., (1997). 17 beta-estradiol regulation of human endothelial cell basal nitric oxide release, independent of cytosolic Ca2+ mobilization. Circ. Res., 81:885–892.
Cheng Y, Wang M, Yu Y, Lawson J, Funk CD, and Fitzgerald GA., (2006). Cyclooxygenases, microsomal prostaglandin E synthase-1, and cardiovascular function. J. Clin. Invest., 116:1391-1399
Church JE, Fulton D., (2006). Differences in eNOS activity because of subcellular localization are dictated by phosphorylation state rather than the local calcium environment. J Biol Chem., 2006 Jan 20;281(3):1477-88. Epub 2005 Oct 28.
Dessy C, Saliez J, Ghisdal P, Daneau G, Lobysheva II, Frerart F, Belge C, Jnaoui K, Noirhomme P, Feron O, Balligand JL, (2005). Endothelial {beta}3-Adrenoreceptors Mediate Nitric Oxide-Dependent Vasorelaxation of Coronary Microvessels in Response to the Third-Generation {beta}-Blocker Nebivolol. Circulation, 112(8): 1198 – 1205.
Dimmeler S, Aicher A, Vasa M, Mildner-Rihm C, Adler K, Tiemann M, Rutten H, Fichtlscherer S, Martin H, Zeiher AM, (2001). HMG-CoA reductase inhibitors (statins) increase endothelial progenitor cells via the PI3-kinase/Akt pathway. J Clin Invest., 108:391–397.
Dobrydneva Y, Williams RL, Morris GZ, Blackmore PF, (2002). Dietary phytoestrogens and their synthetic structural analogues as calcium channel blockers in human platelets. J Cardiovasc Pharmacol, 40:399–410.
Duarte J, Ocete MA, Perez-Vizcaino F, Zarzuelo A, Tamargo J, (1997). Effect of tyrosine kinase and tyrosine phosphatase inhibitors on aortic contraction and induction of nitric oxide synthase. Eur J Pharmacol, 338:25–33.
Erwin PA, Mitchell DA, Sartoretto J, Marletta MA, Michel T., (2006). Subcellular Targeting and Differential S-Nitrosylation of Endothelial Nitric-oxide Synthase. J. Biol. Chem., 281:1, 151-157.
George T. and P. Ramwell, (2004). Nitric Oxide, Donors, & Inhibitors. Chapter 19 in Katzung, BG., Basic & Clinical Pharmacology. McGraw-Hill, 9th Edition, pp. 313 – 318.
Gong M, et al., (2003). HDL-associated estradiol stimulates endothelial NO synthase and vasodilation in an SR-BI-dependent manner. J. Clin. Invest., 111:1579–1587.
Gonzalez E, Kou R, Lin AJ, Golan DE, Michel T., (2002). Subcellular Targeting and Agonist-induced Site-specific Phosphorylation of Endothelial Nitric-oxide Synthase. J. Biol. Chem., 277;42:39554-39560.
Goon, P.K.Y. Lip G.Y.H, Boos, CJ, Stonelake, PS, Blann, AD. (2006). Circulating Endothelial Cells, Endothelial Progenitor Cells, and Endothelial Microparticles in Cancer, Neoplasia, 8:79-88.
Gottstein N, Ewins BA, Eccleston C, Hubbard GP, Kavanagh IC, Minihane AM, Weinberg PD, Rimbach G, (2003). Effect of genistein and daidzein on platelet aggregation and monocyte and endothelial function. Br J Nutr, 89:607–616
Grovers R, Bevers L, De Bree P, Rabelink TJ, (2002). Endothelial nitric oxide synthase activity is linked to its presence at cell–cell contacts. Biochem. J., 361 (193–201) (Printed in Great Britain)
Haynes WG, Ferro CJ, O’Kane KP, Somerville D, Lomax CC, Webb DJ, (1996). Systemic endothelin receptor blockade decreases peripheral vascular resistance and blood pressure in humans. Circulation, 15;93(10):1860-70.
Iaccarino G, Cipolletta E, Fiorillo A, AnnecchiaricoM, Ciccarelli M, Cimini V, Koch WJ, B. Trimarco B, (2002). {beta}2-Adrenergic Receptor Gene Delivery to the Endothelium Corrects Impaired Adrenergic Vasorelaxation in Hypertension. Circulation, 106(3): 349 – 355.
Jordan J, Tank J, Stoffels, Franke MG, Christensen NJ, Luft CF, Boschmann M, (2001). Interaction between {beta}-Adrenergic Receptor Stimulation and Nitric Oxide Release on Tissue Perfusion and Metabolism.J. Clin. Endocrinol. Metab., 86(6): 2803 – 2810.
Kalinowski L, Dobrucki LW, Szczepanska-Konkel M, Jankowski M, Martyniec L, Angielski S, Malinski, T, (2003). Third-Generation {beta}-Blockers Stimulate Nitric Oxide Release From Endothelial Cells Through ATP Efflux: A Novel Mechanism for Antihypertensive Action. Circulation, 107(21): 2747 – 2752.
N S Kirkby, P W F Hadoke, A J Bagnall, and D J Webb (2008). The endothelin system as a therapeutic target in cardiovascular disease: great expectations or bleak house? Br J Pharmacol. 2008 March; 153(6): 1105–1119.
Kleinman, ME, Blei, F, Gurtner, GC, (2005). Circulating Endothelial Progenitor Cells and Vascular Anomalies, Lymphatic Research and Biology, 3;4: 234-239.
Koshimizu T-A, Nasa Y, Tanoue A, Oikawa R, Kawahara Y, Kiyono Y, Adachi T, Tanaka T, Kuwaki T, Mori T, Takeo S, Okamura H, Tsujimoto G., (2006). V1a vasopressin receptors maintain normal blood pressure by regulating circulating blood volume and baroreflex sensitivity. PNAS, 103;20: 7807-7812.
Kotamraju S, Hogg N, Joseph J, Keefer LK, Kalyanaraman B, (2001). Inhibition of oxidized low-density lipoprotein-induced apoptosis in endothelial cells by nitric oxide. Peroxyl radical scavenging as an antiapoptotic mechanism. J Biol Chem, 276:17316–17323.
Kuvin JT, et al., (2002). A novel mechanism for the beneficial vascular effects of high-density lipoprotein cholesterol: enhanced vasorelaxation and increased endothelial nitric oxide synthase expression. Am. Heart J., 144:165–172.
Lahav R, Heffner G, Patterson PH., (1999). An endothelin receptor B antagonist inhibits growth and induces cell death in human melanoma cells in vitro and in vivo. PNAS, 96;20: 11496-11500.
Lantin-Hermoso RL, et al., (1997). Estrogen acutely stimulates nitric oxide synthase activity in fetal pulmonary artery endothelium. Am. J. Physiol., 273:L119–L126.
Laszlo, F, Whittle BJR, Moncada S., (1994). Time dependent enhancement or inhibition of endotoxin-induced vascular injury in rat intestine by nitric oxide synthase inhibitors. Br. J. Pharmacol., 111, 1309–1315.
Laufs U, Werner N, Link A, Endres M, Wassmann S, Jurgens K, Miche E, Bohm M, Nickenig G, (2003). Physical training increases endothelial progenitor cells, inhibits neointima formation, and enhances angiogenesis. Circulation, 109:220 –226.
Li AC, Binder, CJ, Gutierrez, A, Brown, KK, Plotkin, CR, Pattison, JW, Valledor, AF, Davis, RA, Willson, TM, Witztum, JL, Palinski, W, Glass, CK. (2004). Differential inhibition of macrophage foam-cell formation and atherosclerosis in mice by PPAR-alpha, Beta/delta, and gamma. J. Clin. Invest., 114:1564-1576.
Li XP, et al., (2000). Protective effect of high density lipoprotein on endothelium-dependent vasodilatation. Int. J. Cardiol., 73:231–236.
Liu D, Homan LL, Joseph, Dillon JS., (2004). Genistein Acutely Stimulates Nitric Oxide Synthesis in Vascular Endothelial Cells by a Cyclic Adenosine 5′-Monophosphate-Dependent Mechanism, Endocrinology, 145:12, 5532-5539.
Llevadot J, Murasawa S, Kureishi Y, Uchida S, Masuda H, Kawamoto A, Walsh K, Isner JM, Asahara T, (2001). HMG-CoA reductase inhibitor mobilizes bone marrow-derived endothelial progenitor cells. J Clin Invest., 108:399–405.
McDuffie JE, Coaxum SD, Maleque MA, (1999) 5-Hydroxytryptamine evokes endothelial nitric oxide synthase activation in bovine aortic endothelial cell cultures. Proceedings of the Society for Experimental Biology and Medicine, 221, 386-390.
McDuffie JE, Motley ED, Limbird LE, Maleque, MA, (2000). 5-Hydroxytryptamine Stimulates Phosphorylation of p44/p42 Mitogen-Activated Protein Kinase Activation in Bovine Aortic Endothelial Cell Cultures. Journal of Cardiovascular Pharmacology, 35(3):398-402.
McEniery CM, Schmitt M, Qasem A, Webb DJ, Avolio AP, Wilkinson IB, Cockcroft JR, (2004). Nebivolol Increases Arterial Distensibility In Vivo. Hypertension, 44(3): 305 – 310.
Mason RP, Kalinowski L, Jacob RF, Jacoby AM, Malinski BT, (2005). Nebivolol Reduces Nitroxidative Stress and Restores Nitric Oxide Bioavailability in Endothelium of Black Americans. Circulation, 112(24): 3795 – 3801.
McDuffie JE, Motley ED, Limbird LE, Maleque, MA, (2000). 5-Hydroxytryptamine Stimulates Phosphorylation of p44/p42 Mitogen-Activated Protein Kinase Activation in Bovine Aortic Endothelial Cell Cultures. Journal of Cardiovascular Pharmacology, 35(3):398-402.
Mineo C, Yuhanna IS, Quon MJ, Shaul PW., (2003). HDL-induced eNOS activation is mediated by Akt and MAP kinases. J. Biol. Chem., 278:9142–9149.
Mollnau H, Schulz E, Daiber A, Baldus S, Oelze M, August M, Wendt M, Walter U, Geiger C, Agrawal R, Kleschyov AL, Meinertz T. Munzel T, (2003). Nebivolol Prevents Vascular NOS III Uncoupling in Experimental Hyperlipidemia and Inhibits NADPH Oxidase Activity in Inflammatory Cells. Arterioscler. Thromb. Vasc. Biol., 23(4): 615 – 621.
Moncada S., (2006). Adventures in vascular biology: a tale of two mediators. Phil. Trans. R. Soc. B 29 May 2006 vol. 361 no. 1469 735-759
Moncada S, and Higgs EA, (2006). The discovery of nitric oxide and its role in vascular biology. British Journal of Pharmacology, 147, S193–S201
Mukherjee S, Baksi S, Dart RA, Gollub S, Lazar J, Nair C, Schroeder D, Woolf SH, (2003). {beta}-Blockers With Vasodilatory Actions. Chest, 124(4): 1621 – 1621.
Murakami H, Murakami R, Kambe F, Cao X, Takahashi R, Asai T, Hirai T, Numaguchi Y, Okumura K, Seo H, Murohara T., (2006). Fenofibrate activates AMPK and increases eNOS phosphorylation in HUVEC. Biochem Biophys Res Commun., 341(4):973-8. Epub 2006 Jan 24.
Nebivolol is a long-acting, cardioselective beta-blocker currently licensed for the treatment of hypertension.
Nebivolol
http://www.intekom.com/pharm/adcock/nebilet.html – retrieved on 6/20/2006
Nestel PJ, Yamashita T, Sasahara T, Pomeroy S, Dart A, Komesaroff P, Owen A, Abbey M, (1997). Soy isoflavones improve systemic arterial compliance but not plasma lipids in menopausal and perimenopausal women. Arterioscler Thromb Vasc Biol 17:3392–3398.
Nofer J-R, et al., (2004). HDL induces NO-dependent vasorelaxation via the lysophospholipid receptor S1P3. J. Clin. Invest.,113:569–581.
Nolte MS and JH Karam, (2004). Pancreatic Hormones & Antidiabetic Drugs. Chapter 41 in Katzung, BG., Basic & Clinical Pharmacology. McGraw-Hill, 9th Edition, pp.693-715, in particular, Thiazolidinediones, pp.709-710, 713.
Ohkita Mamoru, Masashi Tawa, Kento Kitada and Yasuo Matsumura (2012). Pathophysiological Roles of Endothelin Receptors in Cardiovascular Diseases, J Pharmacol Sci 119, 302 – 313 (2012)
Pott C, Steinritz D, Bölck B, Mehlhorn U, Brixius K, Schwinger RHG, BlochW., (2006). eNOS translocation but not eNOS phosphorylation is dependent on intracellular Ca2+ in human atrial myocardium. Am J Physiol Cell Physiol 290: C1437-C1445.
Ramet ME, et al., (2003). High-density lipoprotein increases the abundance of eNOS protein in human vascular endothelial cells by increasing its half-life. J. Am. Coll. Cardiol., 41:2288–2297.
Reid, Ian A., (2004). Vasoactive Peptides. Chapter 17 in Katzung, BG., Basic & Clinical Pharmacology. McGraw-Hill, 9th Edition, pp. 281 – 297, in particular, Endothelins, pp. 290-293.
Richardson SM, Maleque MA, Motley ED., (2003). 3-Morpholinosyndnonimine inhibits 5-hydroxytryptamine-induced phosphorylation of nitric oxide synthase in endothelial cells.Cell Mol Biol.,49(8):1385-1389.
Ritter JM, Ferro A, Chowienczyk PJ., (2006). Relation between beta-adrenoceptor stimulation and nitric oxide synthesis in vascular control. Eur J Clin Pharmacol., 62 (Supplement 13):109-113.
Rosenzweig A., (2005). Circulating Endothelial Progenitors – Cells as Biomarkers. NEJM., 353;10: 1055-1057.
Rubins et al., (1999). Gemfibrozil for the secondary prevention of coronary heart disease in men with low levels of high-density lipoprotein cholesterol. Veterans Affairs High-Density Lipoprotein Cholesterol Intervention Trial Study Group. N. Engl. J. Med., 341:410–418.
Sanchez FA, Savalia NB, Duran RG, Lal BK, Boric MP, Duran WN., (2006). Functional significance of differential eNOS translocation. Am J Physiol Heart Circ Physiol., May 5; [Epub ahead of print]
Satake N, Shibata S, (1999). The potentiating effect of genistein on the relaxation induced by isoproterenol in rat aortic rings. Gen Pharmacol, 33:221–227. Shaul PW., (2002). Regulation of endothelial nitric oxide synthase: location, location, location. Annu. Rev. Physiol., 64:749–774.
Shaul, PW and Mineo, C, (2004). HDL action on the vascular wall: is the answer NO? J Clin Invest., 15; 113(4): 509–513.
Shin WS, Hong YH, Peng HB, De Caterina R, Libby P, Liao JK, (1996). Nitric oxide attenuates vascular smooth muscle cell activation by interferon. The role of constitutive NF-B activity. J Biol Chem, 271:11317–11324.
Skidgel RA, Stanislavjevic S, Erdos EG., (2006). Kinin- and angiotensin-converting enzyme (ACE) inhibitor-mediated nitric oxide production in endothelial cells. Biol Chem., 387(2):159-65.
Spieker et al., (2002). High-density lipoprotein restores endothelial function in hypercholesterolemic men. Circulation, 105:1399–1402.
Spyridopoulos I, Haendeler J, Urbich C, Brummendorf TH, Oh H, Schneider MD, Zeiher AM, Dimmeler S, (2004). Statins enhance migratory capacity by upregulation of the telomere repeat-binding factor TRF2 in endothelial progenitor cells. Circulation, 110:3136 –3142.
Squadrito F, Altavilla D, Crisafulli A, Saitta A, Cucinotta D, Morabito N, D’Anna R, Corrado F, Ruggeri P, Frisina N, Squadrito G, (2003). Effect of genistein on endothelial function in postmenopausal women: a randomized, double-blind, controlled study. Am J Med, 114:470–476.
Sütsch G, Kiowski W, Yan X-W, Hunziker P, Christen S, Strobel W, Kim J-H, Rickenbacher P, Bertel O., (1998). Short-Term Oral Endothelin-Receptor Antagonist Therapy in Conventionally Treated Patients With Symptomatic Severe Chronic Heart Failure. Circulation, 98:2262-2268
Uittenbogaard A, Shaul PW, Yuhanna IS, Blair A, Smart EJ., (2000). High density lipoprotein prevents oxidized low density lipoprotein-induced inhibition of endothelial nitric-oxide synthase localization and activation in caveolae. J. Biol. Chem., 275:11278–11283.
van der Schouw YT, de Kleijn MJ, Peeters PH, Grobbee DE, (2000). Phyto-oestrogens and cardiovascular disease risk. Nutr Metab Cardiovasc Dis., 10:154–167.
Van Nueten L, Dupont AG, Vertommen C, Goyvaerts H, Robertson JI., (1997). A dose-response trial of nebivolol in essential hypertension. J Hum Hypertens.,11(2):139-44.
Vasa M, Fichtlscherer S, Adler K, Aicher A, Martin H, Zeiher AM, Dimmeler S. (2001a). Increase in circulating endothelial progenitor cells by statin therapy in patients with stable coronary artery disease. Circulation, 103:2885–2890.
Verma S, Szmitko, PE, (2006). The vascular biology of peroxisome proliferator-activated receptors: Modulation of atherosclerosis. Can J Cardiol, 22 (Suppl B):12B-17B.
Walker HA, Dean TS, Sanders TA, Jackson G, Ritter JM, Chowienczyk PJ, (2001). The phytoestrogen genistein produces acute nitric oxide-dependent dilation of human forearm vasculature with similar potency to 17ß-estradiol. Circulation, 103:258–262.
Walter DH, Rittig K, Bahlmann FH, Kirchmair R, Silver M, Murayama T, Nishimura H, Losordo DW, Asahara T, Isner JM, (2002). Statin therapy accelerates reendothelialization: a novel effect involving mobilization and incorporation of bone marrow-derived endothelial progenitor cells. Circulation, 105:3017–3024.
Wang C-H, Ciliberti N, Li S-H, Szmitko PE, Weisel RD, Fedak PWM, Al-Omran M, Cherng W-J, Li R-K, Stanford WL, Verma S., (2004). Rosiglitazone facilitates angiogenic progenitor cell differentiation toward endothelial lineage: a new paradigm in glitazone pleiotropy. Circulation, 109:1392-1400.
Werner N, Junk S, Laufs L, Link A, Walenta K, Bohm M, Nickenig G., (2003). Intravenous transfusion of endothelial progenitor cells reduces neointima formation after vascular injury. Circ Res., 93:e17– e24.
Wilson PW, Abbott RD, Castelli WP, (1988). High density lipoprotein cholesterol and mortality. The Framingham Heart Study.Arteriosclerosis, 8:737–741.
Xu H-L, Feinstein DL, Santizo RA, Koenig HM, Pelligrino DA., (2002).Agonist-specific differences in mechanisms mediating eNOS-dependent pial arteriolar dilation in rats. Am J Physiol Heart Circ Physiol., 282:H237-H243
Yuhanna IS, et al., (2001). High-density lipoprotein binding to scavenger receptor-BI activates endothelial nitric oxide synthase. Nat. Med., 7:853–857.
Zeiher AM, Schachlinger V, Hohnloser SH, Saurbier B, Just H., (1994). Coronary atherosclerotic wall thickening and vascular reactivity in humans. Elevated high-density lipoprotein levels ameliorate abnormal vasoconstriction in early atherosclerosis. Circulation, 89:2525–2532.
[…] Comments « Inhibition of ET-1, ETA and ETA-ETB, Induction of NO production, stimulation of eNOS and Treatment R… […]
[…] http://pharmaceuticalintelligence.com/2012/10/04/inhibition-of-et-1-eta-and-eta-etb-induction-of-no-… […]
[…] http://pharmaceuticalintelligence.com/2012/10/04/inhibition-of-et-1-eta-and-eta-etb-induction-of-no-… […]
[…] http://pharmaceuticalintelligence.com/2012/10/04/inhibition-of-et-1-eta-and-eta-etb-induction-of-no-… […]
[…] http://pharmaceuticalintelligence.com/2012/10/04/inhibition-of-et-1-eta-and-eta-etb-induction-of-no-… […]
PUT IT IN CONTEXT OF CANCER CELL MOVEMENT
The contraction of skeletal muscle is triggered by nerve impulses, which stimulate the release of Ca2+ from the sarcoplasmic reticuluma specialized network of internal membranes, similar to the endoplasmic reticulum, that stores high concentrations of Ca2+ ions. The release of Ca2+ from the sarcoplasmic reticulum increases the concentration of Ca2+ in the cytosol from approximately 10-7 to 10-5 M. The increased Ca2+ concentration signals muscle contraction via the action of two accessory proteins bound to the actin filaments: tropomyosin and troponin (Figure 11.25). Tropomyosin is a fibrous protein that binds lengthwise along the groove of actin filaments. In striated muscle, each tropomyosin molecule is bound to troponin, which is a complex of three polypeptides: troponin C (Ca2+-binding), troponin I (inhibitory), and troponin T (tropomyosin-binding). When the concentration of Ca2+ is low, the complex of the troponins with tropomyosin blocks the interaction of actin and myosin, so the muscle does not contract. At high concentrations, Ca2+ binding to troponin C shifts the position of the complex, relieving this inhibition and allowing contraction to proceed.
Figure 11.25
Association of tropomyosin and troponins with actin filaments. (A) Tropomyosin binds lengthwise along actin filaments and, in striated muscle, is associated with a complex of three troponins: troponin I (TnI), troponin C (TnC), and troponin T (TnT). In (more ) Contractile Assemblies of Actin and Myosin in Nonmuscle Cells
Contractile assemblies of actin and myosin, resembling small-scale versions of muscle fibers, are present also in nonmuscle cells. As in muscle, the actin filaments in these contractile assemblies are interdigitated with bipolar filaments of myosin II, consisting of 15 to 20 myosin II molecules, which produce contraction by sliding the actin filaments relative to one another (Figure 11.26). The actin filaments in contractile bundles in nonmuscle cells are also associated with tropomyosin, which facilitates their interaction with myosin II, probably by competing with filamin for binding sites on actin.
Figure 11.26
Contractile assemblies in nonmuscle cells. Bipolar filaments of myosin II produce contraction by sliding actin filaments in opposite directions. Two examples of contractile assemblies in nonmuscle cells, stress fibers and adhesion belts, were discussed earlier with respect to attachment of the actin cytoskeleton to regions of cell-substrate and cell-cell contacts (see Figures 11.13 and 11.14). The contraction of stress fibers produces tension across the cell, allowing the cell to pull on a substrate (e.g., the extracellular matrix) to which it is anchored. The contraction of adhesion belts alters the shape of epithelial cell sheets: a process that is particularly important during embryonic development, when sheets of epithelial cells fold into structures such as tubes.
The most dramatic example of actin-myosin contraction in nonmuscle cells, however, is provided by cytokinesisthe division of a cell into two following mitosis (Figure 11.27). Toward the end of mitosis in animal cells, a contractile ring consisting of actin filaments and myosin II assembles just underneath the plasma membrane. Its contraction pulls the plasma membrane progressively inward, constricting the center of the cell and pinching it in two. Interestingly, the thickness of the contractile ring remains constant as it contracts, implying that actin filaments disassemble as contraction proceeds. The ring then disperses completely following cell division.
Figure 11.27
Cytokinesis. Following completion of mitosis (nuclear division), a contractile ring consisting of actin filaments and myosin II divides the cell in two.
http://www.ncbi.nlm.nih.gov/books/NBK9961/
This is good. I don’t recall seeing it in the original comment. I am very aware of the actin myosin troponin connection in heart and in skeletal muscle, and I did know about the nonmuscle work. I won’t deal with it now, and I have been working with Aviral now online for 2 hours.
I have had a considerable background from way back in atomic orbital theory, physical chemistry, organic chemistry, and the equilibrium necessary for cations and anions. Despite the calcium role in contraction, I would not discount hypomagnesemia in having a disease role because of the intracellular-extracellular connection. The description you pasted reminds me also of a lecture given a few years ago by the Nobel Laureate that year on the mechanism of cell division.
I actually consider this amazing blog , âSAME SCIENTIFIC IMPACT: Scientific Publishing –
Open Journals vs. Subscription-based « Pharmaceutical Intelligenceâ, very compelling plus the blog post ended up being a good read.
Many thanks,Annette
I actually consider this amazing blog , âSAME SCIENTIFIC IMPACT: Scientific Publishing –
Open Journals vs. Subscription-based « Pharmaceutical Intelligenceâ, very compelling plus the blog post ended up being a good read.
Many thanks,Annette
I actually consider this amazing blog , âSAME SCIENTIFIC IMPACT: Scientific Publishing –
Open Journals vs. Subscription-based « Pharmaceutical Intelligenceâ, very compelling plus the blog post ended up being a good read.
Many thanks,Annette
I actually consider this amazing blog , âSAME SCIENTIFIC IMPACT: Scientific Publishing –
Open Journals vs. Subscription-based « Pharmaceutical Intelligenceâ, very compelling plus the blog post ended up being a good read.
Many thanks,Annette
I actually consider this amazing blog , âSAME SCIENTIFIC IMPACT: Scientific Publishing –
Open Journals vs. Subscription-based « Pharmaceutical Intelligenceâ, very compelling plus the blog post ended up being a good read.
Many thanks,Annette
I actually consider this amazing blog , âSAME SCIENTIFIC IMPACT: Scientific Publishing –
Open Journals vs. Subscription-based « Pharmaceutical Intelligenceâ, very compelling plus the blog post ended up being a good read.
Many thanks,Annette
I actually consider this amazing blog , âSAME SCIENTIFIC IMPACT: Scientific Publishing –
Open Journals vs. Subscription-based « Pharmaceutical Intelligenceâ, very compelling plus the blog post ended up being a good read.
Many thanks,Annette
I actually consider this amazing blog , âSAME SCIENTIFIC IMPACT: Scientific Publishing –
Open Journals vs. Subscription-based « Pharmaceutical Intelligenceâ, very compelling plus the blog post ended up being a good read.
Many thanks,Annette