Українська English

ISSN 2522-9028 (Print)
ISSN 2522-9036 (Online)
DOI: https://doi.org/10.15407/fz

Fiziologichnyi Zhurnal

is a scientific journal issued by the

Bogomoletz Institute of Physiology
National Academy of Sciences of Ukraine

Editor-in-chief: V.F. Sagach

The journal was founded in 1955 as
1955 – 1977 "Fiziolohichnyi zhurnal" (ISSN 0015 – 3311)
1978 – 1993 "Fiziologicheskii zhurnal" (ISSN 0201 – 8489)
1994 – 2016 "Fiziolohichnyi zhurnal" (ISSN 0201 – 8489)
2017 – "Fiziolohichnyi zhurnal" (ISSN 2522-9028)

Fiziol. Zh. 2007; 53(2): 78-89


Modern conception of protein kinasec role in the vascularsmooth muscles tone regulation

I.V. Kizub, O.O. Pavlova, A.I. Solovyov

    Institute of Pharmacology and Toxicology Academy ofMedical Sciences of Ukraine, Kyiv



Abstract

Protein kinase C is an important regulatory enzyme that plays significant role in the vascular tone regulation. Protein kinase C is involved in the vascular smooth muscle cells (SMC) contrac- tility at physiological conditions and its hyperreactivity at differ- ent types of pathology. Myogenic and endothelium-dependent pathways of protein kinase С-mediated vascular tone regulation include a variety of cellular mechanisms. The most important protein kinase C-mediated mechanisms in SMC are the increase of myophilament Ca2+-sensitivity; regulation of plasmolema ion permeability, and proliferative changes in SMC. Protein kinase C-related mechanisms in vascular endotheliocytes include regulation of formation and transduction of humoral and electri- cal signals to SMC that play an important role in the pathologi- cal vasospasm development.

References

  1. Павлова О.О., Сагач В.Ф., Соловйов А.І. Впливблокади протеїнкінази С на зміни кальцієвоїчутливості скоротливого апарату судинних гла-деньких м’язів при вазоспастичних станах різногогенезу // Фізіол. журн. – 2003. – 49, №6. – С.31–37.
  2. Соловьев А.И. Изменения Ca2+-чувствительности сок-ратительных белков гладкомышечных клеток воротнойвены крас при растяжении и гипоксии // Физиол. журн.СССР. – 1990. – 76, №8. – С.1048–1054.
  3. Albert A.P., Piper A.S., Large W.A. Properties of aconstitutively active Ca2+-permeable non-selectivecation channel in rabbit ear artery myocytes // J. Physiol. –2003. – 549. – P.143–156.
  4. Barman S.A., Zhu S., White R.E. PKC activates BKCachannels in rat pulmonary arterial smooth muscle viacGMP–dependent protein kinase // Amer. J. Physiol. LungCell Mol. Physiol. – 2004. – 286. – P.L1275–L1281.
  5. Beckman J.A., Goldfine A.B., Gordon M.B. et al. Inhi-bition of protein kinase Cb prevents impaired endot-helium-dependent vasodilation caused by hypergly-caemia in humans // Circulat. Res. – 2002. – 90. –P.107–111.
  6. Bohlen H.G. Protein kinase ?II in Zucker obese ratscompromises oxygen and flow-mediated regulation ofnitric oxide formation // Amer. J. Physiol. – 2004. –286. – P.H492–H497.
  7. Bohlen H.G., Nase G.P. Arteriolar nitric oxideconcentration is decreased during hyperglycemia-in-duced ?II PKC activation // Ibid. – 2001. – 280. –P.H621–H627.
  8. Bonev A.D., Jaggar J.H., Rubart M., Nelson M.T. Acti-vators of protein kinase C decrease Ca2+ spark fre-quency in smooth muscle cells from cerebral arteries //Ibid. – 1997. – 273. – P.C2090–C2095.
  9. 9. Bonnevier J., Arner A. Action doenstream of cyclicGMP/protein kinase G can reverse proteine kinase C-mediated phosphorylation of CPI-17 and Ca2+ sensiti-zation in smooth muscle // J. Biol. Chem. – 2004. – 279.– P.28998–289003.
  10. 10. Carter R.W., Kanagy N.L. Mechanism of enhancedcalcium sensitivity and alpha 2-AR vasoreactivity inchronic NOS inhibition hypertension // Amer. J.Physiol. Heart Circulat. Physiol. – 2003. – 284, №1. –P.H309–H316.
  11. Chu S., Bohlen H.G. High concentration of glucose inhib-its glomerular endothelial eNOS through a PKC mecha-nism // Amer. J. Physiol. – 2004. – 287. – P.F384–F392.
  12. Dempsey E.C., Newton A.C., Mochley-Rosen D. et al.Protein kinase C isozymes and the regulation of diversecell responses // Ibid. – 2000. – 279. – P.L429–L438.
  13. Denhardt D.T. Signal-transducing protein phosphory-lation cascades mediated by Ras/Rho proteins in themammalian cell: the potential for multiplex signalling //Biochem. J. – 1996. – 318. – P.729–747.
  14. Dessy C., Matsuda N., Hulvershorn J. et al. Evidencefor involvement of the PKC-б, isoform in myogeniccontractions of the coronary microcirculation // Amer.J. Physiol. – 2000. – 279. – P.H916–H923.
  15. Ding Y., Schwartz D., Posner P., Zhong J. Hypotonicswelling stimulates L-type Ca2+ channel activity in vas-cular smooth muscle cells through PKC // Amer. J. Physiol.Cell Physiol. – 2004. – 287, №2. – P.C413–C421.
  16. Eto M., Matsuzawa F., Aikawa S., Ohki S. Mecha-nism for the controlling Ca2+ sensintivity of smoothmuscle contraction // J. Muscl. Res. Cell Motil. – 2005. –26. №1. – P.68.
  17. Ferro T., Neumann P., Gertzberg N. et al. Protein kinaseC-? mediates endothelial barrier dysfunction inducedby TNF-? // Amer. J. Physiol. – 2000. – 278. –P.L1107–1117.
  18. 19. Figueroa X.F., Isakson B.E., Duling B.R. Connexins:gaps in our knowledge of vascular function // Physiol-ogy. – 2004. – 19, №5. – P.277–284.
  19. 20. Gokina N.I., Knot H.J., Nelson M.T., Osol G. In-creased Ca2+ sensitivity as a key mechanism of PKC-induced contraction in pressurized cerebral arteries //Amer. J. Physiol. Heart Circulat. Physiol. – 1999. –277. – P.H1178–H1188.
  20. Griffith T.M. Endothelium–dependent smooth musclehyperpolarization: do gap junctions provide a unifyinghypothesis? // Brit. J. Pharmacol. – 2004. – 141, №6. –P.881–903.
  21. Guo M., Wu M.H., Korompai F., Yuan S.Y. Upregulationof PKC genes and isozymes in cardiovascular tissuesduring early stages of experimental diabetes // Physiol.Genomics. – 2003. – 12. – P.139–146.
  22. Hagen B.M., Bayguinov O., Sanders K.M. b1-Sub-units are required for regulation of coupling betweenCa2+ transients and Ca2+–activated K+ (BK) channelsby protein kinase C // Amer. J. Physiol. Cell Physiol. –2003. – 285. – P.1270–1280.
  23. Haiyan P., Khalil N.B. Direct association of RhoAwith specific domains of PKC-? // Amer. J. Physiol. –2005. – 289. – P.C982–C993.
  24. Harnett K.M., Cao W., Biancani P. Signal–transduc-tion pathways that regulate smooth muscle function I.Signal transduction in phasic (esophageal) and tonic(gastroesophageal sphincter) smooth muscles // Amer.J. Physiol. Gastrointest. Liver Physiol. – 2005. – 288. –P.G407–G416.
  25. Hill M.A., Davis M.J., Song J., Zou H. Calcium de-pendence of indolactam–mediated contractions inresistance vessels // J. Pharmacol. Exp. Ther. – 1996. –276. – P.867–874.
  26. Kevil C.G., Okayama N., Alexander J.S. H2O2–medi-ated permeability II: importance of tyrosine phos-phatase and kinase activity // Amer. J. Physiol. CellPhysiol. – 2001. – 281. – P.C1940–C1947.
  27. 29. Khalil R.A., Morgan K.G. PKC-mediated redistribu-tion of mitogen-activated protein kinase during smoothmuscle cell activation // Amer. J. Physiol. – 1993. –265. – P.C406–C411.
  28. 30. Khalil R.A., VanBreemen C. Sustained contraction ofvascular smooth muscle: calcium influx or C- kinaseactivation? // J. Pharmacol. Exp. Ther. – 1988. – 244. –P.537–542.
  29. Kitamura K., Xiong Z., Teramoto N., Kuriyama H.Roles of inositol trisphosphate and protein kinase-Cin the spontaneous outward current modulated bycalcium release in rabbit portal vein // Pflьg. Arch. –1992. – 421. – P.539–551.
  30. Kizub I., Pavlova A., Soloviev A. Proteine kinase Cmodulates myofilaments Са2+–sensitivity in vascularsmooth muscle: possible role in vasospasm develop-ment // J. Muscle Res. and Cell Motil. – 2005, – 26,№1. – P.70.
  31. Korzick D.H., Laughlin M.H., Bowles D.K. Alterationin PKC signaling underlie enhanced myogenic tone inexercise-trained porcine coronary resistance arteries //J. Appl. Physiol. – 2004. – 96. – P.1425–1432.
  32. Kubo M., Quayle J.M., Standen N.B. Angiotensin IIinhibition of ATP-sensitive K+ currents in rat arterialsmooth muscle cells through protein kinase C // J.Physiol. (London) – 1997. – 503. – P.489–496.
  33. Kunisaki M., Bursell S.E., Clermont A.C. et al. Vita-min E prevents diabetes-induced abnormal retinal bloodflow via the diacylglycerol-protein kinase C pathway// Amer. J. Physiol. – 1995. – 269. – P.E239–E246.
  34. Leach R.M., Hill M., Snetkov V.A. et al. Divergentroles of glycolysis and the mitochondryal electrontransport chain in hypoxic pulmonary vasoconstric-tion of the rat: identity of the hypoxic sensor // J.Physiol. – 2001. – 536, №1. – P.211–224.
  35. Lehenky V., Zelensky S., Stefanov A., Soloviev A.Effectsof nitric oxide donors on a type vascular smoothmuskle preactivation // Cardiovasc. Toxicol. – 2002. –2. – P.151–160.
  36. Li H., Oehrlein S.A., Wallerath T. et al. Activation ofprotein kinase C alpha and/or epsilon enhances transcrip-tion of the human endothelial nitric oxide synthase gene //Mol. Pharmacol. – 1998. – 53. – P.630–637.
  37. 39. Liedtke C.M., Raghuram V., Yun C.C., Wang X. Roleof a PDZ1 domain of NHERF1 in the binding of airwayepithelial RACK1 to NHERF1 // Amer. J. Physiol. CellPhysiol. – 2004. – 286. – P.C1037–C1044.
  38. 40. Liou Y.M., Morgan K.G. Redistribution of proteinkinase C isoforms in association with vascular hy-pertrophy of rat aorta // Amer. J. Physiol. – 1994. –267. – P.C980–C989.
  39. Massett M.P., Ungvari Z., Csiszar A. et al. Differentroles of PKC and MAP kinases in arteriolar constric-tions to pressure and agonists // Ibid. – 2002. – 283. –P.H2282–H2287.
  40. Matsubara M., Hayashi N., Jing T., Titani K.Regulation of endothelial nitric oxide synthase by pro-tein kinase C // J. Biochem. (Tokyo) – 2003. – 133. –P.773–781.
  41. McNair L.L., Salamanca D.A., Khalil R.A. Endothelin-1 promotes Ca2+ antagonist-insensitive coronarysmooth muscle contraction via activation of ?-proteinkinase C // Hypertension. – 2004. – 43. – P.897.
  42. Morgan K.G., Gangopadhyay S.S. Signal transductionin smooth muscle: invited review: cross–bridgeregulation by thin filament–associated proteins // J.Appl. Physiol. – 2001. – 91. – P.953–962.
  43. Nakajima S., Kawakami M., Ueda M. 12-Deoxy-phorbol 13-isobutyrate contracts isolated rat thoracicarteries // Eur. J. Physiol. – 1991. – 195. – P.145–150.
  44. Nakayama K., Obara K., Tanabe Y. et al. Interactiverole of tyrosine kinase, protein kinase C, and Rho/Rhokinase systems in the mechanotransduction of vascu-lar smooth muscles // Biorheology. – 2003. – 40. –P.307–314.
  45. Newton A.C. Regulation of protein kinase C // Curr.Opin. Cell Biol. – 1997. – 9. – Р.161–167.
  46. Ohanian V., Ohanian J. Shaw L. et al. Identification ofprotein kinase C isoforms in rat mesenteric smallarteries and their possible role in agonist-induced con-traction // Circulat. Res. – 1996. – 78. – P.806–812.
  47. 49. Olsson M.C., Patel J.R., Fitzsimons D.P. et al. Basalmyosin light chain phosphorylation is a determinantof Ca2+ sensitivity of force and activation dependenceof the kinetics of myocardial force development // Amer.J. Physiol. Heart Circulat. Physiol. – 2004. – 287. –P.H2712–H2718.
  48. 50. Pass J.M., Zheng Y., Wead W.B. et al. PKC-epsilon acti-vation induces dichotomous cardiac phenotypes andmodulates PKC epsilon-RACK interactions and RACKexpression // Ibid. – 2001. – 280. – P.H946–H955.
  49. Phelps D.T., Ferro T.J., Higgins P.J. et al. Tumor ne-crosis factor induces the peroxynitrite–mediated deple-tion of lung endothelial glutathione via protein kinaseC activation // Amer. J. Physiol. Lung Cell Mol. Physiol. –1995. – 269. – Р.L551–L559.
  50. Sato A., Hattori Y., Fukao M. et al. A role of myofilamentCa2+ sensitivity in enchanced vascular reactivity in car-diomyopathic hamster // Eur. J. Pharmacol. – 1998. –353, №2-3. – P.247–256.
  51. Serfilippi G.L., Ferro T.J., Johnson A. The activationof protein kinase C mediates the alteration in pulmo-nary vasoreactivity induced by tumor necrosis factor-?// Amer. J. Physiol. – 1994. – 267. – P.L282–L290.
  52. Slish D.F., Welsh D.G., Brayden J.E. Diacylglyceroland protein kinase C activate cation channels involvedin myogenic tone // Ibid. – 2002. – 283. – P.H2196–H2201.
  53. Sohn U.D., Cao W., Tang D.-C. et al. Myosin light chainkinase– and PKC–dependent contraction of LES andesophageal smooth muscle // Amer. J. Physiol. Gastro-intest. Liver Physiol. – 2001. – 281. – P.467–478.
  54. Soloviev A., Basilyuk O. Evidence for decrease inmyofilament responsiveness to Ca2+ during hypoxia inspontaneously active vascular smooth vuscle in rats //Exp. Physiol. – 1993. – 18. – P.395–402.
  55. Soloviev A., Bershtein S. The contractile apparatus invascular smooth muscle cells of spontaneously hyper-tensive rats possess increased calcium sensitivity: thepossible role of protein kinase C // J. Hypertens. –1992. – 10. – P.131–136.
  56. Soloviev A., Lehenkyi V., Zelensky S., Hellstrand P.Nitric oxide relaxes rat tail artery smooth muscle bycyclic GMP-independent decrease in calcium sensitiv-ity of myofilaments // Cell Calcium. – 2004. – 36. –P.165–173.
  57. 59. Soloviev A.I., Parshikov A.V., Stefanov A.V. Evidencefor the involvement of protein kinase C in depressionof endothelium-dependent vascular responses in spon-taneously hypertensive rats // J. Vasc. Res. – 1998. –35. – P.325–331.
  58. 60. Soloviev A., Tishkin S., Zelensky S. et al. Ionizingradiation alters myofilament calcium sensitivity in vas-cular smooth muscle: Potential role of protein kinase C// Amer. J. Physiol. Regulat. Integrat. Compar. Physiol.– 2005. – 289. – P. R755–R762.
  59. Soloviev A., Tishkin S., Parshikov A. et al. Mecha-nisms of endothelium dysfunction after ionizedradiation: selective empairement of the nitric oxidecomponent of endothelium–dependent vasodilation //Br. J. Pharmacol. – 2003. – 138. – P.837–842.
  60. Somlyo A.P., Somlyo A.V. Ca2+ sensitivity of smoothmuscle and nonmuscle myosin II: modulated by G pro-teins, kinases, and myosin phosphatase // Physiol. Rev. –2003. – 83. – P.1325–1358.
  61. Thomson S., Clayton A.L., Hazzalin C.A. et al. Thenucleosomal response associated with immediate–earlygene induction is mediated via alternative MAP kinasecascades: MSK1 as a potential histone H3/HMG-14kinase // EMBO J. – 1999. – 18. – P.4779–4793.
  62. Tsai B.M., Wang M. Hypoxic pulmonary vasocon-striction mediated expression by protein kinase C //Amer. J. Physiol. – 2004. – 287. – P.L1215–L1219.
  63. Uehara V., Ishii M., Ishimitsu F., Sugimoto F. Enhancedphospholipase С activity in the vascular wall of sponta-neously hypertensive rats // Hypertension. – 1988. –11. – P.28–33.
  64. Vondriska T.M., Klein J.B., Ping P. Use of functionalproteomics to investigate PKC?–mediated cardio-protection: the signaling module hypothesis // Amer. J.Physiol. Heart Circulat. Physiol. – 2001. – 280. –P.H1434–H1441.
  65. Vondriska T.M., Zhang J., Song C. et al. PKCe–Srcmodules direct signal transduction in NO–induced car-dioprotection: complex formation as a means forcardioprotective signaling // Circulat. Res. – 2001. –88. – P.1306–1313.
  66. Waypa G.B., Marks J.D., Mack M.M. et al. Mito-chondrial reactive oxygen species trigger calcium in-creases during hypoxia in pulmonary arterial myocytes// Ibid. – 2002. – 91, №8. – P.719–726.
  67. 69. Wesselman J.P.M., Spaan J.A.E., Van Bavel E. Role ofprotein kinase C in myogenic calsium–contractioncoupling of rat cannulated mesenteric small arteries //Clin. Exp. Pharmacol. Physiol. – 2001. – 28, №10. –P.848–855.
  68. 70. Wu H.M., Yuan Y., Zawieja D.C. et al. Role of phos-pholipase C, protein kinase C, and calcium in VEGF-induced venular hyperpermeability // Amer. J. Physiol. –1999. – 276. – P.H535–H542.
  69. Xiao Z.L., Andrada M.J.P., Biancani P., Behar J. Reactiveoxygen species (H2O2): effects on the gallbladder muscleof guinea pigs // Amer. J. Physiol. Gastrointest. LiverPhysiol. – 2002. – 282. – P.300–306.
  70. Zharikov S.I., Herrera H., Block E.R. Role of membranepotential in hypoxic inhibition of L-arginine uptake bylung endothelial cells // Amer. J. Physiol. – 1997. – 272.– P.L78–L84.
  71. Zhong J., Wang G.X., Hatton W.J. et al. Regulation ofvolume-sensitive outwardly rectifying anion channelsin pulmonary arterial smooth muscle cells by proteinkinase C // Amer. J. Physiol. Cell. Physiol. – 2002. –283. – P.C1627–C1636.

© National Academy of Sciences of Ukraine, Bogomoletz Institute of Physiology, 2014-2024.