Disorganization by calcium antagonists of actin microfilament in aortic smooth muscle cells

Sasaki, Yasuharu; Kanno, Kimiyoshi; Hidaka, Hiroyoshi

doi:10.1152/ajpcell.1987.253.1.c71

Cited by 21 publications

(9 citation statements)

References 26 publications

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“…Three N-glycan chains of human EPO consist of the tetra-antennary structure with or without N-acetyllactosamine repeating units (Tsuda, et al, 1988). The O-linked sugar chain is composed of Gal-GalNAc and sialic acids (Sasaki, et al, 1987). The production and secretion of the mature EPO also relies upon the integrity of the N-and O-linked chains.…”

Section: Epo Expression Structure and Receptor Role In Cells And Timentioning

confidence: 99%

Erythropoietin and Oxidative Stress

Maiese

Chong

Hou

et al. 2008

CNR

110

113

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Unmitigated oxidative stress can lead to diminished cellular longevity, accelerated aging, and accumulated toxic effects for an organism. Current investigations further suggest the significant disadvantages that can occur with cellular oxidative stress that can lead to clinical disability in a number of disorders, such as myocardial infarction, dementia, stroke, and diabetes. New therapeutic strategies are therefore sought that can be directed toward ameliorating the toxic effects of oxidative stress. Here we discuss the exciting potential of the growth factor and cytokine erythropoietin for the treatment of diseases such as cardiac ischemia, vascular injury, neurodegeneration, and diabetes through the modulation of cellular oxidative stress. Erythropoietin controls a variety of signal transduction pathways during oxidative stress that can involve Janus-tyrosine kinase 2, protein kinase B, signal transducer and activator of transcription pathways, Wnt proteins, mammalian forkhead transcription factors, caspases, and nuclear factor κB. Yet, the biological effects of erythropoietin may not always be beneficial and may be poor tolerated in a number of clinical scenarios, necessitating further basic and clinical investigations that emphasize the elucidation of the signal transduction pathways controlled by erythropoietin to direct both successful and safe clinical care. KeywordsAlzheimer's disease; Akt; angiogenesis; apoptosis; cancer; cardiac; caspases; diabetes; endothelial; erythropoietin; forkhead; FoxO; GSK-3β; inflammation; mitochondria; NF-κB; renal; STATs; Wnt OXIDATIVE STRESSInitial work in pathways that can lead to oxidative stress by early investigators observed that increased metabolic rates could be detrimental to animals in an elevated oxygen environment. More current studies point to the potential aging mechanisms and accumulated toxic effects for an organism that are tied to oxidative stress (Maiese, et al., 2008a NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript in organisms, or at least the rate of oxygen consumption in organisms, has intrigued several investigators. Pearl proposed that increased exposure to oxygen through an increased metabolic rate could lead to a shortened life span (Pearl, 1928). Subsequent work by multiple investigators has furthered this hypothesis by demonstrating that increased metabolic rates could be detrimental to animals in an elevated oxygen environment . When one moves to more current work, oxygen free radicals and mitochondrial DNA mutations have become associated with oxidative stress injury, aging mechanisms, and accumulated toxicity for an organism (Yui and Matsuura, 2006).Oxygen free radicals can be generated in elevated quantities during the reduction of oxygen and subsequently lead to cell injury and apoptosis. Oxidative stress occurs as a result of the development of reactive oxygen species that consist of oxygen free radicals and other chemical entities. These agents can involve superoxide free radicals, hydrogen peroxide, sin...

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Section: Epo Expression Structure and Receptor Role In Cells And Timentioning

confidence: 99%

Erythropoietin and Oxidative Stress

Maiese

Chong

Hou

et al. 2008

CNR

110

113

View full text Add to dashboard Cite

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“…Three N-glycan chains of human EPO consist of the tetra-antennary structure with or without N-acetyllactosamine repeating units [4]. The O-linked sugar chain is composed of Gal-GalNAc and sialic acids [5].…”

Section: The Molecular Determinants For the Biological Activity Of Epomentioning

confidence: 99%

Erythropoietin on a Tightrope: Balancing Neuronal and Vascular Protection between Intrinsic and Extrinsic Pathways

Chong

Maiese³

2004

Neurosignals

102

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Enthusiasm for erythropoietin (EPO) as a broad cytoprotective agent continues to increase at an almost exponential rate. The premise that EPO was required only for erythropoiesis was eventually shed by recent work demonstrating the existence of EPO and its receptor in other organs and tissues outside of the liver and the kidney, such as the brain and heart. As a result, EPO has been identified as a possible candidate in the formulation of therapeutic strategies for both cardiac and nervous system diseases. EPO has been shown to mediate an array of vital cellular functions that involve progenitor stem cell development, cellular protection, angiogenesis, DNA repair, and cellular longevity. An important requirement to achieve the goal of preventing or even reducing cellular injury by any cytoprotective agent is the ability to uncover the cellular pathways that ultimately drive a cell to its demise. We present for consideration several critical cellular pathways modulated by EPO that involve Janus kinase 2 (Jak2), the serine-threonine kinase Akt, forkhead transcription factors, glycogen synthase kinase-3β (GSK-3β), cellular calcium, protein kinase C, caspases, as well as the control of inflammatory microglial activation. As we continue to gain new insight into these pathways, EPO should emerge as a critical agent for the development, maturation, and survival of cells throughout the body.

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“…The contraction in response to adrenoceptor stimulation in Ca2"-free solution is attributed almost entirely to release of intracellular Ca2 + (Fleckenstein, 1977;Weiss, 1981). Cultured vascular smooth muscle cells treated with HA1077 showed a dose-dependent loss or a decrease in size and length of the actin-containing microfilament structure (Sasaki et al, 1987). Neither verapamil nor diltiazem in doses up to 100yM induced reorganization of the actin microfilament structure.…”

Section: Introductionmentioning

confidence: 95%

Vasodilator actions of HA1077 in vitro and in vivo putatively mediated by the inhibition of protein kinase

Asano

Suzuki

Tsuchiya

et al. 1989

British J Pharmacology

Self Cite

130

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1 The in vitro and in vivo vasorelaxant effects of HA1077, 1-(5-isoquinolinesulphonyl)-homopiperazine HC1, a novel vasodilator were examined. 2 The inhibitory effects of HA1077 on contractile responses to various agonists were examined on strips of rabbit aorta. The concentration-response curves to 5-hydroxytryptamine, prostaglandin F2., histamine, angiotensin II, noradrenaline and dopamine were concentration-dependently shifted to the right in the presence of HA1077 (0.3-3.0pM). 3 The in vivo vasodilator effects of HA1077 were examined in the constant-pressure autoperfused coronary vascular bed of dogs. Intra-coronary administration of HA1077 (3-30jpg per dog) dosedependently increased coronary blood flow (CBF), with no effect on mean blood pressure (MBP) or heart rate (HR). Intra-coronary infusion of atropine, propranolol or diphenhydramine did not modify the in vivo coronary vasodilator response to HA1077. 6 The effects of HA1077 on various enzymes considered to be related to the regulation of smooth muscle contraction were examined. HA1077 had little effect on cyclic nucleotide phosphodiesterases, yet it potently inhibited protein kinases such as cyclic nucleotide dependent protein kinases and Ca2 +/calmodulin dependent myosin light chain kinase.7 The present study demonstrates that HA1077 is a novel type of arterial vasodilator.

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Disorganization by calcium antagonists of actin microfilament in aortic smooth muscle cells

Cited by 21 publications

References 26 publications

Erythropoietin and Oxidative Stress

Erythropoietin and Oxidative Stress

Erythropoietin on a Tightrope: Balancing Neuronal and Vascular Protection between Intrinsic and Extrinsic Pathways

Vasodilator actions of HA1077 in vitro and in vivo putatively mediated by the inhibition of protein kinase

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