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153. Pro-contractile action of the Na,K-ATPase/Src-kinase signaling pathway in the vascular wall

Author

Bouzinova, Elena, Hangaard, Lise, Xie, Zijian, Staehr, Christian, Aalkjær, Christian, and Matchkov, Vladimir

Subjects
NA+/K+-ATPASE
Abstract

Aim: Na,K-ATPase is essential for maintaining the transmembrane ion gradient and might initiate various intracellular signaling. These signals possibly act through a modification of the local ion concentrations or via Src-kinase activation. It is known that inhibition of the α-2 isoform of Na,K-ATPase by ouabain elevates blood pressure. Consequently, ouabain was shown to potentiate arterial contraction in vitro. In contrast, we have demonstrated that siRNA-induced down-regulation of the α-2 isoform Na,K-ATPase expression reduced arterial sensitivity to agonist stimulation and prevented the effect of ouabain. Here we demonstrate results of our research on the mechanisms involved in the modulation of vascular wall contractility by ouabain-sensitive Na,K-ATPase. Methods: The experiments were performed using rat mesenteric arteries in isometric myograph conditions. To inhibit kinase activity a Src-family selective tyrosine kinase inhibitor, PP2, and pNaKtide - a membrane-permeable small peptide which antagonizes ouabain-induced activation of Src-kinase were used. Results: The pro-contractile action of ouabain is associated with activation of Src. This is supported by Western blot analyses showing activation of Src by ouabain and its inhibition by pNaKtide. Src was also activated by agonist (noradrenaline - NA) stimulation. Src-dependent potentiation of vasoconstriction was associated with sensitization of contractile machinery to [Ca2+]i, as evident from MYPT (myosin phosphatase targeting protein) phosphorylation assay. Down-regulation of the α-2 isoform Na,K-ATPase prevented the inhibitory effect of Src inhibitors on arterial contraction. Conclusions: The pro-contractile action of ouabain-sensitive Na,K-ATPase inhibition is associated with Src-kinase inhibition suggesting the role of this signaling pathway in regulation of vascular tone and peripheral resistance.

Published
2015

154. Fast and controlled growth of two-dimensional layered ZrTe3 nanoribbons by chemical vapor deposition.

Author

Yu, Xu, Wen, Xiaokun, Zhang, Wenfeng, Yang, Li, Wu, Hao, Lou, Xun, Xie, Zijian, Liu, Yuan, and Chang, Haixin

Subjects
CHEMICAL vapor deposition, NANORIBBONS, CHARGE density waves, DIAMAGNETISM, TRANSITION metals
Abstract

Quasi-one-dimensional (1D)/two-dimensional (2D) ZrTe3 attracts intense interest as a typical charge density wave (CDW)-bearing material. However, the conventional chemical vapor transport (CVT) synthesis of bulk ZrTe3 is limited by high time consumption, even up to weeks, and low morphological controllability, so it is highly desirable to develop feasible methods for fast and controlled ZrTe3 growth, and so far, these have not been demonstrated. In this work, we first demonstrated that ZrTe3 nanoribbons can be grown directly by a modified chemical vapor deposition (CVD) method. The growth time is significantly reduced to less than 90 min, and the size of ZrTe3 nanoribbons can be well tuned by controlling the growth time and growth temperature. Moreover, differing from most of the other transition metal trichalcogenides (TMTCs), we reveal that ZrTe3 nanoribbons exhibit both competing and synergistic magnetic properties originating from their intrinsic diamagnetism and unexpected ferromagnetism, which can be attributed to their structural imperfection and edge-states due to the reduced dimensionality. Such observable ferromagnetism might favor the exploration of their spin-electronic applications. [ABSTRACT FROM AUTHOR]

Published
2019
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155. Smooth muscle Ca 2+ sensitization causes hypercontractility of middle cerebral arteries in mice bearing the familial hemiplegic migraine type 2 associated mutation.

Author

Staehr, Christian, Hangaard, Lise, Bouzinova, Elena V, Kim, Sukhan, Rajanathan, Rajkumar, Boegh Jessen, Peter, Luque, Nathan, Xie, Zijian, Lykke-Hartmann, Karin, Sandow, Shaun L, Aalkjaer, Christian, and Matchkov, Vladimir V

Abstract

Familial hemiplegic migraine type 2 (FHM2) is associated with inherited point-mutations in the Na,K-ATPase α2 isoform, including G301R mutation. We hypothesized that this mutation affects specific aspects of vascular function, and thus compared cerebral and systemic arteries from heterozygote mice bearing the G301R mutation (Atp1a2+/−G301R) with wild type (WT). Middle cerebral (MCA) and mesenteric small artery (MSA) function was compared in an isometric myograph. Cerebral blood flow was assessed with Laser speckle analysis. Intracellular Ca2+ and membrane potential were measured simultaneously. Protein expression was semi-quantified by immunohistochemistry. Protein phosphorylation was analysed by Western blot. MSA from Atp1a2+/−G301R and WT showed similar contractile responses. The Atp1a2+/−G301R MCA constricted stronger to U46619, endothelin and potassium compared to WT. This was associated with an increased depolarization, although the Ca2+ change was smaller than in WT. The enhanced constriction of Atp1a2+/−G301R MCA was associated with increased cSrc activation, stronger sensitization to [Ca2+]i and increased MYPT1 phosphorylation. These differences were abolished by cSrc inhibition. Atp1a2+/−G301R mice had reduced resting blood flow through MCA in comparison with WT mice. FHM2-associated mutation leads to elevated contractility of MCA due to sensitization of the contractile machinery to Ca2+, which is mediated via Na,K-ATPase/Src-kinase/MYPT1 signalling. [ABSTRACT FROM AUTHOR]

Published
2019
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157. Downregulation of cardiac myocyte [Na.sup.+]-[K.sup.+]-ATPase by adenovirus-mediated expression of an [Alpha]-subunit fragment

Author

KOMETIANI, PETER, ASKARI, AMIR, LIU, JIANG, XIE, ZIJIAN, and ASKARI, FREDERICK K.

Subjects
Muscle cells -- Physiological aspects, Adenosine triphosphatase -- Physiological aspects, Adenoviruses -- Physiological aspects, Heart failure -- Physiological aspects, Rats -- Physiological aspects, Cardiac glycosides -- Physiological aspects, Calcium in the body -- Physiological aspects, Biological sciences
Abstract

Kometiani, Peter, Amir Askari, Jiang Liu, Zijian Xie, and Frederick K. Askari. Downregulation of cardiac myocyte [Na.sup.+]-[K.sup.+]-ATPase by adenovirus-mediated expression of an [Alpha]-subunit fragment. Am J Physiol Heart Circ Physiol 280: H1415-H1421, 2001.--Cultured rat cardiac myocytes and A7r5 cells were transfected with an adenoviral vector used earlier for in vivo expression of functional [[Alpha].sub.2]-isoform of the catalytic subunit of rat [Na.sup.+]-[K.sup.+]-ATPase. Expressions of truncated forms of [[Alpha].sub.2], but little or no intact [[Alpha].sub.2], were detected, suggesting the rapid degradation of [[Alpha].sub.2] in these cultured cells. In neonatal myocytes normally containing the [[Alpha].sub.1]- and the [[Alpha].sub.3]-isoforms, expression of the [[Alpha].sub.2]-fragment led to 1) a significant decrease in the level of endogenous [[Alpha].sub.1]-protein and a modest decrease in [[Alpha].sub.3]-protein, 2) decreases in mRNAs of [[Alpha].sub.1] and [[Alpha].sub.3], 3) decrease in [Na.sup.+]-[K.sup.+]-ATPase function measured as ouabain-sensitive [Rb.sup.+] uptake, 4) increase in intracellular [Ca.sup.2+] concentration similar to that induced by ouabain, and 5) eventual loss of cell viability. These findings indicate that the [[Alpha].sub.2]-fragment downregulates endogenous [Na.sup.+]-[K.sup.+]-ATPase most likely by dominant negative interference either with folding and/or assembly of the predominant housekeeping [[Alpha].sub.1]-isoform or with signal transducing function of the enzyme. Demonstration of rise in intracellular [Ca.sup.2+] resulting from [[Alpha].sub.1]-downregulation 1) does not support the previously suggested special roles of less abundant [[Alpha].sub.2]- and [Alpha].sub.3]-isoforms in the regulation of cardiac [Ca.sup.2+], 2) lends indirect support to proposals that observed decrease in total [Na.sup.+]-[K.sup.+]-ATPase of the failing heart may be a mechanism to compensate for impaired cardiac contractility, and 3) suggests the potential therapeutic utility of dominant negative inhibition of [Na.sup.+]-[K.sup.+]-ATPase. calcium; cardiac glycosides; dominant negative; heart failure; ouabain

Published
2001

158. Metabolic regulation of [Na.sup.+]/[P.sub.i]-cotransporter-1 gene expression in H4IIE cells

Author

XIE, ZIJIAN, LI, HUI, LIU, LIQIN, KAHN, BARBARA B., NAJJAR, SONIA M., and SHAH, WAQAR

Subjects
Insulin -- Research, Metabolic regulation -- Research, Phosphatidylinositol -- Research, Gene expression -- Research, Biological sciences
Abstract

Xie, Zijian, Hui Li, Liqin Liu, Barbara B. Kahn, Sonia M. Najjar, and Waqar Shah. Metabolic regulation of [Na.sup.+]/[P.sub.i]-cotransporter-1 gene expression in H4IIE cells. Am J Physiol Endocrinol Metab 278: E648-E655, 2000.--We showed that the rat [Na.sup.+]/[P.sub.i] cotransporter-1 (RNaPi-1) gene was regulated by insulin and glucose in rat hepatocytes. The aim of this work was to elucidate signaling pathways of insulin-mediated metabolic regulation of the RNaPi-1 gene in H4IIE cells. Insulin increased RNaPi-1 mRNA abundance in the presence of glucose and decreased RNaPi-1 mRNA in the absence of glucose, clearly establishing an involvement of metabolic signals for insulin-induced upregulation of the RNaPi-1 gene. Pyruvate and insulin increased RNaPi-1 expression but downregulated L-pyruvate kinase, indicating the existence of gene-specific metabolic signals. Although fructose, glycerol, and lactate could support insulin-induced upregulation of the RNaPi-1 gene, compounds entering metabolism beyond pyruvate oxidation, such as acetate and citrate, could not, suggesting that RNaPi-l-specific metabolic signals are generated at or above pyruvate oxidation. Wortmannin, LY-294002, and rapamycin abolished the insulin effect on the RNaPi-1 gene, whereas expression of dominant negative [Asn.sup.17] Ras and mitogen-activating protein kinase (MAPK) kinase (MEK) inhibitor PD-98059 exhibited no effect. Thus we herein propose that metabolic regulation of RNaPi-1 expression by insulin is mediated through the phosphatidylinositol 3-kinase/p70 ribosomal S6 kinase pathways, but not the Ras/MAPK pathway. rat [Na.sup.+]/[P.sub.i] cotransporter-1; insulin; Ras; phosphatidylinositol 3-kinase; p70 ribosomal S6 kinase

Published
2000

159. Regulation of Renal Function and Structure by the Signaling Na/K-ATPase

Author

Xie, Jeffrey X., Li, Xin, and Xie, Zijian

Subjects
src-Family Kinases, Animals, Humans, Kidney Diseases, Phosphorylation, Sodium-Potassium-Exchanging ATPase, Kidney, Protein Processing, Post-Translational, Article, Signal Transduction
Abstract

The Na/K-ATPase as an essential ion pump was discovered more than 50 years ago (Skou (1989) Biochim. Biophys. Acta 1000, 439-446; Feraille and Doucet (2001) Physiol. Rev. 81, 345-418). The signaling function of Na/K-ATPase has been gradually appreciated over the last 20 years, first from the studies of regulatory effects of ouabain on cardiac cell growth. Several reviews on this topic have been written during the last few years (Schoner and Scheiner-Bobis (2007) Am. J. Physiol. Cell. Physiol. 293, C509-C536; Xie and Cai (2003) Mol. Interv. 3, 157 - 168; Bagrov et al. (2009) Pharmacol. Rev. 61, 9-38; Tian and Xie (2008) Physiology 23, 205-211; Fontana et al. (2013) FEBS J. 280, 5450-5455; Blanco and Wallace (2013) Am. J. Physiol. Renal Physiol. 305, F797-F812). This article will focus on the molecular mechanism of Na/K-ATPase-mediated signal transduction and its potential regulatory role in renal physiology and diseases.

Published
2013

160. Attenuation of Na/K-ATPase Mediated Oxidant Amplification with pNaKtide Ameliorates Experimental Uremic Cardiomyopathy

Author

Liu, Jiang, primary, Tian, Jiang, additional, Chaudhry, Muhammad, additional, Maxwell, Kyle, additional, Yan, Yanling, additional, Wang, Xiaoliang, additional, Shah, Preeya T., additional, Khawaja, Asad A., additional, Martin, Rebecca, additional, Robinette, Tylor J., additional, El-Hamdani, Adee, additional, Dodrill, Michael W., additional, Sodhi, Komal, additional, Drummond, Christopher A., additional, Haller, Steven T., additional, Kennedy, David J., additional, Abraham, Nader G., additional, Xie, Zijian, additional, and Shapiro, Joseph I., additional

Published
2016
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161. Rapamycin Attenuates Cardiac Fibrosis in Experimental Uremic Cardiomyopathy by Reducing Marinobufagenin Levels and Inhibiting Downstream Pro‐Fibrotic Signaling

Author

Haller, Steven T., primary, Yan, Yanling, additional, Drummond, Christopher A., additional, Xie, Joe, additional, Tian, Jiang, additional, Kennedy, David J., additional, Shilova, Victoria Y., additional, Xie, Zijian, additional, Liu, Jiang, additional, Cooper, Christopher J., additional, Malhotra, Deepak, additional, Shapiro, Joseph I., additional, Fedorova, Olga V., additional, and Bagrov, Alexei Y., additional

Published
2016
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163. Na/K-ATPase signaling regulates collagen synthesis through microRNA-29b-3p in cardiac fibroblasts

Author

Drummond, Christopher A., primary, Hill, Michael C., additional, Shi, Huilin, additional, Fan, Xiaoming, additional, Xie, Jeffrey X., additional, Haller, Steven T., additional, Kennedy, David J., additional, Liu, Jiang, additional, Garrett, Michael R., additional, Xie, Zijian, additional, Cooper, Christopher J., additional, Shapiro, Joseph I., additional, and Tian, Jiang, additional

Published
2016
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165. The Na/K-ATPase Oxidant Amplification Loop Regulates Aging.

Author

Sodhi, Komal, Nichols, Alexandra, Mallick, Amrita, Klug, Rebecca L., Liu, Jiang, Wang, Xiaoliang, Srikanthan, Krithika, Goguet-Rubio, Perrine, Nawab, Athar, Pratt, Rebecca, Lilly, Megan N., Sanabria, Juan R., Xie, Zijian, Abraham, Nader G., and Shapiro, Joseph I.

Subjects
CELLULAR aging, ADENOSINE triphosphatase, FIBROBLASTS, APOPTOSIS, OXIDATIVE stress
Abstract

As aging involves oxidant injury, we examined the role of the recently described Na/K-ATPase oxidant amplification loop (NKAL). First, C57Bl6 old mice were given a western diet to stimulate oxidant injury or pNaKtide to antagonize the NKAL. The western diet accelerated functional and morphological evidence for aging whereas pNaKtide attenuated these changes. Next, human dermal fibroblasts (HDFs) were exposed to different types of oxidant stress in vitro each of which increased expression of senescence markers, cell-injury, and apoptosis as well as stimulated the NKAL. Further stimulation of the NKAL with ouabain augmented cellular senescence whereas treatment with pNaKtide attenuated it. Although N-Acetyl Cysteine and Vitamin E also ameliorated overall oxidant stress to a similar degree as pNaKtide, the pNaKtide produced protection against senescence that was substantially greater than that seen with either antioxidant. In particular, pNaKtide appeared to specifically ameliorate nuclear oxidant stress to a greater degree. These data demonstrate that the NKAL is intimately involved in the aging process and may serve as a target for anti-aging interventions. [ABSTRACT FROM AUTHOR]

Published
2018
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184. CD36 and Na/K-ATPase-α1 Form a Proinflammatory Signaling Loop in Kidney

Author

Kennedy, David J., primary, Chen, Yiliang, additional, Huang, Wenxin, additional, Viterna, Jamie, additional, Liu, Jiang, additional, Westfall, Kristen, additional, Tian, Jian, additional, Bartlett, David J., additional, Tang, W.H. Wilson, additional, Xie, Zijian, additional, Shapiro, Joseph I., additional, and Silverstein, Roy L., additional

Published
2013
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194. Identification of Hydroxyxanthones as Na/K-ATPase Ligands

Author

Zhang, Zhongbing, primary, Li, Zhichuan, additional, Tian, Jiang, additional, Jiang, Wei, additional, Wang, Yin, additional, Zhang, Xiaojin, additional, Li, Zhuorong, additional, You, Qidong, additional, Shapiro, Joseph I., additional, Si, Shuyi, additional, and Xie, Zijian, additional

Published
2010
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196. Spironolactone Attenuates Experimental Uremic Cardiomyopathy by Antagonizing Marinobufagenin

Author

Tian, Jiang, primary, Shidyak, Amjad, additional, Periyasamy, Sankaridrug M., additional, Haller, Steven, additional, Taleb, Mohamed, additional, El-Okdi, Nasser, additional, Elkareh, Jihad, additional, Gupta, Shalini, additional, Gohara, Sabry, additional, Fedorova, Olga V., additional, Cooper, Christopher J., additional, Xie, Zijian, additional, Malhotra, Deepak, additional, Bagrov, Alexei Y., additional, and Shapiro, Joseph I., additional

Published
2009
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