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Apolipoprotein E4 stimulates cAMP response element-binding protein transcriptional activity through the extracellular signal-regulated kinase pathway

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JOURNAl OF BIOlOGICAl CHEMISTRY 2001年第5期276卷 3046-3053页

作者： Ohkubo, N Mitsuda, N Tamatani, M Yamaguchi, A lee, YD Ogihara, T Vitek, MP Tohyama, M Osaka Univ Grad Sch Med Dept Anat & Neurosci Suita Osaka 5650871 Japan Osaka Univ Grad Sch Med Dept Geriatr Med Suita Osaka 5650871 Japan CREST Japan Sci & Technol Yokohama Kanagawa Japan Ajou Univ Sch Med Dept Anat Suwon 442749 South Korea Duke Univ Med Ctr Div Neurol Durham NC 27710 USA

Inheritance of the epsilon4 allele of the apolipoprotein E gene (APOE4) is a major risk factor for the development of Alzheimer's disease (AD). Although the association between APOE4 and AD is well documented, the mechanism by which apolipoprotein E exerts an isoform-specific effect on neurons in disease is unknown. In this report, we demonstrate that apoE4 stimulates the transcriptional activity of cAMP-response element-binding protein (CREB) by activating the extracellular signal-regulated kinase (ERK) cascade in rat primary hippocampal neurons. In contrast, apoE3 was unable to stimulate CREB transcriptional activity and unable to activate the ERK pathway. Elevation of intracellular Ca2+ levels are also involved because treatment with receptor-associated protein, nifedipine, MK801, removal of Ca2+ from the medium and dantrolene all served to inhibit calcium elevation and attenuate the activation of CREB, Treatment with an apoE peptide was also found to facilitate transcription of the CREB-dependent genes, c-fos and Bcl-2. In contrast to treatment with apoE3, our findings suggest apoE4 and apoE-peptide induce a novel signaling pathway.

关键词：抗原 CD95 抗原分化载脂蛋白E3 载脂蛋白E4 载脂蛋白E类/遗传学载脂蛋白E类/代谢载脂蛋白E类/生理学钙/代谢钙通道 l型/代谢 cAMP反应元件结合蛋白质/遗传学 cAMP反应元件结合蛋白质/代谢环AMP依赖性蛋白激酶类/代谢酶激活海马/代谢 lDl受体相关蛋白质1 膜糖蛋白类丝裂原激活蛋白激酶类/代谢神经细胞黏附分子l1 神经细胞黏附分子类神经元/代谢磷酰化蛋白质丝氨酸苏氨酸激酶/代谢原癌基因蛋白质c-bcl-2/生物合成原癌基因蛋白质c-fos/生物合成受体免疫受体脂蛋白/代谢受体 N-甲基-D-天冬氨酸/代谢重组蛋白质类/代谢丝氨酸/代谢反式激活(遗传学)/生理学动物大鼠

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Cardiac hypertrophy and impaired relaxation in transgenic mice overexpressing triadin 1

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JOURNAl OF BIOlOGICAl CHEMISTRY 2001年第6期276卷 4142-4149页

作者： Kirchhefer, U Neumann, J Baba, HK Begrow, F Kobayashi, YM Reinke, U Schmitz, W Jones, lR Univ Munster Inst Pharmakol & Toxikol D-48149 Munster Germany Univ Munster Gerhard Domagk Inst Pathol D-48149 Munster Germany Indiana Univ Sch Med Dept Med Krannert Inst Cardiol Indianapolis IN 46202 USA

Triadin 1 is a major transmembrane protein in cardiac junctional sarcoplasmic reticulum (SR), which forms a quaternary complex with the ryanodine receptor (Ca2+ release channel), junctin, and calsequestrin. To better understand the role of triadin 1 in excitation-contraction coupling in the heart, we generated transgenic mice with targeted overexpression of triadin 1 to mouse atrium and ventricle, employing the alpha -myosin heavy chain promoter to drive protein expression. The protein was overexpressed 5-fold in mouse ventricles, and overexpression was accompanied by cardiac hypertrophy. The levels of two other junctional SR proteins, the ryanodine receptor and junctin, were reduced by 55% and 73%, respectively in association with triadin 1 overexpression, whereas the levels of calsequestrin, the Ca2+ binding protein of junctional SR, and of phospholamban and SERCA2a, Ca2+-handling proteins of the free SR, were unchanged. Cardiac myocytes from triadin 1-over-expressing mice exhibited depressed contractility;Ca2+ transients decayed at a slower rate, and cell shortening and relengthening were diminished. The extent of depression of cell shortening of triadin 1-overexpressing cardiomyocytes was rate-dependent, being more depressed under low stimulation frequencies (0.5 Hz), but reaching comparable levels at higher frequencies of stimulation (5 Hz). Spontaneously beating, isolated work-performing heart preparations overexpressing triadin 1 also relaxed at a slower rate than control hearts, and failed to adapt to increased afterload appropriately. The fast time inactivation constant, tau (1), of the l-type Ca2+ channel was prolonged in transgenic cardiomyocytes. Our results provide evidence for the coordinated regulation of junctional SR protein expression in heart independent of free SR protein expression, and furthermore suggest an important role for triadin 1 in regulating the contractile properties of the heart during excitation-contraction coupling.

关键词：碱基序列钙/代谢钙通道 l型/代谢肌集钙蛋白/代谢心脏扩大/遗传学载体蛋白质类 DNA引物小鼠转基因肌蛋白质类/遗传学肌蛋白质类/生理学动物小鼠

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Protein phosphatase 2A is associated with class C l-type calcium channels (Ca_v1.2) and antagonizes channel phosphorylation by cAMP-dependent protein kinase

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JOURNAl OF BIOlOGICAl CHEMISTRY 2000年第50期275卷 39710-39717页

作者： Davare, MA Horne, MC Hell, JW Univ Wisconsin Dept Pharmacol Madison WI 53706 USA

Phosphorylation by cAMP-dependent protein kinase (PKA) regulates a vast number of cellular functions. An important target for PKA in brain and heart is the class C l-type Ca2+ channel (Ca(v)1.2). PKA phosphorylates serine 1928 in the central, pore-forming alpha (1C) subunit of this channel. Regulation of channel activity by PRA requires a proper balance between phosphorylation and dephosphorylation. For hat and specific signaling, PKA is recruited to this channel by an protein kinase A anchor protein (Davare, M. A, Dong, F., Rubin, C. S., and Hell, J.W (1999) J. Biol. Chem. 274, 39280-39287), A phosphatase may be associated with the channel to effectively balance serine 1928 phosphorylation by channel-bound PKA Dephosphorylation of this site is mediated by a serine/threonine phosphatase that is inhibited by okadaic acid and microcystin. We show that immunoprecipitation of the channel complex hom rat brain results in coprecipitation of PP2A Stoichiometric: analysis indicates that about 80% of the channel complexes contain PP2A PP2A directly and stably binds to the C-terminal 557 amino acids of alpha (1C). This interaction does not depend on serine 1928 phosphorylation and is not altered by PP2A catalytic site inhibitors. These results indicate that the PP2A-alpha (1C) interaction constitutively recruits PP2A to the channel complex rather than being a transient substrate-catalytic site interaction. Functional assays with the immunoisolated class C channel complex showed that channel-associated PP2A effectively reverses serine 1928 phosphorylation by endogenous PHA. Our findings demonstrate that both PKA and PP2A are integral components of the class C l-type Ca2+ channel that determine the phosphorylation level of serine 1928 and thereby channel activity.

关键词：氨基酸类/化学脑/代谢钙通道 l型/代谢催化域细胞系环AMP依赖性蛋白激酶类/拮抗剂和抑制剂环AMP依赖性蛋白激酶类/代谢酶抑制剂/药理学大肠杆菌/代谢谷胱甘肽转移酶/代谢免疫印迹法半数抑制浓度离子载体/药理学微囊藻毒素类黑软海绵素A/药理学肽类环/药理学磷酰化沉淀素试验蛋白质结合蛋白激酶C/代谢蛋白质结构三级重组融合蛋白质类/代谢丝氨酸/化学苏氨酸/化学动物人类大鼠

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Modulation of the smooth-muscle l-type Ca²⁺ channel α1 subunit (α1C-b) by the β2a subunit:: a peptide which inhibits binding of β to the I-II linker of α1 induces functional uncoupling

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BIOCHEMICAl JOURNAl 2000年第part3期348卷 657-665页

作者： Hohaus, A Poteser, M Romanin, C Klugbauer, N Hofmann, F Morano, I Haase, H Groschner, K Graz Univ Inst Pharmakol & Toxikol A-8010 Graz Austria Max Delbruck Ctr Mol Med D-13092 Berlin Germany Johannes Kepler Univ Linz Inst Biophys A-4040 Linz Austria Tech Univ Munich Inst Pharmakol & Toxikol D-80802 Munich Germany

Modulation of the smooth-muscle Ca2+ channel alpha 1C-b subunit by the auxiliary beta 2a subunit was studied in the HEK 293 (cell line from human embryonic kidney cells) expression system. In addition, we tested whether the alpha 1-beta interaction in functional channels is sensitive to an 18-amino-acid synthetic peptide that corresponds to the sequence of the defined major interaction domain in the cytoplasmic I-II linker of alpha 1C (AID-peptide). Ca2+ channels derived by co-expression of alpha 1C-b and beta 2a subunits exhibited an about 3-fold higher open probability (P-0) than alpha 1C-b channels. High-P-0 gating of alpha *** 2a channels was associated with the occurrence of long-lasting channel openings [mean open time (tau) > 10 ms] which were rarely observed in alpha 1C-b channels. Modulation of fast gating by the beta 2a subunit persisted in the cell-free, inside-out recording configuration. Biochemical experiments showed that the AID-peptide binds with appreciable affinity to beta 2 subunits of native Ca2+ channels. Binding of the beta 2 protein to immobilized AID-peptide was specifically inhibited (K-i of 100 nM) by preincubation with free (uncoupled) AID-peptide, but not by a corresponding scrambled peptide. Administration of the AID-peptide (10 mu M) to the cytoplasmic side of inside-out patches induced a substantial reduction of P-0 of alpha *** 2a channels. The scrambled control peptide failed to affect alpha *** 2a channels, and the AID-peptide (10 mu M) did not modify alpha 1C-b channel function in the absence of expressed beta 2a subunit. Our results demonstrate that the beta 2a subunit controls fast gating of alpha 1C-b channels, and suggest the alpha 1-beta interaction domain in the cytoplasmic I-II linker of alpha 1C (AID) as a possible target of modulation of the channel. Moreover, our data are consistent with a model of alpha 1-beta interaction that is based on multiple interaction sites, including AID as a determinant of the

关键词：钙通道 l型/化学钙通道 l型/代谢细胞系细胞质/代谢离子通道闸门肌平滑/代谢肽碎片/代谢蛋白质结合大鼠 Wistar 动物人类大鼠

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Ethanol regulates calcium channel subunits by protein kinase C δ-dependent and -independent mechanisms

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JOURNAl OF BIOlOGICAl CHEMISTRY 2000年第33期275卷 25717-25722页

作者： Walter, HJ McMahon, T Dadgar, J Wang, D Messing, RO Univ Calif San Francisco Dept Neurol San Francisco CA 94143 USA Univ Calif San Francisco Grad Programs Neurosci & Biomed Sci San Francisco CA 94143 USA Ernest Gallo Clin & Res Ctr Emeryville CA 94608 USA

Chronic exposure to ethanol increases the number of functional l-type voltage-gated calcium channels in neural cells. In PC12 cells, this adaptive response is mediated by protein kinase C delta (PKC delta), but the mechanisms by which this occurs are not known. Since expression of several different calcium channel subunits can increase the abundance of functional l-type channels, we sought to identify which subunits are regulated by ethanol. Incubation of PC12 cells with 120-150 mM ethanol for 6 days increased levels of alpha(1C), alpha(2), and beta(1b) subunit immunoreactivity in cell membranes and selectively increased the abundance of mRNA encoding the alpha(1C-1) splice variant of alpha(1C). In cells expressing a fragment of PKC delta (delta V1) that selectively inhibits PKC delta, there was no increase in membrane-associated alpha(1C), alpha(2), and beta(1b) immunoreactivity following chronic ethanol exposure. However, ethanol still increased levels of alpha(1C-1) mRNA in these cells. These results indicate that ethanol increases the abundance of l-type channels by at least two mechanisms;one involves increases in mRNA encoding a splice variant of alpha(1C) and the other is post-transcriptional, rate-limiting, and requires PKC delta.

关键词：选择性剪接碱基序列印迹法蛋白质钙通道 l型/化学钙通道 l型/遗传学钙通道 l型/代谢 DNA引物/代谢 DNA 互补/代谢剂量效应关系药物乙醇/药理学同工酶类/化学同工酶类/代谢同工酶类/生理学分子序列数据 PC12细胞蛋白激酶C/化学蛋白激酶C/代谢蛋白激酶C/生理学蛋白激酶Cδ RNA 信使/代谢逆转录聚合酶链反应核糖核酸酶类/代谢时间因素增量调节动物大鼠

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Role of the C terminus of the α_1C (Ca_v1.2) subunit in membrane targeting of cardiac l-type calcium channels

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JOURNAl OF BIOlOGICAl CHEMISTRY 2000年第33期275卷 25436-25444页

作者： Gao, TY Bünemann, M Gerhardstein, Bl Ma, H Hosey, MM Northwestern Univ Sch Med Dept Mol Pharmacol & Biol Chem Chicago IL 60611 USA

We have previously demonstrated that formation of a complex between l-type calcium (Ca2+) channel alpha(1C) (Ca(V)1.2) and beta subunits was necessary to target the channels to the plasma membrane when expressed in tsA201 cells. In the present study, we identified a region in the C terminus of the alpha(1C) subunit that was required for membrane targeting. Using a series of C-terminal deletion mutants of the alpha(1C) subunit, a domain consisting of amino acid residues 1623-1666 ("targeting domain") in the C terminus of the alpha(1C) subunit has been identified to be important for correct targeting of l-type Ca2+ channel complexes to the plasma membrane. Although cells expressing the wild-type alpha(1C) and beta(2a) subunits exhibited punctate clusters of channel complexes along the plasma membrane with little intracellular staining, co-expression of deletion mutants of the alpha(1C) subunit that lack the targeting domain with the beta(2a) subunit resulted in an intracellular localization of the channels. In addition, three other regions in the C terminus of the alpha(1C) subunit that were downstream of residues 1623-1666 were found to contribute to membrane targeting of the l-type channels. Deletion of these domains in the alpha(1C) subunit resulted in a reduction of plasma membrane-localized channels, and a concomitant increase in channels localized intracellularly, Taken together, these results have demonstrated that a targeting domain in the C terminus of the alpha(1C) subunit was required for proper plasma membrane localization of the l-type Ca2+ channels.

关键词：钙通道 l型/化学钙通道 l型/代谢钙通道 l型/生理学细胞系细胞膜/代谢荧光抗体技术基因缺失免疫印迹法配体诱变定点膜片钳术沉淀素试验脯氨酸/化学蛋白质结合蛋白质结构三级转染人类

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Proteolytic processing of the C terminus of the α_1C subunit of l-type calcium channels and the role of a proline-rich domain in membrane tethering of proteolytic fragments

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JOURNAl OF BIOlOGICAl CHEMISTRY 2000年第12期275卷 8556-8563页

作者： Gerhardstein, Bl Gao, TY Bünemann, M Puri, TS Adair, A Ma, H Hosey, MM Northwestern Univ Sch Med Dept Mol Pharmacol & Biol Chem Chicago IL 60611 USA

Although most l-type calcium channel alpha(1C) subunits isolated from heart or brain are similar to 190-kDa proteins that lack similar to 50 kDa of the C terminus, the C-terminal domain is present in intact cells. To test the hypothesis that the C terminus is processed but remains functionally associated with the channels, expressed, full-length alpha(1C) subunits mere cleaved in vitro by chymotrypsin to generate a 190-kDa C-terminal truncated protein and C-terminal fragments of 30-56 kDa, These hydrophilic C-terminal fragments remained membrane-associated, A C-terminal proline-rich domain (PRD) was identified as the mediator of membrane association. The alpha(1C) PRD bound to SH3 domains in Src, lyn, Hck, and the channel beta(2) subunit. Mutant alpha(1C) Subunits lacking either similar to 50 kDa of the C terminus or the PRD produced increased barium currents through the channels, demonstrating that these domains participate in the previously described (Wei, X., Neely, a., lacerda, A. E, Olcese, r,, Stefani, E,, Perez-Reges, E., and Birnbaumer, l,, (1994) J. Biol. Chem. 269, 1635-1640) inhibition of channel function by the C terminus.

关键词：钡/代谢结合部位钙通道 l型/遗传学钙通道 l型/代谢环AMP依赖性蛋白激酶类/代谢导电性谷胱甘肽转移酶/遗传学谷胱甘肽转移酶/代谢心室/代谢细胞内膜/代谢肽碎片/遗传学肽碎片/代谢磷酰化脯氨酸蛋白质结合蛋白质加工转译后重组融合蛋白质类/代谢 src同源域动物兔

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A model of the l-type Ca²⁺ channel in rat ventricular myocytes:: ion selectivity and inactivation mechanisms

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JOURNAl OF PHYSIOlOGY-lONDON 2000年第1期529卷 139-158页

作者： Sun, l Fan, JS Clark, JW Palade, PT Univ Texas Med Branch Dept Physiol & Biophys Galveston TX 77555 USA Rice Univ Dept Elect & Comp Engn Houston TX 77005 USA

1. We have developed a mathematical model of the l-type Ca2+ current, which is based on data from whole-cell voltage clamp experiments on rat ventricular myocytes. Ion substitution methods were employed to investigate the ionic selectivity of the channel. Experiments were configured with Na+, Ca2+ or Ba2+ as the majority current carrier. 2. The amplitude of current through the channel is attenuated in the presence of extracellular Ca2+ or Ba2+. Our model accounts for channel selectivity by using a, modified Goldman-Hodgkin-Katz (GHK) configuration that employs voltage-dependent channel binding functions for external divalent ions. Stronger binding functions were used for Ca2+ than for Ba2+. 3. Decay of the ionic current during maintained depolarization was characterized by means of voltage- and Ca2+-dependent inactivation pathways embedded in a five-state dynamic channel model. Particularly, Ca2+ first binds to calmodulin and the Ca2+-calmodulin complex is the mediator of Ca2+ inactivation. Ba2+-dependent inactivation was characterized using the same scheme, but with a decreased binding to calmodulin. 4. A reduced amount of steady-state inactivation, as evidenced by a U-shaped curve at higher depolarization levels (>40 mV) in the presence of [Ca2+](o), was observed in double-pulse protocols used to study channel inactivation. To characterize this phenomenon, a mechanism was incorporated into the model whereby Ca2+ or Ba2+ also inhibits the voltage-dependent inactivation pathway. 5. The five-state dynamic channel model was also used to simulate single channel activity. Calculations of the open probability of the channel model are generally consistent with experimental data. A sixth state can be used to simulate modal activity by way of introducing long silent intervals. 6. Our model has been tested extensively using experimental data from a wide variety of voltage clamp protocols and bathing solution manipulations. It provides: (a) biophysically based explanations of

关键词：算法钡/代谢钙/代谢钙通道 l型/代谢电生理学离子通道闸门/生理学膜电位/生理学模型理论心肌/细胞学心肌/代谢膜片钳术通透性肌浆网/代谢钠/代谢动物大鼠

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Protein kinase C evokes quantal catecholamine release from PC12 cells via activation of l-type Ca²⁺ channels

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JOURNAl OF BIOlOGICAl CHEMISTRY 2000年第35期275卷 26786-26791页

作者： Taylor, SC Green, KN Carpenter, E Peers, C Univ Leeds Inst Cardiovasc Res Leeds LS2 9JT W Yorkshire England

Application of the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) to PC12 cells under resting conditions evoked quantal catecholamine secretion, as detected amperometrically, This effect was not mimicked by 4 alpha-phorbol-12,13-didecanoate, another phorbol ester, which is inactive with respect to protein kinase C activation, and was prevented by the protein kinase C inhibitor bisindolylmaleimide, TPA also caused a rise of [Ca2+](i) in Fura-2-loaded PC12 cells, and again this was not mimicked by 4 alpha-phorbol-12,13-didecanoate and could be blocked by bisindolylmaleimide, TPA-evoked secretion was entirely dependent on extracellular Ca2+ and was fully abolished by nifedipine, as were TPA-induced rises of [Ca2+](i). Resting membrane potential, monitored using perforated patch recordings, was unaffected by TPA. However, a small (6-8 mV) hyperpolarizing shift in the voltage dependence of Ca2+ channel currents (determined using whole-cell patch clamp recordings) was induced by TPA, and this could be fully prevented by nifedipine. In contrast to results with depolarizing stimuli, which evoke exocytosis because of Ca2+ influx through N-type channels in these cells, the present results indicate that protein kinase C activation leads directly to quantal catecholamine secretion in the absence of depolarizing stimuli via a selective shift in the activation of l-type Ca2+ channels.

关键词：钙通道 l型/代谢儿茶酚胺类/代谢电化学酶激活膜电位 PC12细胞蛋白激酶C/代谢十四酰佛波乙酯/药理学动物大鼠

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Changes in the mechanisms involved in uterine contractions during pregnancy in guinea-pigs

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JOURNAl OF PHYSIOlOGY-lONDON 2000年第3期523卷 785-798页

作者： Coleman, HA Hart, JDE Tonta, MA Parkington, HC Monash Univ Dept Physiol Clayton Vic Australia

1. The mechanisms involved in contraction in guinea-pig myometrium were compared at mid- and late pregnancy. Tension was recorded simultaneously with either membrane potential or cytoplasmic calcium ([Ca2+](i)) in strips exposed briefly to prostaglandin F-2 alpha (PGF). 2. PGF-induced increases in tension were underpinned by action potentials followed by sustained depolarization and biphasic increases in [Ca2+](i) at mid- (peak, 879 +/- 199 nM;sustained, 298 +/- 35 nM, n = 11) and late pregnancy (peak, 989 +/- 302 nM;sustained 178 +/- 33 nM, n = 8). 3. At mid- and late pregnancy, nifedipine (10(-6) M) reduced (a) the PGF-induced increase in tension to 84 and 35%, (b) the level attained during the depolarization by 2 and 12 mV and (c) the peak rise in [Ca2+](i) to 42 and 17%. The sustained rises in [Ca2+](i) were resistant to nifedipine. 4. In Ca2+-free solution (containing 1 mM EGTA), PGF elicited an increase in tension that was 26% of that in 2.5 mM Ca2+ and an increase in [Ca2+](i) (24% of the sustained level) at midpregnancy but no increase in tension or [Ca2+](i) at term. 5. At both stages of pregnancy, PGF decreased the level of [Ca2+](i) required to elicit increases in tension comparable to those evoked by high K-o(+). The slope of the tension-[Ca2+](i) curves were steeper in mid- than in late pregnancy. 6. In conclusion, at mid-pregnancy, the contractile response of the guinea-pig myometrium to PGF involves Ca2+ influx through l-type voltage-operated Ca2+ channels (VOCCs) and by receptor-operated mechanisms, release of Ca2+ from intracellular stores, and an increase in the sensitivity of the contractile apparatus to Ca2+. At term the situation is different: a modest increase in the sensitivity of the contractile apparatus to Ca2+ persists and there is a major reliance on Ca2+ influx through VOCCs.

关键词：钙/代谢钙/药理学钙通道阻滞药/药理学钙通道 l型/药物作用钙通道 l型/代谢内质网/代谢硝苯地平/药理学妊娠动物/生理学前列腺素F类/药理学子宫收缩/药物作用子宫收缩/生理学动物女(雌)性豚鼠妊娠

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