Publications
150 results found
Levy E, Sastre M, 1999, X11 modulation of β-amyloid precursor protein cellular stabilization and reduction of amyloid β-protein secretion, Alzheimer's Disease and Related Disorders, Editors: Wiley, Ltd, Pages: 397-404
Sastre M, Turner RS, Levy E, 1998, X11 interaction with β-amyloid precursor protein modulates its cellular stabilization and reduces amyloid β-protein secretion, JOURNAL OF BIOLOGICAL CHEMISTRY, Vol: 273, Pages: 22351-22357, ISSN: 0021-9258
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- Citations: 127
Sastre M, Galea E, Feinstein D, et al., 1998, Metabolism of agmatine in macrophages: modulation by lipopolysaccharide and inhibitory cytokines, BIOCHEMICAL JOURNAL, Vol: 330, Pages: 1405-1409, ISSN: 0264-6021
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- Citations: 59
Callado LF, Meana JJ, Grijalba B, et al., 1998, Selective increase of α<sub>2A</sub>-adrenoceptor agonist binding sites in brains of depressed suicide victims, JOURNAL OF NEUROCHEMISTRY, Vol: 70, Pages: 1114-1123, ISSN: 0022-3042
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- Citations: 109
Sastre M, Regunathan S, Reis DJ, 1997, Uptake of agmatine into rat brain synaptosomes: Possible role of cation channels, JOURNAL OF NEUROCHEMISTRY, Vol: 69, Pages: 2421-2426, ISSN: 0022-3042
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- Citations: 56
Sastre M, Garcia-Sevilla JA, 1997, Densities of I2-imidazoline receptors, α2-adrenoceptors and monoamine oxidase B in brains of suicide victims, Neurochemistry International: the journal for the publication of cellular and molecular aspects of neurochemistry, Vol: 30, Pages: 63-72
Sastre M, Regunathan S, Galea E, et al., 1996, Agmatinase activity in rat brain: A metabolic pathway for the degradation of agmatine, JOURNAL OF NEUROCHEMISTRY, Vol: 67, Pages: 1761-1765, ISSN: 0022-3042
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- Citations: 121
GarciaSevilla JA, Escriba PV, Sastre M, et al., 1996, Immunodetection and quantitation of imidazoline receptor proteins in platelets of patients with major depression and in brains of suicide victims, ARCHIVES OF GENERAL PSYCHIATRY, Vol: 53, Pages: 803-810, ISSN: 0003-990X
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- Citations: 89
Escriba PV, Alemany R, Sastre M, et al., 1996, Pharmacological modulation of immunoreactive imidazoline receptor proteins in rat brain: Relationship with non-adrenoceptor [H-3]-idazoxan binding sites, BRITISH JOURNAL OF PHARMACOLOGY, Vol: 118, Pages: 2029-2036, ISSN: 0007-1188
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- Citations: 37
Busquets X, Ventayol P, Sastre M, et al., 1996, Age-dependent increases in protein kinase C-alpha beta immunoreactivity and activity in the human brain: Possible in vivo modulatory effects on guanine nucleotide regulatory G(i) proteins, BRAIN RESEARCH, Vol: 710, Pages: 28-34, ISSN: 0006-8993
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- Citations: 8
Sastre M, Ventayol P, Garcia-Sevilla, 1996, Decreased density of I2-imidazoline receptors in the postmortem brains of heroin addicts, Neuroreport, Vol: 7, Pages: 509-512
ESCRIBA PV, SASTRE M, GARCIASEVILLA JA, 1995, DISRUPTION OF CELLULAR SIGNALING PATHWAYS BY DAUNOMYCIN THROUGH DESTABILIZATION OF NONLAMELLAR MEMBRANE STRUCTURES, PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, Vol: 92, Pages: 7595-7599, ISSN: 0027-8424
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- Citations: 95
GARCIASEVILLA JA, SASTRE M, ESCRIBA PV, 1995, AGE-DEPENDENT INCREASES OF IMMUNOREACTIVE IMIDAZOLINE RECEPTORS IN THE HUMAN BRAIN - POSSIBLE ASSOCIATION OF A 29/30-KDA PROTEIN WITH THE I-2-IMIDAZOLINE RECEPTOR IDENTIFIED BY [H-3] IDAZOXAN, NEUROSCIENCE LETTERS, Vol: 184, Pages: 133-136, ISSN: 0304-3940
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- Citations: 24
BUSQUETS X, ESCRIBA PV, SASTRE M, et al., 1995, LOSS OF PROTEIN-KINASE C-ALPHA-BETA IN BRAIN OF HEROIN-ADDICTS AND MORPHINE-DEPENDENT RATS, JOURNAL OF NEUROCHEMISTRY, Vol: 64, Pages: 247-252, ISSN: 0022-3042
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- Citations: 41
Sastre M, Escriba PV, Reis DJ, et al., 1995, Decreased number and immunoreactivity of I2-imidazoline receptors in the frontal cortex of suicide victims., Pages: 520-522
Garcia-Sevilla JA, Miralles A, Sastre M, et al., 1995, I2-imidazoline receptors in the healthy and pathologic human brain, Ann.N.Y. Acad. Sci., Vol: 763, Pages: 178-193
Sastre M, García-Sevilla JA, 1994, Alpha 2-adrenoceptor subtypes identified by [3H]RX821002 binding in the human brain: the agonist guanoxabenz does not discriminate different forms of the predominant alpha 2A subtype., J Neurochem, Vol: 63, Pages: 1077-1085, ISSN: 0022-3042
Competition [3H]RX821002 ([3H]2-methoxyidazoxan) binding experiments with alpha 2-adrenoceptor subtype-specific antagonists--BRL 44408 (alpha 2A selectively), ARC 239 (alpha 2B selective), and others--were performed to delineate through rigorous computer modeling receptor subtypes in the postmortem human brain. In the hippocampus, hypothalamus, cerebellum, and brainstem the whole population of alpha 2-adrenoceptors appears to belong to the alpha 2A subtype (100%; Bmax = 34-90 fmol/mg of protein). In the frontal cortex, the predominant receptor was the alpha 2A subtype (87%; Bmax = 53 fmol/mg of protein), although a small population of the alpha 2B/C subtype (13%; Bmax = 8 fmol/mg of protein) was also detected. In the caudate nucleus, a mixed population of alpha 2A (64%; Bmax = 9 fmol/mg of protein) and alpha 2B/C (36%; Bmax = 5 fmol/mg of protein) subtypes was detected. In the cortex and caudate and in the presence of ARC 239 (to mask the alpha 2B/C-adrenoceptors), competition experiments with the agonist guanoxabenz clearly modeled the high- and low-affinity states of the alpha 2A subtype. In the presence of ARC 239 and the GTP analogue guanylyl-5'-imidodiphosphate together with NaCl and EDTA (to eliminate the high-affinity alpha 2A-adrenoceptor) guanoxabenz only recognized the low-affinity alpha 2A-adrenoceptor. The results indicate that in the human brain the predominant alpha 2-adrenoceptor is of the alpha 2A subtype and that this functionally relevant receptor subtypes is not heterogeneous in nature.
ESCRIBA PV, SASTRE M, WANG H, et al., 1994, IMMUNODETECTION OF PUTATIVE IMIDAZOLINE RECEPTOR PROTEINS IN THE HUMAN AND RAT-BRAIN AND OTHER TISSUES, NEUROSCIENCE LETTERS, Vol: 178, Pages: 81-84, ISSN: 0304-3940
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- Citations: 49
GABILONDO AM, MEANA JJ, BARTUREN F, et al., 1994, MU-OPIOID RECEPTOR AND ALPHA(2)-ADRENOCEPTOR AGONIST BINDING-SITES IN THE POSTMORTEM BRAIN OF HEROIN-ADDICTS, PSYCHOPHARMACOLOGY, Vol: 115, Pages: 135-140, ISSN: 0033-3158
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- Citations: 50
Escriba PV, Sastre M, Garcia-Sevilla JA, 1994, Increased density of guanine nucleotide-binding proteins in the postmortem brains of heroin addicts., Arch Gen Psychiatry, Vol: 51, Pages: 494-501, ISSN: 0003-990X
OBJECTIVE: To directly evaluate the guanine nucleotide-binding (G) protein subunits alpha, beta, and gamma, which are involved in the signal transduction of opioid receptors, in the postmortem brains of heroin addicts who had died of an opiate overdose. METHODS: Specimens of the frontal cortex (Brodmann's area 9) were collected from 11 heroin addicts and 10 control subjects without a history of drug abuse. The biochemical status of human brain G protein subunits during opiate dependence was studied by means of immunoblotting techniques. Solubilized G proteins were separated by gel electrophoresis, transferred to pyroxylin membranes (western blotting) labeled with specific antiserum samples, and quantitated by image analysis after enhanced chemoluminescence. RESULTS: In the frontal cortex, relevant increases in the immunoreactivities of G alpha i 1/2 (19% +/- 4%, P < .005), G alpha o (29% +/- 7%, P < .005), and G alpha s (26% +/- 5%, P < .005) but not of G alpha i3 were found in heroin addicts compared with age- and sex-matched controls. Moreover, the amount of G protein beta-subunit immunoreactivity was also consistently increased (27% +/- 8%, P < .01) compared with controls in the same brain region. These G protein changes in the brains of human opiate addicts paralleled (with the exception of G alpha s) those obtained in the brains of morphine hydrochloride-dependent rats. The increase in G alpha s immunoreactivity that was observed in the rat brain only after the short-term morphine administration (24% +/- 3%, P < .005) suggests that the increase in G alpha s immunoreactivity in the brains of human addicts could be the cellular response to a deadly overdose of heroin. CONCLUSIONS: Alterations in the density of specific Gi and Go protein subunits that are coupled to mu-opioid and other opioid receptors may be of clinical relevance in opiate tolerance, dependence, and abstinence syndrome.
BUSQUETS X, ESCRIBA PV, SASTRE M, et al., 1994, CHRONIC HEROIN/MORPHINE ADMINISTRATION DECREASES PROTEIN-KINASE-C IMMUNOREACTIVITY IN THE HUMAN AND RAT-BRAIN, BRITISH JOURNAL OF PHARMACOLOGY, Vol: 112, Pages: U171-U171, ISSN: 0007-1188
ESCRIBA PV, SASTRE M, GARCIASEVILLA JA, 1994, HEXAMETHYLENE BISACETAMIDE INDUCES THE DISSOCIATION OF G-PROTEINS AND PROTEIN-KINASE-C FROM THE PLASMA-MEMBRANE, BIOPHYSICAL JOURNAL, Vol: 66, Pages: A29-A29, ISSN: 0006-3495
Sastre M, Garcia-Sevilla JA, 1994, Density of alpha-2A adrenoceptors and Gi proteins in the human brain: Ratio of high affinity sites to antagonist sites and effect of age, J. Pharmacol. Exp. Ther., Vol: 669, Pages: 1062-1072
Sastre M, García-Sevilla JA, 1993, Opposite age-dependent changes of alpha 2A-adrenoceptors and nonadrenoceptor [3H]idazoxan binding sites (I2-imidazoline sites) in the human brain: strong correlation of I2 with monoamine oxidase-B sites., J Neurochem, Vol: 61, Pages: 881-889, ISSN: 0022-3042
In the postmortem human brain (27 specimens of frontal cortex, Brodmann area 9), the specific binding of the antagonists [3H]RX 821002 (2-methoxyidazoxan) to alpha 2A-adrenoceptors and that of [3H]idazoxan to I2-imidazoline sites (a nonadrenoceptor mitochondrial site) were determined in parallel to study the effect of aging (range, 4-89 years) on both brain proteins. The density of alpha 2A-adrenoceptors and age were negatively correlated (r = -0.71; p < 0.001). In contrast, the density of I2-imidazoline sites was positively correlated with aging (r = 0.59; p < 0.005). The ratio of receptor densities (alpha 2A/I2) also showed a marked negative correlation with age (r = -0.76; p < 0.001). In an age-selected group (range, 10-89 years), the density of monoamine oxidase (MAO)-B sites labeled by [3H]Ro 19-6327 (lazabemide) also showed a positive correlation with age (r = 0.80; p < 0.005). In these subjects, the density of I2-imidazoline sites correlated well with the density of MAO-B sites (r = 0.70; p < 0.005). The ratio of the density of these sites (MAO-B/I2) did not correlate with the age of the subject at death (r = -0.15). In the human frontal cortex, idazoxan displayed very low affinity (Ki = 89 microM) against the binding of [3H]Ro 19-6327 to MAO-B, which discounted a direct interaction of [3H]idazoxan with the active center of the enzyme and indicated that the I2-imidazoline site cannot be identified with MAO-B.(ABSTRACT TRUNCATED AT 250 WORDS)
ESCRIBA PV, SASTRE M, GARCIASEVILLA JA, 1993, INCREASED DENSITY OF GUANINE NUCLEOTIDE-BINDING (G) PROTEINS IN THE FRONTAL-CORTEX OF HEROIN-ADDICTS, BRITISH JOURNAL OF PHARMACOLOGY, Vol: 108, Pages: P30-P30, ISSN: 0007-1188
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- Citations: 1
Miralles A, Olmos G, Sastre M, et al., 1993, Discrimination and pharmacological characterization of I2-imidazoline sites with [3H]idazoxan and alpha-2 adrenoceptors with [3H]RX821002 (2-methoxy idazoxan) in the human and rat brains., J Pharmacol Exp Ther, Vol: 264, Pages: 1187-1197, ISSN: 0022-3565
The alpha-2 adrenoceptor antagonist idazoxan has been shown to also recognize with high affinity nonadrenoceptor sites (I2-imidazoline sites). In contrast, the 2-methoxy derivative of idazoxan, 2-methoxy idazoxan (RX821002), binds almost exclusively to alpha-2 adrenoceptors. The purpose of this study was to assess and extend the pharmacological characterization of I2-imidazoline sites and alpha-2 adrenoceptors in the human and rat brains. Competition studies with several imidazoli(di)ne/guanidine drugs and other nonrelated structures were performed in cortical membranes against [3H]idazoxan (4 nM in the presence of 10(-6) M I-epinephrine to prevent binding to alpha-2 adrenoceptors) or [3H]RX821002 (1 nM). Drugs such as cirazoline, guanoxan, naphazoline, tolazoline, clonidine, bromoxidine (UK 14,304) and phenylbiguanide displaced [3H]idazoxan from two distinct binding sites, which suggested the existence of two affinity states for I2-imidazoline sites that were not modulated by MgCl2 or the nucleotide analog guanylyl-5'-imido-diphosphate. Binding affinities at the low-affinity site (KiL) were consistently more than 2 orders of magnitude lower than binding affinities at the high-affinity site (KiH), and there was a good correlation between KiH and KiL values for a given drug in the human (r = 0.89) and rat (r = 0.92) brains. For 18 to 22 drugs, the Ki values in the human brain correlated well with the corresponding Ki values in the rat brain both for I2-imidazoline sites (r = 0.94) and alpha-2 adrenoceptors (r = 0.97). However, the Ki values for I2-imidazoline sites did not correlate with the Ki values for alpha-2 adrenoceptors in human and rat brains. The order of drug potency for the I2-imidazoline sites was: guanoxan (1.3 nM) approximately cirazoline > idazoxan approximately naphazoline > clonidine > phentolamine > RX821002 > (8aR, 12aS, 13aS)-3-methoxy-12-methanesulfonyl-5,6,8a,9,10,11,12,12a,13,13a- decahydro-8H-isoquino[2,1-g]-naphthyridine (RS 15
Sastre M, Garcia-Sevilla JA, 1993, Opposite age-dependent changes of α2-adrenoceptors and non-adrenoceptor [3H]idazoxan binding sites (I2-imidazoline sites) in the human brain: coexpression of I2-sites with MAO-B, J. Neurochem., Vol: 61, Pages: 881-889
Klotz LH, Sastre M, Freihoff D, et al., Noradrenaline upregulates the anti-inflammatory peroxisome proliferator-activated receptor gamma, NEUROBIOLOGY OF AGING, Vol: 23, Pages: S228-S228, ISSN: 0197-4580
Sastre M, Freihoff D, Klockgether T, et al., Role of NSAIDs and peroxisome proliferator-activated receptor γ-agonists on APP processing, NEUROBIOLOGY OF AGING, Vol: 23, Pages: S223-S224, ISSN: 0197-4580
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- Citations: 1
Freihoff D, Dumitrescu-Ozimek L, Sastre M, et al., Identification and characterisation of Alzheimer-like inflammatory changes in APP (V7171) transgenic mice, NEUROBIOLOGY OF AGING, Vol: 23, Pages: S224-S224, ISSN: 0197-4580
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