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M Buttini

Publications and source records attributed to M Buttini.

24 records · Page 2Linked to original sources
PubMed1995

Cloning of rat interleukin-3 receptor beta-subunit from cultured microglia and its mRNA expression in vivo.

The high-affinity receptors for interleukin-3 (IL-3), GM-CSF, and IL-5 are composed of a ligand binding (alpha-) and a transducing (beta-) subunit. Two distinct transducing subunits (clones AIC2A and AIC2B) have been cloned from mouse, whereas in humans, only one (common) beta-subunit (beta c) has been found. A PCR-based cloning strategy was used to obtain a full-length cDNA sequence from rat microglia including 5'-untranslated regions. Sequence analysis revealed a number of features indicative of the presence of only one beta-subunit in the rat. Most likely, the new rIL-3R beta cDNA is the rat equivalent of human respective murine (AIC2B) beta c subunits. Regulation of rIL-3R beta mRNA expression was investigated in cultured microglia and in vivo. Purified microglia expressed significant amounts of rIL-3R beta mRNA. Addition of lipopolysaccharide (LPS) resulted in a marked upregulation of rIL-3R beta mRNA within approximately 4 hr. No downregulation was observed within 1 week's treatment. No rIL-3R beta mRNA was detectable in normal rat brain. However, 3 hr after a single injection of LPS into the tail vein of a rat, a marked induction of receptor mRNA occurred in a variety of brain regions. Transcriptional rates subsided significantly after 24 hr. rIL-3R beta mRNA was visualized by in situ hybridizations with cRNA antisense probes in ramified cells formerly characterized as microglial cells. rIL-3R beta mRNA was also induced in rat brain after occlusion of middle cerebral artery (MCAO).(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗
PubMed1994

Induction of interleukin-1 beta mRNA after focal cerebral ischaemia in the rat.

The expression of interleukin-1 beta (IL-1 beta) mRNA in the brain in response to cerebral ischaemia in rats was examined using in situ hybridization histochemistry. Focal cerebral ischaemia was induced in spontaneously hypertensive rats by permanent occlusion of the left middle cerebral artery (MCAO). Whereas no IL-1 beta mRNA could be detected in non-operated and sham-operated rats, middle cerebral artery occlusion induced the expression of IL-1 beta mRNA within 15 min in the ischaemic brain regions prone to become necrotic after 1-2 days. The message appeared as spot-like signals, reached a peak after 3 h and then declined to undetectable levels within 4 days. Additionally, a pronounced but brief induction of IL-1 beta mRNA could be detected 1 h after MCAO in the meninges near the watershed zone. The results demonstrate that the inflammatory cytokine IL-1 beta is induced in a time-dependent way after brain ischaemia.

Animals↗
PubMed1993

Differential distribution of calcineurin A alpha isoenzyme mRNA's in rat brain.

Specific antisense oligonucleotide probes for the alpha isoforms of the catalytic subunit (A-subunit) of calcineurin were prepared and the distribution of A alpha 1 and A alpha 2 mRNA's has been studied in rat brain using in situ hybridization histochemistry. Clear regional differences have been observed for the A alpha 1 and A alpha 2 isoforms. The predominant form, A alpha 1, was found to be preferentially expressed in the caudate putamen, the pyramidal cell layer of the hippocampus, specific cortical cell layers, the cerebellar granular cell layer and some other brain areas. On the other hand, the A alpha 2 isoform, although being generally less abundant than A alpha 1, gave an intense autoradiography signal in the dentate gyrus of the hippocampus and was the major transcript in the amygdala, the superior and the inferior colliculus, the central gray matter and the reticular formation. These regional differences might reflect specific functions exerted by the two alternatively spliced isoenzymes in the CNS and opens the perspective of interfering with defined calcineurin-dependent signal transduction pathways using isoform-specific compounds.

Animals↗
PubMed1992

M1 muscarinic receptors mediate intracellular calcium release in NB-OK1 human neuroblastoma cells.

Muscarine acetylcholine receptors were characterized in NB-OK1 cells using radioligand (3H-NMS) binding experiments and second messenger (calcium and phosphatidylinositol (PI) turnover) studies. In radioligand binding experiments the displacement curves of pirenzepine (KI = 1.3 x 10(-8) M), AF-DX 116 (KI = 8.2 x 10(-7) M), methoctramine (KI = 8.4 x 10(-8) M) and parafluorohexahydrosiladifenidol (pF-HHSiD) (KI = 1.8 x 10(-8) M) were monophasic and indicated the presence of M1 muscarinic receptors. Schild analysis with the muscarinic antagonists pirenzepine, AF-DX 116, methoctramine and pF-HHSiD yielded pA2 values of 8.40 +/- 0.13, 6.48 +/- 0.09, 7.61 +/- 0.12 and 7.22 +/- 0.08 in the calcium experiments and pA2 values of 8.13 +/- 0.30 and 6.26 +/- 0.26, 7.65 +/- 0.16 and 7.46 +/- 0.11, respectively, in the PI turnover experiments. These results indicate that both the carbachol-induced increase in intracellular calcium and the increase in PI turnover are mediated by M1 muscarinic receptors. In calcium free buffer, stimulation with carbachol induced similar responses to those seen under control conditions. From functional and radioligand binding experiments we conclude that the muscarinic receptor expressed in NB-OK1 cells is the M1 subtype. In addition, the M1 receptor-induced calcium response is related to PI turnover and is independent on extracellular calcium.

Calcium↗
PubMed1991

Pharmacological properties of cloned muscarinic receptors expressed in A9 L cells; comparison with in vitro models.

The effects of a series of muscarinic agonists and antagonists at cloned m1 and m3 muscarinic receptors expressed in mouse fibroblast A9 L cells have been compared with their effects in in vitro models of M1 (rat superior cervical ganglion) and M3 (guinea-pig ileum) muscarinic receptors. A good correlation existed between the potencies of muscarinic agonists at cloned m1 muscarinic receptors and the M1 sites in rat ganglion (r = 0.80) as well as at cloned m3 receptors and guinea-pig ileum M3 receptors (r = 0.87). However, cross correlations of potencies in rat ganglion and cloned m3 receptors as well as in guinea-pig ileum and in cloned m1 receptors also yielded relatively high correlation coefficients (0.71 and 0.91, respectively). Low correlation coefficients were found for the maximal responses of muscarinic agonists in rat ganglion and cloned m1 receptors (0.53) and in guinea-pig ileum and cloned m3 receptors (0.36). A high correlation between pA2 values of muscarinic antagonists at cloned m1 receptors and in rat ganglion (r = 0.97) and between cloned m3 receptors and guinea-pig ileum (r = 0.98) was found. Cross correlation of pA2 values in rat ganglion and cloned m3 receptors and in guinea-pig ileum and cloned m1 receptors yielded correlation coefficients of 0.82 and 0.72, respectively. The data indicate that the cloned muscarinic receptor sites seem similar to the corresponding endogenous sites. The good correlations in corresponding but also non-corresponding receptor models reflect the relatively low selectivity of the majority of the compounds investigated.

Animals↗