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Biomedical subjects

P Galli

Publications and source records attributed to P Galli.

At least 19 recordsLinked to original sources
PubMed1999

Factor(s) from nonmacrophage bone marrow stromal cells inhibit Lewis lung carcinoma and B16 melanoma growth in mice.

Bone marrow stroma produces positive and negative growth regulators which constitute the hematopoietic microenvironment. As many tumors metastasize to the bones, these regulators may also influence tumor growth. Hematopoietic cytokines may indeed exert both positive and negative effect on tumor growth. We report that, when mixed with tumor cells. adherent bone marrow cells inhibit primary tumor growth and metastases formation in mice transplanted with Lewis lung carcinoma or B16 melanoma. Peritoneal macrophages or lymph node cells did not exert any influence. The tumor inhibition was apparently due to soluble factor(s) released by marrow stromal cells. In cocultures with B16 melanoma cells, adherent bone marrow cells exerted a significant antiproliferative effect which was increased by previous culture of the bone marrow cells with granulocyte-macrophage colony-stimulating factor but not with macrophage colony-stimulating factor. Neither neutralizing antibodies against tumor necrosis factor-alpha, transforming growth factor-beta or interferon alpha/beta nor addition of Escherichia coli lipopolysaccharide to generate inflammatory cytokines could affect the antiproliferative effect of bone marrow stromal cells. The bone marrow stroma factor(s) which inhibit tumor growth might, therefore, be a novel growth regulator.

Animals↗
PubMed1998

Heavy metals concentrations in acanthocephalans parasites compared to their fish host.

A number of authors have demonstrated that heavy metal concentrations in intestinal Helminths are higher than those found in the tissues of their final hosts. In this work, Pb and Cr concentrations in the Acanthocephalan Acanthocephalus anguillae were measured by means of electrothermal atomic absorption spectrometry. The metal concentrations measured in the whole body of Acanthocephalans were compared to those in the liver of their fish hosts (Leuciscus cephalus) sampled in the Lambro river (Northern Italy). The results show higher concentrations of Pb and Cr in the parasites, respectively approximately 200 times and approximately 60 times higher than that of the host liver. These results corroborate the usefulness of parasites in the monitoring of biologically available metal concentrations in aquatic ecosystems that are non severely polluted.

Acanthocephala↗
PubMed1998

Populations of acanthocephalus anguillaePomphorhynchus laevis in rivers with different pollution levels

The distribution of two acanthocephalan species (Pomphorhynchus laevisAcanthocephalus anguillae) in the chub (Leuciscus cephalus) was studied in four river reaches characterized by different levels of pollution: the River Ticino near Abbiategrasso (unpolluted), the Naviglio Grande Canal, in Milano (slightly polluted), the River Lambro near Merone village (polluted) and the River Lambro near Monza (severely polluted).Pomphorhynchus laevis was restricted to the unpolluted and the slightly polluted sites, while the intensity of A. anguillae increased proportionally to water pollution. These differences were partially explained by the variation in abundance of their intermediate hosts (Echinogammarus stammeri for P. laevisAsellus aquaticus for A. anguillae). Data on the occurrence of P. laevis and A. anguillae showed a significant negative binomial frequency distribution, suggesting their tendency to be aggregated within the host populations of L. cephalus.

Journal Article↗
PubMed1997

Priming of cultured neurons with sabeluzole results in long-lasting inhibition of neurotoxin-induced tau expression and cell death.

Sabeluzole was described to have antiischemic, antiepileptic, and cognitive-enhancing properties, and is currently under development for Alzheimer's disease. Recently, it was reported that repeated treatments with sabeluzole protect cultured rat hippocampal neurons against NMDA- and glutamate-induced neurotoxicity. We evaluated the possibility that sabeluzole elicits neuroprotection by acting, either directly or indirectly, on tau proteins. We found that repeated treatments during development of primary cultures of cerebellar granule cells with nanomolar concentrations of sabeluzole resulted in mature cells that were resistant to the excitotoxicity induced by glutamate. Also, sabeluzole treatment specifically prevented the glutamate-induced increase of tau expression without modifying the basal pattern of expression of tau proteins, as shown by measurement of mRNA and protein levels. In human neuroblastoma cell line SH-SY5Y, differentiated by treatment with retinoic acid, doxorubicin increased tau immunoreactivity, and later induced cell death. Both effects were prevented by sabeluzole. Our data indicate that increased tau expression is a common response to different types of cells to neurotoxic agents, and that sabeluzole-induced neuroprotection is functionally associated with the prevention of the injury-mediated increase of tau expression.

Animals↗
PubMed1997

Effects of epidermal growth factor on the [3H]-thymidine uptake in the SK-N-SH and SH-SY5Y human neuroblastoma cell lines.

The studies on the factors that regulate the biology of the neuroblastoma cell lines may offer important information on the development of tissues and organs that derive from the neural crest. In the present paper we study the action of epidermal growth factor (EGF) on two human neuroblastoma cell lines: SK-N-SH which is composed at least of two cellular phenotypes (neuroblastic and melanocytic/glial cells), and its pure neuroblastic subclone SH-SY5Y. The results show that EGF (10 ng/ml) significantly stimulates the incorporation of [3H]-thymidine in the SK-N-SH cells only in the presence of fetal bovine serum (FBS) (control = 58,285 +/- 9327 cpm; EGF = 75,523 +/- 4457, p < 0.05). Such effect is not observed in the presence of a chemical defined medium, that is, in the absence of FBS (control = 100,997 +/- 4375; EGF = 95,268 +/- 4683; NS) In the SH-SY5Y cells the EGF does not modify the incorporation of [3H]-thymidine either in the presence of 10% of BFS (control = 113,838 +/- 6978; EGF = 119,434 +/- 9441; NS) or in its absence (control = 46,197 +/- 3335; EGF = 44,472 +/- 3493; NS). The results here reported suggest that: a) EGF may affect the proliferation of cells derived from a primary human neuroblastoma; b) this is evident by the EGF-induced increase of [3H]-thymidine incorporation in SK-N-SH cells; c) it is required the presence of other growth factors, present in the FBS, for the mitogenic action to be accomplished; d) since the pure neuroblastic SH-SY5Y cell line are refractory to the EGF, the effects observed in SK-N-SH cells probably occur on the melanocytic/glial cell subpopulation.

Epidermal Growth Factor↗
PubMed1996

Melatonin-induced T-helper cell hematopoietic cytokines resembling both interleukin-4 and dynorphin.

We have reported that melatonin exerts colony stimulating activity and rescues bone marrow cells from apoptosis induced either in vivo or in vitro by cancer chemotherapy compounds. We proposed that melatonin regulates interleukin-4 (IL-4) production in bone marrow T-helper cells and that IL-4 stimulates adherent stromal cells to produce colony stimulating factors (CSF). However, in further investigations we did not find any direct evidence of the ability of melatonin to stimulate IL4. We found that besides anti-IL4 monoclonal antibody (mAb), the opioid antagonist naltrexone also neutralized the colony stimulating activity and part of the hematopoietic protection exerted by melatonin. SDS-PAGE and immunoblotting analysis of supernatants of bone marrow T-helper cells incubated overnight with melatonin revealed the presence of two proteins with an apparent molecular weight of 15 and 67 kDa, which were recognized by both anti-common opioid sequence (Tyr-Gly-Gly-Phe) and anti-IL4 mAbs. When Abs against known opioid peptides were tested, only anti-dynorphin B Ab labeled the 67 kDa but not the 15 kDa protein. These melatonin-induced-opioids (MIO) were separated by gel filtration. The lower molecular weight MIO (MIO15) seems to mediate the naltrexone-sensitive hematopoietic effects of melatonin. Consistently, we found the presence of opioid receptors in adherent bone marrow cells. Apparently, the higher molecular weight protein, MIO67, was responsible for the naltrexone-insensitive part of the melatonin-induced hematopoietic rescue. These melatonin-induced T-helper cell products which resemble both IL-4 and dynorphin B might represent a new family of opioid peptides with hematopoietic and immune functions.

Animals↗
PubMed1996

Metabotropic and ionotropic transducers of glutamate signal inversely control cytoplasmic Ca2+ concentration and excitotoxicity in cultured cerebellar granule cells: pivotal role of protein kinase C.

We investigated the functional role of metabotropic glutamate receptors (mGluRs) in modulating glutamate-affected neuronal intracellular calcium concentration ([Ca2+]i) and cell viability in rat cerebellar granule cells. The mGluR agonist trans-1-amino-cyclopentane-1,3-dicarboxylic acid (tACPD) induced a transient increase in [Ca2+]i, which seemed to be developmentally regulated and maximal at 4 days in vitro. In addition, tACPD significantly prevented the [Ca2+]i rise produced by glutamate or by N-methyl-D-aspartate. The mGluR antagonists L-2-amino-3-phosphonopropionic and (+)-alpha-methyl-4-carboxyphenylglycine blocked the effects of tACPD but intrinsically, they magnified the glutamate-mediated [Ca2+]i elevation. The tACPD-mediated decrease in [Ca2+]i rise occurred under experimental conditions superimposable on those producing neuroprotection in glutamate-exposed cultures. tACPD affected neither [Ca2+]i elevation due to KCI nor that evoked by the calcium ionophore A 23187. The inhibitory effect of tACPD was also unaffected by K+ channel blockade produced by tetraethylammonium. The tACPD effects were fully mimicked by quisqualate and (RS)-3,5-dihydroxyphenylglycine, whereas they were only partially reproduced by (2S,1'S,2'S)-2-carboxycyclopropyl-glycine. L-2-Amino-4-phosphonobutyrate was inactive in preventing glutamate-mediated [Ca2+]i rise and neurotoxicity. The tACPD inhibitory responses seemed to be highly sensitive to protein kinase C blockade by bisindolylmaleimide or staurosporine, whereas they were weakly affected by the cAMP analogue dibutyryl cAMP. The protein kinase C activator 4beta-phorbol-12,13-dibutyrate reproduced mGluR-mediated inhibition of both glutamate-induced [Ca2+]i rise and neurotoxicity. In summary, these data suggest that activation of mGluR1-5 subtypes reduce glutamate-mediated (Ca2+]i rise through a mechanism involving protein kinase C activation. Such an effect results in neuroprotection.

Animals↗
PubMed1995

Inhibition of glutamate-induced neurotoxicity by a tau antisense oligonucleotide in primary culture of rat cerebellar granule cells.

Short-term exposure of primary cultures of cerebellar granule cells from neonatal rat brain to high concentrations of glutamate resulted in a significant increase of both immunoreactivity to and mRNA levels of tau protein. Time-course experiments revealed the increases of tau immunoreactivity and mRNA levels to be maximal 2 h after the glutamate pulse. To investigate the relationship between newly synthesized tau protein and glutamate-induced neurotoxicity, neurons were preincubated with a specific tau antisense oligonucleotide. This treatment resulted in (i) inhibition of the glutamate-induced increase of tau immunoreactivity and (ii) a decrease in the sensitivity of the neurons to neurotoxic concentrations of glutamate. These data indicate that induction of the cytoskeleton-associated tau protein participates in the cascade of events promoted by glutamate leading to neurodegeneration.

Animals↗
PubMed1995

Opposing regulation of amyloid precursor protein by ionotropic and metabotropic glutamate receptors.

The effects of the ionotropic glutamate receptor (iGluR) selective agonist N-methyl-D-aspartate (NMDA) on amyloid precursor protein (APP) levels were investigated in primary cultures of rat cerebellar granule cells. Both immunocytochemistry and immunoblotting techniques showed increased APP levels 4 h after a 15 min pulse with NMDA. This effect was completely prevented by incubating the neurones in the presence of the selective metabotropic GluR (mGluR) agonist 1S,3R-ACPD. This phenomenon was related, in terms of doses and time, with the observed 1S,3R-ACPD-mediated protection on NMDA-induced granule cell death. Our findings indicate that APP metabolism is differentially regulated by the stimulation of various GluR subtypes. The GluR-mediated changes in APP content might participate in the control of neuronal viability.

Amyloid beta-Protein Precursor↗
PubMed1994

Lack of vasoactive intestinal peptide-releasing property in prolactin cells from ovariectomized rats: contribution of post-transductional impairments.

We have demonstrated recently that in menopausal women and in ovariectomized rats the deficiency of circulating oestrogens impairs vasoactive intestinal peptide (VIP) efficacy in stimulating prolactin (PRL) release. The present study was designed to investigate whether the lack of VIP-induced PRL release after ovariectomy is a consequence of a defect at the receptor-transductional or post-transductional level. For this purpose we evaluated the VIP receptor function, by measuring VIP-stimulated cyclic adenosine monophosphate (AMP) formation, and the efficacy of the cyclic AMP-dependent PRL release in pituitary cells from control and ovariectomized animals. We observed that VIP induced a significantly higher stimulation of adenylate cyclase in pituitary homogenates from ovariectomized rats than in those from control animals. This effect appeared to be linked to an increased efficiency of the Gs coupling protein, because superimposable results were obtained by using the non-hydrolysable guanosine triphosphate (GTP) analogue, 5-guanylylimidodiphosphate. On the contrary, the cyclic AMP analogue, 8-Br-cAMP, that potently stimulated PRL release from control pituitary cells was completely ineffective in cells from ovariectomized rats. The present data indicate that in PRL-secreting cells from ovariectomized rats a defect in the post-transductional mechanism that couples the VIP receptor to PRL secretion, rather than a reduction of receptor function, possibly accounts for the lack of VIP efficacy.

Adenylyl Cyclases↗
PubMed1992

Metal uptake in neurone cultures: a systematic study.

We present the first comparative study of the uptake of metal ions by neurons, performed for Zn, Cr, Co, Mo, Al, Ni, Mn and Cd. The study reveals substantial differences in the uptake of different metals, under similar exposure procedures. In particular, we found very large uptakes for aluminium and molybdenum. We also found significant effects of excitatory substances, in particular kainate, as stimulants of uptake of some of the metals.

Animals↗
PubMed1989

Beta-adrenoceptor desensitization in a model of experimental asthma in guinea-pigs.

We investigated the possible occurrence of the desensitization of pulmonary beta-receptors in a model of experimental asthma such as the ovalbumin sensitized guinea-pig. Although some differences were observed between normal and asthmatic guinea-pigs, the desensitization procedure (isoproterenol (ISO) 10(-6) M x 20 min x 2) markedly impaired the relaxing capacity of ISO, epinephrine (EPI) and procaterol. With the beta 2 agonist procaterol, the sensitized tissues seemed to be more sensitive compared to normal. In parallel, the desensitization procedure produced a greater decrease in the relaxing capacity of procaterol in the sensitized tracheas. On the other hand, the two unselective beta-agonists (ISO and EPI) did not seem to discriminate between the two experimental conditions used. These data suggest that the immunological disturbance due to the active sensitization may induce a modification in beta-adrenoceptor reactivity. The results obtained with EPI after anaphylactic challenge are in agreement with this. In fact, the relaxing capacity of EPI was markedly reduced by antigen challenge.

Adrenergic beta-Agonists↗
PubMed1977

Adrenergic supersensitivity of the pupil in idiopathic headache.

In idiopathic headache (IH) sufferers, phenylephrine and fenfluramine induce a pupillary dilatation respectively greater and lesser than in controls. The difference may be due to a supersensitivity of the iris alpha adrenoceptors caused by a deficiency of noradrenaline in the iris adrenergic nerve terminal of the IH sufferer. These findings seem to support the hypothesis of a brain receptorial, monoamine supersensitivity in IH.

Adult↗