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6. Hyccin, the Molecule Mutated in the Leukodystrophy Hypomyelination and Congenital Cataract (HCC), Is a Neuronal Protein.

Author

Gazzerro, Elisabetta, Baldassari, Simona, Giacomini, Caterina, Musante, Veronica, Fruscione, Floriana, La Padula, Veronica, Biancheri, Roberta, Scarfì, Sonia, Prada, Valeria, Sotgia, Federica, Duncan, Ian D, Zara, Federico, Werner, Hauke B, Lisanti, Michael P, Nobbio, Lucilla, Corradi, Anna, Minetti, Carlo, Gazzerro, Elisabetta, Baldassari, Simona, Giacomini, Caterina, Musante, Veronica, Fruscione, Floriana, La Padula, Veronica, Biancheri, Roberta, Scarfì, Sonia, Prada, Valeria, Sotgia, Federica, Duncan, Ian D, Zara, Federico, Werner, Hauke B, Lisanti, Michael P, Nobbio, Lucilla, Corradi, Anna, and Minetti, Carlo

Abstract

"Hypomyelination and Congenital Cataract", HCC (MIM #610532), is an autosomal recessive disorder characterized by congenital cataract and diffuse cerebral and peripheral hypomyelination. HCC is caused by deficiency of Hyccin, a protein whose biological role has not been clarified yet. Since the identification of the cell types expressing a protein of unknown function can contribute to define the physiological context in which the molecule is explicating its function, we analyzed the pattern of Hyccin expression in the central and peripheral nervous system (CNS and PNS). Using heterozygous mice expressing the b-galactosidase (LacZ) gene under control of the Hyccin gene regulatory elements, we show that the gene is primarily expressed in neuronal cells. Indeed, Hyccin-LacZ signal was identified in CA1 hippocampal pyramidal neurons, olfactory bulb, and cortical pyramidal neurons, while it did not colocalize with oligodendroglial or astrocytic markers. In the PNS, Hyccin was detectable only in axons isolated from newborn mice. In the brain, Hyccin transcript levels were higher in early postnatal development (postnatal days 2 and 10) and then declined in adult mice. In a model of active myelinogenesis, organotypic cultures of rat Schwann cells (SC)/Dorsal Root Ganglion (DRG) sensory neurons, Hyccin was detected along the neurites, while it was absent from SC. Intriguingly, the abundance of the molecule was upregulated at postnatal days 10 and 15, in the initial steps of myelinogenesis and then declined at 30 days when the process is complete. As Hyccin is primarily expressed in neurons and its mutation leads to hypomyelination in human patients, we suggest that the protein is involved in neuron-to-glia signalling to initiate or maintain myelination.

Published
2012

7. Hyccin, the Molecule Mutated in the Leukodystrophy Hypomyelination and Congenital Cataract (HCC), Is a Neuronal Protein

Author

Gazzerro, Elisabetta, primary, Baldassari, Simona, additional, Giacomini, Caterina, additional, Musante, Veronica, additional, Fruscione, Floriana, additional, La Padula, Veronica, additional, Biancheri, Roberta, additional, Scarfì, Sonia, additional, Prada, Valeria, additional, Sotgia, Federica, additional, Duncan, Ian D., additional, Zara, Federico, additional, Werner, Hauke B., additional, Lisanti, Michael P., additional, Nobbio, Lucilla, additional, Corradi, Anna, additional, and Minetti, Carlo, additional

Published
2012
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9. RANTES Modulates the Release of Glutamate in Human Neocortex.

Author

Musante, Veronica, Longordo, Fabio, Neri, Elisa, Pedrazzi, Marco, Kalfas, Fotios, Severi, Paolo, Raiteri, Maurizio, and Pittaluga, Anna

Subjects
*CHEMOKINES, *GLUTAMIC acid, *G proteins, *PHOSPHORYLATION, *EXOCYTOSIS, *IMMUNOGLOBULINS
Abstract

The effects of the recombinant chemokine human RANTES (hRANTES) on the release of glutamate from human neocortex glutamatergic nerve endings were investigated. hRANTES facilitated the spontaneous release of d [³H]D-aspartate ([³H]D-ASP) by binding Pertussis toxin-sensitive G-protein-coupled receptors (GPCRs), whose activation caused Ca2+ mobilization from inositol trisphosphate-sensitive stores and cytosolic tyrosine kinase-mediated phosphorylations. Facilitation of release switched to inhibition when the effects of hRANTES on the 12mMK+-evoked [³H]D-ASP exocytosis were studied. Inhibition of exocytosis relied on activation of Pertussis toxin-sensitive GPCRs negatively coupled to adenylyl cyclase. Both hRANTES effects were prevented by met-RANTES, an antagonist at the chemokine receptors (CCRs) of the CCR1, CCR3, and CCR5 subtypes. Interestingly,humanneocortex glutamatergic nerve endings seem to possess all three receptor subtypes. Blockade of CCR1 and CCR5 by antibodies against the extracellular domain of CCRs prevented both the hRANTES effect on [ 3H]D-ASP release, whereas blockade of CCR3 prevented inhibition, but not facilitation, of release. The effects ofRANTESon the spontaneous and the evoked release of [³H]D-ASP were also observed in experiments with mouse cortical synaptosomes, which may therefore represent an appropriate animal model to study RANTES-induced effects on neurotransmission. It is concluded that glutamate transmission can be modulated in opposite directions by RANTES acting at distinct CCR receptor subtypes coupled to different transduction pathways, consistent with the multiple and sometimes contrasting effects of the chemokine. [ABSTRACT FROM AUTHOR]

Published
2008
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