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Oh, Jun-Young,Rhee, Sangmyung,Silva, Alcino J.,Lee, Yong-Seok,Kim, Hyong Kyu Elsevier 2017 Neuroscience Letters Vol.649 No.-
<P><B>Abstract</B></P> <P>Glutamate is the major excitatory neurotransmitter in the central nervous system, and related signaling involves both AMPA and NMDA subtype receptors. The expression of glutamate receptors is dynamically regulated during development. Recent studies showed that the dysregulation of glutamate receptor expression and function is associated with neurodevelopmental disorders including intellectual disability. Previously, a Noonan syndrome (NS)-associated SHP2 mutation (SHP2<SUP>D61G</SUP>) was shown to increase the synaptic delivery of AMPA receptor, subsequently impairing synaptic plasticity and learning in adult mice. However, how the mutant SHP2 affects glutamate receptor expression during development is not known. Here, we found that the SHP2<SUP>D61G</SUP> differentially regulates the expression of AMPA and NMDA receptors depending on the stage of neuronal maturation. In cultured neurons (immature stage; DIV 6), overexpression of SHP2<SUP>D61G</SUP> significantly increased the average size and the number of NMDA receptor-containing particles, but not those with AMPA receptors. In early matured neurons (DIV 12), SHP2<SUP>D61G</SUP> significantly increased only the average size of AMPA receptor particles, and subsequently increased their number in matured neurons (DIV 18). Importantly, all the changes described above for SHP2<SUP>D61G</SUP> neurons were reversed by inhibiting MAPK. These data demonstrate that the increased activation of MAPK signaling pathway by SHP2<SUP>D61G</SUP> could deregulate the surface expression of synaptic receptors during neuronal development, which likely contributes to cognitive impairments in NS patients.</P> <P><B>Highlights</B></P> <P> <UL> <LI> A Noonan syndrome-associated mutation in SHP2 increases NMDA receptor expression in premature neurons. </LI> <LI> This mutation increases the size of AMPA receptor clusters in early maturing neurons. </LI> <LI> The SHP2 mutation also increases both the size and the number of AMPA receptor clusters in mature neurons. </LI> <LI> The altered expressions of glutamate receptors by mutant SHP2 can be reversed by inhibiting the MAPK signaling pathway. </LI> </UL> </P>
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Solitary peripheral osteomas of the jaws
Franca, Talita Ribeiro Tenorio De,Gueiros, Luiz Alcino Monteiro,Castro, Jurema Freire Lisboa De,Catunda, Ivson,Leao, Jair Carneiro,Perez, Danyel Elias Da Cruz Korean Academy of Oral and Maxillofacial Radiology 2012 Imaging Science in Dentistry Vol.42 No.2
Osteoma is a benign osteogenic tumor composed of cancellous or compact bone, classified as peripheral, central, or extraskeletal. Peripheral osteomas are uncommon. Excluding the maxillary sinuses, the maxilla is a rare site for osteomas. The purpose of this report was to describe clinicopathological and radiological features of two peripheral osteomas occurring in the jaws, one located in the mandible and another in the edentulous maxillary alveolar ridge. The tumors were asymptomatic and were fully excised without any complications or recurrence. The lesions were submitted to histopathological analysis and diagnosed as peripheral osteoma, compact type.
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Solitary peripheral osteomas of the jaws
Talita Ribeiro Tenório de França,Luiz Alcino Monteiro Gueiros,Jurema Freire Lisboa de Castro,Ivson Catunda,Jair Carneiro Leão,Danyel Elias da Cruz Perez 대한구강악안면방사선학회 2012 Imaging Science in Dentistry Vol.42 No.2
Osteoma is a benign osteogenic tumor composed of cancellous or compact bone, classified as peripheral, central, or extraskeletal. Peripheral osteomas are uncommon. Excluding the maxillary sinuses, the maxilla is a rare site for osteomas. The purpose of this report was to describe clinicopathological and radiological features of two peripheral osteomas occurring in the jaws, one located in the mandible and another in the edentulous maxillary alveolar ridge. The tumors were asymptomatic and were fully excised without any complications or recurrence. The lesions were submitted to histopathological analysis and diagnosed as peripheral osteoma, compact type.
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Excitatory neuron–specific SHP2-ERK signaling network regulates synaptic plasticity and memory
Ryu, Hyun-Hee,Kim, TaeHyun,Kim, Jung-Woong,Kang, Minkyung,Park, Pojeong,Kim, Yong Gyu,Kim, Hyopil,Ha, Jiyeon,Choi, Ja Eun,Lee, Jisu,Lim, Chae-Seok,Kim, Chul-Hong,Kim, Sang Jeong,Silva, Alcino J.,Kaang AAAS 2019 Science signaling Vol.12 No.571
<P><B>Cell type–specific RASopathy</B></P><P>The neurodevelopmental disorder Noonan syndrome is often caused by activating mutations in the phosphatase SHP2 that enhance RAS signaling. However, SHP2 is present in multiple neuron types as well as glia; thus, where the mutant protein has its pathological effects is unclear. Ryu <I>et al.</I> examined one NS-associated SHP2 mutation in isolated cell types from mice and determined that its presence in only excitatory neurons resulted in electrophysiological and cognitive effects. This was because certain adaptor proteins that interact with SHP2 to mediate RAS signaling are abundant in excitatory but not inhibitory neurons. These findings reveal that cell type–specific variations within the RAS signaling network underlie the phenotypes of NS and possibly other “RASopathies”.</P><P>Mutations in RAS signaling pathway components cause diverse neurodevelopmental disorders, collectively called RASopathies. Previous studies have suggested that dysregulation in RAS–extracellular signal–regulated kinase (ERK) activation is restricted to distinct cell types in different RASopathies. Some cases of Noonan syndrome (NS) are associated with gain-of-function mutations in the phosphatase SHP2 (encoded by <I>PTPN11</I>); however, SHP2 is abundant in multiple cell types, so it is unclear which cell type(s) contribute to NS phenotypes. Here, we found that expressing the NS-associated mutant SHP2<SUP>D61G</SUP> in excitatory, but not inhibitory, hippocampal neurons increased ERK signaling and impaired both long-term potentiation (LTP) and spatial memory in mice, although endogenous SHP2 was expressed in both neuronal types. Transcriptomic analyses revealed that the genes encoding SHP2-interacting proteins that are critical for ERK activation, such as GAB1 and GRB2, were enriched in excitatory neurons. Accordingly, expressing a dominant-negative mutant of GAB1, which reduced its interaction with SHP2<SUP>D61G</SUP>, selectively in excitatory neurons, reversed SHP2<SUP>D61G</SUP>-mediated deficits. Moreover, ectopic expression of GAB1 and GRB2 together with SHP2<SUP>D61G</SUP> in inhibitory neurons resulted in ERK activation. These results demonstrate that RAS-ERK signaling networks are notably different between excitatory and inhibitory neurons, accounting for the cell type–specific pathophysiology of NS and perhaps other RASopathies.</P>
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