Regulation of Nogo and Nogo receptor during the development of the entorhino-hippocampal pathway and after adult hippocampal lesions

Mingorance, Ana; Fontana, Xavier; Solé, Marta Sanz; Burgaya, Ferràn; Ureña, Jesús; Teng, Felicia Yu Hsuan; Tang, Bor Luen; Hunt, David; Anderson, Patrick N.; Bethea, John R.; Schwab, Martin E.; Soriano, Eduardo; Rı́o, José Antonio del

doi:10.1016/j.mcn.2004.01.001

Cited by 97 publications

(81 citation statements)

References 69 publications

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“…The changes in Nogo-A observed in the present study are in contrast to the relatively minor changes observed in models of experimental spinal cord injury (SCI; Josephson et al, 2001;Huber et al, 2002;Hunt et al, 2002bHunt et al, , 2003Wang et al, 2002b). However, in other models of CNS injury such as hippocampal deafferentation, global ischemia and kainic acid lesions, a marked increase of Nogo-A mRNA was observed (Zhou et al, 2003;Meier et al, 2003;Mingorance et al, 2004). These reports indicate that the expression of Nogo-A is not generally injury-induced and imply a role for Nogo-A in some, but not all, CNS injury models.…”

Section: Discussioncontrasting

confidence: 77%

“…Although the expression of Nogo-A in neurons under normal conditions has previously been described (Grandpre et al, 2000;Josephson et al, 2001;Huber et al, 2002;Hunt et al, 2002b;Liu et al, 2002b;Wang et al, 2002b;Jin et al, 2003;Mingorance et al, 2004), the function of neuronal Nogo-A remains unclear. However, as a member of the reticulon family of genes (Oertle and Schwab, 2003), Nogo (RTN-4) has been suggested to play a role in cellular physiology and protein trafficking (van de Velde et al, 1994;Grandpre et al, 2000;Teng et al, 2004).…”

Section: Discussionmentioning

confidence: 97%

“…In a subset of animals, a focal increase of NgR expression in the external capsule was observed, that may be caused by impaired axonal transport with accumulation of NgR at the site of axonal injury or an upregulation of NgR in these animals. NgR has been reported to be upregulated early following deafferentiation injury to the hippocampus or global cerebral ischemia (Zhou et al, 2003;Meier et al, 2003;Mingorance et al, 2004). The importance of increased NgR in CNS injury remains to be established, although preserved or increased NgR expression in ipsilateral white matter tracts combined with increased Nogo-A levels may cause further inhibition of axonal regeneration or sprouting following CNS injury (Grandpre et al, 2002;Li and Strittmatter, 2003).…”

Section: Discussionmentioning

confidence: 99%

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Selective temporal and regional alterations of Nogo-A and small proline-rich repeat protein 1A (SPRR1A) but not Nogo-66 receptor (NgR) occur following traumatic brain injury in the rat

Marklund

Fulp

Shimizu

et al. 2006

Experimental Neurology

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Axons show a poor regenerative capacity following traumatic central nervous system (CNS) injury, partly due to the expression of inhibitors of axonal outgrowth, of which Nogo-A is considered the most important. We evaluated the acute expression of Nogo-A, the Nogo-66 receptor (NgR) and the novel small proline-rich repeat protein 1A (SPRR1A, previously undetected in brain), following experimental lateral fluid percussion (FP) brain injury in rats. Immunofluorescence with antibodies against Nogo-A, NgR and SPRR1A was combined with antibodies against the neuronal markers NeuN and microtubule-associated protein (MAP)-2 and the oligodendrocyte marker RIP, while Western blot analysis was performed for Nogo-A and NgR. Brain injury produced a significant increase in Nogo-A expression in injured cortex, ipsilateral external capsule and reticular thalamus from days 1-7 post-injury (P < 0.05) compared to controls. Increased expression of Nogo-A was observed in both RIP-and NeuN positive (+) cells in the ipsilateral cortex, in NeuN (+) cells in the CA3 region of the hippocampus and reticular thalamus and in RIP (+) cells in white matter tracts. Alterations in NgR expression were not observed following traumatic brain injury (TBI). Brain injury increased the extent of SPRR1A expression in the ipsilateral cortex and the CA3 at all post-injury time-points in NeuN (+) cells. The marked increases in Nogo-A and SPRR1A in several important brain regions suggest that although inhibitors of axonal growth may be upregulated, the injured brain is also capable of expressing proteins promoting axonal outgrowth following TBI. KeywordsNogo-A; Nogo-66 receptor; Small proline-rich repeat protein 1A (SPRR1A); Traumatic brain injury; Oligodendrocytes

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Section: Discussioncontrasting

confidence: 77%

Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 99%

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Selective temporal and regional alterations of Nogo-A and small proline-rich repeat protein 1A (SPRR1A) but not Nogo-66 receptor (NgR) occur following traumatic brain injury in the rat

Marklund

Fulp

Shimizu

et al. 2006

Experimental Neurology

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“…In human, increased immunoreactivity of NogoA-positive hippocampal neurons was observed in Alzheimer disease [9] and temporal lobe epilepsy [3]. The increase was also present in the experimental models of brain diseases including epilepsy [28,41] or brain injury [26,28,30].…”

Section: Introductionmentioning

confidence: 89%

“…NogoA is mainly expressed by oligodendrocytes in the adult CNS, but several brain regions containing NogoA-expressing neurons were also identified [12]. It is generally believed that NogoA expression in adult brain is characteristic for plastic CNS regions like cortex, dorsal root ganglia and of course hippocampus [28,30,34]. In human, increased immunoreactivity of NogoA-positive hippocampal neurons was observed in Alzheimer disease [9] and temporal lobe epilepsy [3].…”

Section: Introductionmentioning

confidence: 99%

Minocycline but not valproic acid influence the density of NogoA-immunoreactive neurons in the hilus of the dentate gyrus of the rats subjected to intracerebral haematoma

et al. 2014

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Association study of Nogo‐related genes with schizophrenia in a Japanese case–control sample

Jitoku

Hattori

Iwayama

et al. 2011

American J of Med Genetics Pt B

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Many studies have suggested that myelin dysfunction may be causally involved in the pathogenesis of schizophrenia. Nogo (RTN4), myelin-associated glycoprotein (MAG) and oligodendrocyte myelin glycoprotein (OMG) all bind to the common receptor, Nogo-66 receptor 1 (RTN4R). We examined 68 single nucleotide polymorphisms (SNPs) (51 with genotyping and 17 with imputation analysis) from these four genes for genetic association with schizophrenia, using a 2,120 case-control sample from the Japanese population. Allelic tests showed nominally significant association of two RTN4 SNPs (P = 0.047 and 0.037 for rs11894868 and rs2968804, respectively) and two MAG SNPs (P = 0.034 and 0.029 for rs7249617 and rs16970218, respectively) with schizophrenia. The MAG SNP rs7249617 also showed nominal significance in a genotypic test (P = 0.017). In haplotype analysis, the MAG haplotype block including rs7249617 and rs16970218 showed nominal significance (P = 0.008). These associations did not remain significant after correction for multiple testing, possibly due to their small genetic effect. In the imputation analysis of RTN4, the untyped SNP rs2972090 showed nominally significant association (P = 0.032) and several imputed SNPs showed marginal associations. Moreover, in silico analysis (PolyPhen) of a missense variant (rs11677099: Asp357Val), which is in strong linkage disequilibrium with rs11894868, predicted a deleterious effect on Nogo protein function. Despite a failure to detect robust associations in this Japanese cohort, our nominally positive signals, taken together with previously reported biological and genetic findings, add further support to the "disturbed myelin system theory of schizophrenia" across different populations.

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Regulation of Nogo and Nogo receptor during the development of the entorhino-hippocampal pathway and after adult hippocampal lesions

Cited by 97 publications

References 69 publications

Selective temporal and regional alterations of Nogo-A and small proline-rich repeat protein 1A (SPRR1A) but not Nogo-66 receptor (NgR) occur following traumatic brain injury in the rat

Selective temporal and regional alterations of Nogo-A and small proline-rich repeat protein 1A (SPRR1A) but not Nogo-66 receptor (NgR) occur following traumatic brain injury in the rat

Minocycline but not valproic acid influence the density of NogoA-immunoreactive neurons in the hilus of the dentate gyrus of the rats subjected to intracerebral haematoma

Association study of Nogo‐related genes with schizophrenia in a Japanese case–control sample

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