Contributions
Abstract: EP1459
Type: Poster Sessions
Abstract Category: Pathology and pathogenesis of MS - Experimental models
Background: Nerve Growth Factor (NGF) and its receptors, TrkA and p75NTR, are involved in the interplay of the nervous and immune system, especially in inflammatory conditions such as Multiple Sclerosis (MS) and its experimental model Experimental Autoimmune Encephalomyelitis.
Goals: The expression of TrkA, p75NTR and NGF in the spinal cord in EAE was investigated.
Methods: MOG-EAE mice were examined at three time-points (preclinical (D10), acute (D20) and chronic (D50)) compared to controls. The expression of TrkA, p75NTR and NGF were studied by RT-PCR, Western blotting and immunohistochemistry.
Results: Increased expression was observed of TrkA-mRNA at D20 (4.82-fold, p=0.0002) and D50 (4.25-fold, p= 0.0016), whereas p75NTR-mRNA and NGF-mRNA were up-regulated at D50 compared to D0 ((2.1-fold, p < 0.0001), (5.2-fold, p < 0.0001) respectively). At protein level, Western blotting of the spinal cord samples revealed an increase of TrkA, p75NTR and NGF at D20 and D50 (p < 0.0001). Increased expression of TrkA at D10 (p=0.048), D20 and D50 (p < 0.0001) was observed immunohistochemically in the white matter of spinal cord. p75NTR was increased at D20 and D50 (p< 0.0001). NGF in the white matter showed high expression at D20 and D50 compared to D0 (p< 0.0001). Ιn the grey matter, TrkA and p75NTR were increased at D20 (p < 0.0001, p= 0.0011 respectively). NGF was highly expressed at D20 and D50 compared to D0 (p< 0.0001, p=0.001, respectively).
Conclusions: The expression profile of NGF and its receptors, TrkA and p75NTR, in areas of inflammatory demyelination indicates their possible involvement in the underlying pathology and reorganization of degenerated spinal cord during the course of EAE.
Disclosure: Nickoleta Delivanoglou: Nothing to disclose
Olga Touloumi: Nothing to disclose
Roza Lagoudaki: Nothing to disclose
Evangelia Kesidou: Nothing to disclose
Paschalis Theotokis: Nothing to disclose
Evangelia Nousiopoulou: Nothing to disclose
Nikolina Dafi: Nothing to disclose
Marina Boziki: Nothing to disclose
Nikolaos Grigoriadis: Nothing to disclose
Ioannis Charalampopoulos: Nothing to disclose
Constantina Simeonidou: Nothing to disclose
Abstract: EP1459
Type: Poster Sessions
Abstract Category: Pathology and pathogenesis of MS - Experimental models
Background: Nerve Growth Factor (NGF) and its receptors, TrkA and p75NTR, are involved in the interplay of the nervous and immune system, especially in inflammatory conditions such as Multiple Sclerosis (MS) and its experimental model Experimental Autoimmune Encephalomyelitis.
Goals: The expression of TrkA, p75NTR and NGF in the spinal cord in EAE was investigated.
Methods: MOG-EAE mice were examined at three time-points (preclinical (D10), acute (D20) and chronic (D50)) compared to controls. The expression of TrkA, p75NTR and NGF were studied by RT-PCR, Western blotting and immunohistochemistry.
Results: Increased expression was observed of TrkA-mRNA at D20 (4.82-fold, p=0.0002) and D50 (4.25-fold, p= 0.0016), whereas p75NTR-mRNA and NGF-mRNA were up-regulated at D50 compared to D0 ((2.1-fold, p < 0.0001), (5.2-fold, p < 0.0001) respectively). At protein level, Western blotting of the spinal cord samples revealed an increase of TrkA, p75NTR and NGF at D20 and D50 (p < 0.0001). Increased expression of TrkA at D10 (p=0.048), D20 and D50 (p < 0.0001) was observed immunohistochemically in the white matter of spinal cord. p75NTR was increased at D20 and D50 (p< 0.0001). NGF in the white matter showed high expression at D20 and D50 compared to D0 (p< 0.0001). Ιn the grey matter, TrkA and p75NTR were increased at D20 (p < 0.0001, p= 0.0011 respectively). NGF was highly expressed at D20 and D50 compared to D0 (p< 0.0001, p=0.001, respectively).
Conclusions: The expression profile of NGF and its receptors, TrkA and p75NTR, in areas of inflammatory demyelination indicates their possible involvement in the underlying pathology and reorganization of degenerated spinal cord during the course of EAE.
Disclosure: Nickoleta Delivanoglou: Nothing to disclose
Olga Touloumi: Nothing to disclose
Roza Lagoudaki: Nothing to disclose
Evangelia Kesidou: Nothing to disclose
Paschalis Theotokis: Nothing to disclose
Evangelia Nousiopoulou: Nothing to disclose
Nikolina Dafi: Nothing to disclose
Marina Boziki: Nothing to disclose
Nikolaos Grigoriadis: Nothing to disclose
Ioannis Charalampopoulos: Nothing to disclose
Constantina Simeonidou: Nothing to disclose