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Mecp2 regulatestnfaduring zebrafish embryonic development and acute inflammation
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| Zeitschriftentitel: | Disease Models & Mechanisms |
|---|---|
| Personen und Körperschaften: | , , , , , , , , |
| In: | Disease Models & Mechanisms, 2017 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
The Company of Biologists
|
| Schlagwörter: |
| author_facet |
van der Vaart, M. Svoboda, O. Weijts, B. G. Espín-Palazón, R. Sapp, V. Pietri, T. Bagnat, M. Muotri, A. R. Traver, D. van der Vaart, M. Svoboda, O. Weijts, B. G. Espín-Palazón, R. Sapp, V. Pietri, T. Bagnat, M. Muotri, A. R. Traver, D. |
|---|---|
| author |
van der Vaart, M. Svoboda, O. Weijts, B. G. Espín-Palazón, R. Sapp, V. Pietri, T. Bagnat, M. Muotri, A. R. Traver, D. |
| spellingShingle |
van der Vaart, M. Svoboda, O. Weijts, B. G. Espín-Palazón, R. Sapp, V. Pietri, T. Bagnat, M. Muotri, A. R. Traver, D. Disease Models & Mechanisms Mecp2 regulatestnfaduring zebrafish embryonic development and acute inflammation General Biochemistry, Genetics and Molecular Biology Immunology and Microbiology (miscellaneous) Medicine (miscellaneous) Neuroscience (miscellaneous) |
| author_sort |
van der vaart, m. |
| spelling |
van der Vaart, M. Svoboda, O. Weijts, B. G. Espín-Palazón, R. Sapp, V. Pietri, T. Bagnat, M. Muotri, A. R. Traver, D. 1754-8411 1754-8403 The Company of Biologists General Biochemistry, Genetics and Molecular Biology Immunology and Microbiology (miscellaneous) Medicine (miscellaneous) Neuroscience (miscellaneous) http://dx.doi.org/10.1242/dmm.026922 <jats:p>Mutations in MECP2 cause Rett syndrome, a severe neurological disorder with autism-like features. Duplication of MECP2 also causes severe neuropathology. Both diseases display immunological abnormalities that suggest a role for MeCP2 in controlling immune and inflammatory responses. Here, we used mecp2-null zebrafish to study the potential function of Mecp2 as an immunological regulator. Mecp2-deficiency resulted in an increase in neutrophil infiltration and upregulated expression of the pro- and anti-inflammatory cytokines Il1b and Il10 as a secondary response to disturbances in tissue homeostasis. In contrast, expression of the pro-inflammatory cytokine tumor necrosis factor alpha (Tnfa) was consistently downregulated in mecp2-null animals during development, representing the earliest developmental phenotype described for MeCP2-deficiency to date. Expression of tnfa was unresponsive to inflammatory stimulation, and was partially restored by re-expression of functional mecp2. Thus, Mecp2 is required for tnfa expression during zebrafish development and inflammation. Finally, RNA sequencing of mecp2-null embryos revealed dysregulated processes predictive for Rett syndrome phenotypes.</jats:p> Mecp2 regulates<i>tnfa</i>during zebrafish embryonic development and acute inflammation Disease Models & Mechanisms |
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The Company of Biologists, 2017 |
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The Company of Biologists, 2017 |
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| title |
Mecp2 regulatestnfaduring zebrafish embryonic development and acute inflammation |
| title_unstemmed |
Mecp2 regulatestnfaduring zebrafish embryonic development and acute inflammation |
| title_full |
Mecp2 regulatestnfaduring zebrafish embryonic development and acute inflammation |
| title_fullStr |
Mecp2 regulatestnfaduring zebrafish embryonic development and acute inflammation |
| title_full_unstemmed |
Mecp2 regulatestnfaduring zebrafish embryonic development and acute inflammation |
| title_short |
Mecp2 regulatestnfaduring zebrafish embryonic development and acute inflammation |
| title_sort |
mecp2 regulates<i>tnfa</i>during zebrafish embryonic development and acute inflammation |
| topic |
General Biochemistry, Genetics and Molecular Biology Immunology and Microbiology (miscellaneous) Medicine (miscellaneous) Neuroscience (miscellaneous) |
| url |
http://dx.doi.org/10.1242/dmm.026922 |
| publishDate |
2017 |
| physical |
|
| description |
<jats:p>Mutations in MECP2 cause Rett syndrome, a severe neurological disorder with autism-like features. Duplication of MECP2 also causes severe neuropathology. Both diseases display immunological abnormalities that suggest a role for MeCP2 in controlling immune and inflammatory responses. Here, we used mecp2-null zebrafish to study the potential function of Mecp2 as an immunological regulator. Mecp2-deficiency resulted in an increase in neutrophil infiltration and upregulated expression of the pro- and anti-inflammatory cytokines Il1b and Il10 as a secondary response to disturbances in tissue homeostasis. In contrast, expression of the pro-inflammatory cytokine tumor necrosis factor alpha (Tnfa) was consistently downregulated in mecp2-null animals during development, representing the earliest developmental phenotype described for MeCP2-deficiency to date. Expression of tnfa was unresponsive to inflammatory stimulation, and was partially restored by re-expression of functional mecp2. Thus, Mecp2 is required for tnfa expression during zebrafish development and inflammation. Finally, RNA sequencing of mecp2-null embryos revealed dysregulated processes predictive for Rett syndrome phenotypes.</jats:p> |
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| author | van der Vaart, M., Svoboda, O., Weijts, B. G., Espín-Palazón, R., Sapp, V., Pietri, T., Bagnat, M., Muotri, A. R., Traver, D. |
| author_facet | van der Vaart, M., Svoboda, O., Weijts, B. G., Espín-Palazón, R., Sapp, V., Pietri, T., Bagnat, M., Muotri, A. R., Traver, D., van der Vaart, M., Svoboda, O., Weijts, B. G., Espín-Palazón, R., Sapp, V., Pietri, T., Bagnat, M., Muotri, A. R., Traver, D. |
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| description | <jats:p>Mutations in MECP2 cause Rett syndrome, a severe neurological disorder with autism-like features. Duplication of MECP2 also causes severe neuropathology. Both diseases display immunological abnormalities that suggest a role for MeCP2 in controlling immune and inflammatory responses. Here, we used mecp2-null zebrafish to study the potential function of Mecp2 as an immunological regulator. Mecp2-deficiency resulted in an increase in neutrophil infiltration and upregulated expression of the pro- and anti-inflammatory cytokines Il1b and Il10 as a secondary response to disturbances in tissue homeostasis. In contrast, expression of the pro-inflammatory cytokine tumor necrosis factor alpha (Tnfa) was consistently downregulated in mecp2-null animals during development, representing the earliest developmental phenotype described for MeCP2-deficiency to date. Expression of tnfa was unresponsive to inflammatory stimulation, and was partially restored by re-expression of functional mecp2. Thus, Mecp2 is required for tnfa expression during zebrafish development and inflammation. Finally, RNA sequencing of mecp2-null embryos revealed dysregulated processes predictive for Rett syndrome phenotypes.</jats:p> |
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| spelling | van der Vaart, M. Svoboda, O. Weijts, B. G. Espín-Palazón, R. Sapp, V. Pietri, T. Bagnat, M. Muotri, A. R. Traver, D. 1754-8411 1754-8403 The Company of Biologists General Biochemistry, Genetics and Molecular Biology Immunology and Microbiology (miscellaneous) Medicine (miscellaneous) Neuroscience (miscellaneous) http://dx.doi.org/10.1242/dmm.026922 <jats:p>Mutations in MECP2 cause Rett syndrome, a severe neurological disorder with autism-like features. Duplication of MECP2 also causes severe neuropathology. Both diseases display immunological abnormalities that suggest a role for MeCP2 in controlling immune and inflammatory responses. Here, we used mecp2-null zebrafish to study the potential function of Mecp2 as an immunological regulator. Mecp2-deficiency resulted in an increase in neutrophil infiltration and upregulated expression of the pro- and anti-inflammatory cytokines Il1b and Il10 as a secondary response to disturbances in tissue homeostasis. In contrast, expression of the pro-inflammatory cytokine tumor necrosis factor alpha (Tnfa) was consistently downregulated in mecp2-null animals during development, representing the earliest developmental phenotype described for MeCP2-deficiency to date. Expression of tnfa was unresponsive to inflammatory stimulation, and was partially restored by re-expression of functional mecp2. Thus, Mecp2 is required for tnfa expression during zebrafish development and inflammation. Finally, RNA sequencing of mecp2-null embryos revealed dysregulated processes predictive for Rett syndrome phenotypes.</jats:p> Mecp2 regulates<i>tnfa</i>during zebrafish embryonic development and acute inflammation Disease Models & Mechanisms |
| spellingShingle | van der Vaart, M., Svoboda, O., Weijts, B. G., Espín-Palazón, R., Sapp, V., Pietri, T., Bagnat, M., Muotri, A. R., Traver, D., Disease Models & Mechanisms, Mecp2 regulatestnfaduring zebrafish embryonic development and acute inflammation, General Biochemistry, Genetics and Molecular Biology, Immunology and Microbiology (miscellaneous), Medicine (miscellaneous), Neuroscience (miscellaneous) |
| title | Mecp2 regulatestnfaduring zebrafish embryonic development and acute inflammation |
| title_full | Mecp2 regulatestnfaduring zebrafish embryonic development and acute inflammation |
| title_fullStr | Mecp2 regulatestnfaduring zebrafish embryonic development and acute inflammation |
| title_full_unstemmed | Mecp2 regulatestnfaduring zebrafish embryonic development and acute inflammation |
| title_short | Mecp2 regulatestnfaduring zebrafish embryonic development and acute inflammation |
| title_sort | mecp2 regulates<i>tnfa</i>during zebrafish embryonic development and acute inflammation |
| title_unstemmed | Mecp2 regulatestnfaduring zebrafish embryonic development and acute inflammation |
| topic | General Biochemistry, Genetics and Molecular Biology, Immunology and Microbiology (miscellaneous), Medicine (miscellaneous), Neuroscience (miscellaneous) |
| url | http://dx.doi.org/10.1242/dmm.026922 |