Neuron-Glia Crosstalk: Investigating Immune-Cell Modulation in the CNP1 Null Mutant Mouse Article Swipe
Myelin sheaths built by oligodendrocytes in the central nervous system (CNS) are not only important insulators that enable the fast saltatory propagation of action potentials but also fulfill metabolic support functions to their underlying axons. 2’,3’-cyclic nucleotide 3’ phos- phodiesterase (CNP1) constitutes 4% of total CNS myelin proteins and is disease-relevant in humans and mice. First, a homozygous missense mutation in CNP1 was recently associated with a hypomyelinating dystrophy in humans and second, a reduced CNP1 gene expression causes an age-dependent catatonia-depression syndrome in mouse and man. \n \nBy immunohistochemistry and RNA-Seq. on purified myelin-enriched fractions, we aimed at investigating which changes occur at early ages in CNP1 null mutants and may thus be initial mediators of disease pathology. We found that signs of neuroinflammation and neu- rodegeneration were largely absent at the age of P18 but obvious at P75, suggesting that the earlier age represents a prodromal phase of pathology. Nevertheless, by sensitive qRT-PCR, we identified the anti-inflammatory Tnfaip6 and the alarmin Il-33 upregulated in mutant myelin as early as P20 consistent with the idea that these molecules are secreted by CNP1 deprived oligodendrocytes. Although these candidates are thus possible initial disease modi- fiers, it remains to be analyzed in future experiments, whether they are indeed oligodendro- cyte-derived, since subsequent analyses by qRT-PCR questioned, that P20 can be fully re- garded as prodromal stage of CNP1-related pathology. \n \nWhen analyzing astroglial and microglial RNAs in purified myelin at P75, we noted that as- trocytes exhibit features of A1 (C3, Ggta1, Gbp2) and A2 (Cd109, Cd14, Emp1) cells, and that microglia express pro-inflammatory M1 markers (Ccl6, Fcgr3, Cd86) as well as M2 mark- ers (Clec7a, Trem2) typical for phagocytosing cells. Additionally, Toll-like-receptors (Tlr) 1 and 2 were found upregulated. A subsequent immunohistochemical analysis of CNP1- MyD88-double mutants identified the TLR-associated MyD88-pathway in microglia as in- strumental in inducing axonal pathology in CNP1-deficient mice. \n \nFinally, we hypothesized that the previously reported pathology of cytosolic channels in CNP1 null mutant myelin results in a quantitative alteration of transported mRNAs and pro- teins. By qRT-PCR we found Mbp-mRNA higher in abundance in myelin of mutants at P20, compatible with the idea that an increased local translation of this mRNA is causatively linked to the reported earlier closure of cytosolic myelin channels due to an increased presence of MPB-protein, the only myelin protein absolutely necessary for myelin compaction. At P75 we found Fth1-mRNA, which is reported to be extremely abundant in myelin, reduced by 70% in CNP1 null mutants. This may be of relevance for the pathology since the secretion of Fth1 by oligodendrocytes is suggested to serve as a protective mechanism against iron- induced axonopathy. At P75 we also found the abundance of MCT1 protein, an oligoden- droglial axon supporting monocarboxylate transporter, reduced. Hence, the pathology of cytosolic myelin channels may indeed disrupt the transport of proteins essential for axonal support.
Related Topics
Concepts
Myelin
Biology
Neuroinflammation
Mutant
Oligodendrocyte
Microglia
Immune system
Cell biology
Null allele
Neuroscience
Missense mutation
Downregulation and upregulation
Central nervous system
Immunology
Mutation
Genetics
Gene
Inflammation
Metadata
- Type
- dissertation
- Language
- en
- Landing Page
- https://doi.org/10.53846/goediss-9749
- https://ediss.uni-goettingen.de/bitstream/11858/14546/1/Promotion_Aicher_ediss.pdf
- OA Status
- gold
- References
- 200
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W4322740237
All OpenAlex metadata
Raw OpenAlex JSON
- OpenAlex ID
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https://openalex.org/W4322740237Canonical identifier for this work in OpenAlex
- DOI
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https://doi.org/10.53846/goediss-9749Digital Object Identifier
- Title
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Neuron-Glia Crosstalk: Investigating Immune-Cell Modulation in the CNP1 Null Mutant MouseWork title
- Type
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dissertationOpenAlex work type
- Language
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enPrimary language
- Publication year
-
2023Year of publication
- Publication date
-
2023-01-01Full publication date if available
- Authors
-
Marie Louise AicherList of authors in order
- Landing page
-
https://doi.org/10.53846/goediss-9749Publisher landing page
- PDF URL
-
https://ediss.uni-goettingen.de/bitstream/11858/14546/1/Promotion_Aicher_ediss.pdfDirect link to full text PDF
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YesWhether a free full text is available
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goldOpen access status per OpenAlex
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https://ediss.uni-goettingen.de/bitstream/11858/14546/1/Promotion_Aicher_ediss.pdfDirect OA link when available
- Concepts
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Myelin, Biology, Neuroinflammation, Mutant, Oligodendrocyte, Microglia, Immune system, Cell biology, Null allele, Neuroscience, Missense mutation, Downregulation and upregulation, Central nervous system, Immunology, Mutation, Genetics, Gene, InflammationTop concepts (fields/topics) attached by OpenAlex
- Cited by
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0Total citation count in OpenAlex
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200Number of works referenced by this work
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10Other works algorithmically related by OpenAlex
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| abstract_inverted_index.2 | 281 |
| abstract_inverted_index.A | 285 |
| abstract_inverted_index.a | 56, 66, 73, 144, 326, 430 |
| abstract_inverted_index.4% | 42 |
| abstract_inverted_index.A1 | 244 |
| abstract_inverted_index.A2 | 249 |
| abstract_inverted_index.At | 389, 437 |
| abstract_inverted_index.By | 335 |
| abstract_inverted_index.M1 | 259 |
| abstract_inverted_index.M2 | 267 |
| abstract_inverted_index.We | 117 |
| abstract_inverted_index.an | 79, 354, 375, 447 |
| abstract_inverted_index.as | 166, 168, 220, 264, 266, 299, 429 |
| abstract_inverted_index.at | 96, 101, 129, 136, 234, 347 |
| abstract_inverted_index.be | 111, 196, 216, 398, 412 |
| abstract_inverted_index.by | 3, 150, 179, 210, 404, 423 |
| abstract_inverted_index.in | 5, 51, 60, 69, 83, 104, 163, 198, 231, 297, 302, 306, 319, 325, 341, 343, 401, 406 |
| abstract_inverted_index.is | 49, 361, 395, 425 |
| abstract_inverted_index.it | 193 |
| abstract_inverted_index.of | 22, 43, 114, 121, 132, 147, 223, 243, 289, 316, 329, 345, 358, 369, 378, 413, 421, 444, 458, 467 |
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| abstract_inverted_index.to | 31, 195, 364, 374, 397, 427 |
| abstract_inverted_index.we | 94, 153, 236, 309, 337, 391, 439 |
| abstract_inverted_index.70% | 405 |
| abstract_inverted_index.CNS | 45 |
| abstract_inverted_index.P18 | 133 |
| abstract_inverted_index.P20 | 169, 214 |
| abstract_inverted_index.P75 | 390, 438 |
| abstract_inverted_index.age | 131, 142 |
| abstract_inverted_index.and | 48, 53, 71, 85, 88, 108, 123, 158, 228, 248, 254, 280, 332 |
| abstract_inverted_index.are | 11, 177, 186, 203 |
| abstract_inverted_index.as- | 239 |
| abstract_inverted_index.but | 25, 134 |
| abstract_inverted_index.can | 215 |
| abstract_inverted_index.due | 373 |
| abstract_inverted_index.ers | 269 |
| abstract_inverted_index.for | 273, 386, 415, 470 |
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| abstract_inverted_index.may | 109, 411, 462 |
| abstract_inverted_index.not | 12 |
| abstract_inverted_index.re- | 218 |
| abstract_inverted_index.the | 6, 18, 130, 140, 155, 159, 172, 294, 312, 351, 365, 380, 416, 419, 442, 456, 465 |
| abstract_inverted_index.was | 62 |
| abstract_inverted_index.(C3, | 245 |
| abstract_inverted_index.3’ | 37 |
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| abstract_inverted_index.Fth1 | 422 |
| abstract_inverted_index.MCT1 | 445 |
| abstract_inverted_index.P20, | 348 |
| abstract_inverted_index.P75, | 137, 235 |
| abstract_inverted_index.RNAs | 230 |
| abstract_inverted_index.This | 410 |
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| abstract_inverted_index.also | 26, 440 |
| abstract_inverted_index.axon | 450 |
| abstract_inverted_index.fast | 19 |
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| abstract_inverted_index.mRNA | 360 |
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| abstract_inverted_index.pro- | 333 |
| abstract_inverted_index.that | 16, 119, 139, 174, 213, 238, 255, 311, 353 |
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| abstract_inverted_index.this | 359 |
| abstract_inverted_index.thus | 110, 187 |
| abstract_inverted_index.well | 265 |
| abstract_inverted_index.were | 126, 282 |
| abstract_inverted_index.with | 65, 171, 350 |
| abstract_inverted_index.(CNS) | 10 |
| abstract_inverted_index.(Tlr) | 278 |
| abstract_inverted_index.CNP1- | 290 |
| abstract_inverted_index.Cd14, | 251 |
| abstract_inverted_index.Cd86) | 263 |
| abstract_inverted_index.Emp1) | 252 |
| abstract_inverted_index.Gbp2) | 247 |
| abstract_inverted_index.Il-33 | 161 |
| abstract_inverted_index.aimed | 95 |
| abstract_inverted_index.built | 2 |
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| abstract_inverted_index.mRNAs | 331 |
| abstract_inverted_index.mark- | 268 |
| abstract_inverted_index.mice. | 54 |
| abstract_inverted_index.modi- | 191 |
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| abstract_inverted_index.noted | 237 |
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| abstract_inverted_index.phos- | 38 |
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| abstract_inverted_index.signs | 120 |
| abstract_inverted_index.since | 207, 418 |
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| abstract_inverted_index.their | 32 |
| abstract_inverted_index.these | 175, 184 |
| abstract_inverted_index.total | 44 |
| abstract_inverted_index.which | 98, 394 |
| abstract_inverted_index.(CNP1) | 40 |
| abstract_inverted_index.(Ccl6, | 261 |
| abstract_inverted_index.Fcgr3, | 262 |
| abstract_inverted_index.First, | 55 |
| abstract_inverted_index.Ggta1, | 246 |
| abstract_inverted_index.Hence, | 455 |
| abstract_inverted_index.Myelin | 0 |
| abstract_inverted_index.Trem2) | 271 |
| abstract_inverted_index.absent | 128 |
| abstract_inverted_index.action | 23 |
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| abstract_inverted_index.causes | 78 |
| abstract_inverted_index.cells, | 253 |
| abstract_inverted_index.cells. | 275 |
| abstract_inverted_index.enable | 17 |
| abstract_inverted_index.fiers, | 192 |
| abstract_inverted_index.future | 199 |
| abstract_inverted_index.garded | 219 |
| abstract_inverted_index.higher | 340 |
| abstract_inverted_index.humans | 52, 70 |
| abstract_inverted_index.indeed | 204, 463 |
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| abstract_inverted_index.mutant | 164, 322 |
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| abstract_inverted_index.(Cd109, | 250 |
| abstract_inverted_index.Tnfaip6 | 157 |
| abstract_inverted_index.against | 433 |
| abstract_inverted_index.alarmin | 160 |
| abstract_inverted_index.central | 7 |
| abstract_inverted_index.changes | 99 |
| abstract_inverted_index.closure | 368 |
| abstract_inverted_index.disease | 115, 190 |
| abstract_inverted_index.disrupt | 464 |
| abstract_inverted_index.earlier | 141, 367 |
| abstract_inverted_index.exhibit | 241 |
| abstract_inverted_index.express | 257 |
| abstract_inverted_index.fulfill | 27 |
| abstract_inverted_index.induced | 435 |
| abstract_inverted_index.initial | 112, 189 |
| abstract_inverted_index.largely | 127 |
| abstract_inverted_index.markers | 260 |
| abstract_inverted_index.mutants | 107, 292, 346 |
| abstract_inverted_index.myelin, | 402 |
| abstract_inverted_index.nervous | 8 |
| abstract_inverted_index.obvious | 135 |
| abstract_inverted_index.protein | 383 |
| abstract_inverted_index.qRT-PCR | 211, 336 |
| abstract_inverted_index.reduced | 74, 403 |
| abstract_inverted_index.remains | 194 |
| abstract_inverted_index.results | 324 |
| abstract_inverted_index.second, | 72 |
| abstract_inverted_index.sheaths | 1 |
| abstract_inverted_index.support | 29 |
| abstract_inverted_index.typical | 272 |
| abstract_inverted_index.whether | 201 |
| abstract_inverted_index.(Clec7a, | 270 |
| abstract_inverted_index.Although | 183 |
| abstract_inverted_index.Mbp-mRNA | 339 |
| abstract_inverted_index.RNA-Seq. | 89 |
| abstract_inverted_index.abundant | 400 |
| abstract_inverted_index.analyses | 209 |
| abstract_inverted_index.analysis | 288 |
| abstract_inverted_index.analyzed | 197 |
| abstract_inverted_index.channels | 318, 372, 461 |
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| abstract_inverted_index.droglial | 449 |
| abstract_inverted_index.features | 242 |
| abstract_inverted_index.inducing | 303 |
| abstract_inverted_index.missense | 58 |
| abstract_inverted_index.mutants. | 409 |
| abstract_inverted_index.mutation | 59 |
| abstract_inverted_index.possible | 188 |
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| abstract_inverted_index.protein, | 446 |
| abstract_inverted_index.proteins | 47, 468 |
| abstract_inverted_index.purified | 91, 232 |
| abstract_inverted_index.qRT-PCR, | 152 |
| abstract_inverted_index.recently | 63 |
| abstract_inverted_index.reduced. | 454 |
| abstract_inverted_index.reported | 314, 366, 396 |
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| abstract_inverted_index.support. | 472 |
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| abstract_inverted_index.trocytes | 240 |
| abstract_inverted_index.abundance | 342, 443 |
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| abstract_inverted_index.cytosolic | 317, 370, 459 |
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| abstract_inverted_index.essential | 469 |
| abstract_inverted_index.extremely | 399 |
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| abstract_inverted_index.saltatory | 20 |
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| abstract_inverted_index.Fth1-mRNA, | 393 |
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