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Likewise, while pre-cNF and s-cNF in NF1 patients apparently originate only among various types of cutaneous adnexal structures, they occur among relatively few of all possible adnexae even in patients with numerous cNF. Therefore, while Nf1 DI transformations increase the probability that neurofibromas will occur, the mechanism s that actually triggers pNFs and cNF remains unknown.

Despite the considerable quantity of excessive innervation in the s-cNF, the likely origin from a small subset of sensory fibers associated with a specific adnexa suggests that relatively few DRG neurons may account for the excessive sprouting in each cNF. The capacity for excessive sprouting by C fibers has been shown in transgenic mouse lines designed to overproduce various neurotrophic factors in keratinocytes [ 76 , ]. Our observations indicate that the trigger for the occurrence of a pre-cNF and potential subsequent evolution into a cNF involves a local trophic interaction between nonpeptidergic C-fiber endings and their associated terminal SC at any type of adnexa that is a normal site where these endings are located.

Whereas C fibers are typically regarded as nociceptors involved in pain sensation, there is increasing evidence that many, if not most, are normally involved in local homeostatic monitoring and maintenance of target structures. The normal expression of GAP among C fibers may be indicative of an ongoing remodeling of their sensory endings and associated terminal glia as part of a normal homeostatic monitoring subliminal maintenance which regularly fluctuates in response to transient tissue stressors, becoming especially exaggerated as part of wound repair [ 29 , 35 , 49 , , , — ].

Possibly, the adnexae themselves may exert some degree of paracrine tropism, specifically attracting critical cells from already-established NFs or other sites. Others have proposed possible seeding from mature neurofibromas and the existence of precursor lesions involving a specific neurofibroma precursor cell [ 8 , ]. Comparable to the NF1 pre-cNF, hamartia are microscopic lesions well-documented in the Tuberous Sclerosis Complex that precede and evolve into hamartomas [ 10 ].

Rather, they appear to involve an initial trophic interaction between cutaneous C fiber sensory endings and their terminal SC associated with skin adnexae that may involve ARTN and NTRN signaling through c-Ret receptors on both the innervation and SC. This suggests that the pre-cNF and the evolution to cNF may arise on the basis of dysplasia [ 13 ] and not simply neoplasia in accordance with the canonical two-hit model.

As such, therapeutic strategies that target the c-Ret signaling mechanism at the earliest appearance of a s-cNF may prevent the further development or maintenance of the cNF. Secondary antibodies produced no detectable labeling above background autofluorescence in s-cNF. Example pairs of secondary antibody fluorescence in the absence of primary antibodies A-E as compared to autofluorescence F.

Note the autofluorescence of vascular profiles likely due to the presence of albumen arrowheads. Staining revealed MCs abnormally numerous and diffusely distributed throughout s-cNF S2B Fig as was known previously [ 19 , 26 , 63 , ]. Likewise, mast cells were diffusely distributed within the pre-cNF at a higher density than the surrounding dermis S2A Fig. Note a capsule broad red arrows that contain a PGP-labeled large-caliber axon at the core open yellow arrowheads.

Browse Subject Areas? Click through the PLOS taxonomy to find articles in your field. Abstract In addition to large plexiform neurofibromas pNF , NF1 patients are frequently disfigured by cutaneous neurofibromas cNF and are often afflicted with chronic pain and itch even from seemingly normal skin areas. Introduction Multiple cutaneous neurofibromas cNF are characteristic of neurofibromatosis type 1 NF1 patients who have an autosomal dominant loss-of-function mutation of an NF1 allele. Biopsy specimen Skin biopsies were collected from 19 NF1 patients 20—64 years old; Fig 1 and 16 genetically and somesthetically normal subjects 24—70 years old.

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Summary of the incidence and locations of the pre-cNF among the biopsies of 19 NF1 patients. Table 1. Chemomorphometric analysis CMA antibody specifications. Fig 2. Immunofluorescence profile of pre-cNF among dermal papilla and hair follicles. Fig 3. Immunofluorescence profile of pre-cNF among sweat ducts and glands. Fig 4. Fig 6. Structural organization of s-cNF around an adnexal core perpendicular. Fig 7. Structural organization of an s-cNF around an adnexal core parallel. Fig 8. Multi-molecular immunofluorescence characteristics of s-cNF aberrant innervation.

Fig 9. Structural organization of s-cNF Consistent with the pre-cNF hypothesis, immunolabeling of serial sections from numerous 3—6 mm cNF, cut perpendicular or parallel to the skin surface Figs 6 and 7 , respectively , revealed that each had an adnexal structure imbedded at the core that was associated with a massive dense concentration of aberrant innervation that extensively co-labeled for GAP and PGP Figs 7A—7C and 8A—8C.

Aberrant pre-cNF innervation. Aberrant s-cNF innervation. SC precursor cells. SC related mRNA detection. Unidentified cells. Mast cells, compartmentalizing cells, and sensory corpuscles. Potential neural signaling mechanisms between aberrant innervation and nSC That the aberrant innervation in pre-cNF and s-cNF was overwhelmingly composed of nonpeptidergic C fibers suggested the possible presence of ligands and receptors for two major neurotrophic factor systems that promote outgrowth of C fibers: the nerve growth factor NGF family and glial-derived neurotrophic factor GDNF family [ 75 — 78 ], Section E in S1 Text.

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GDNF family of neurotrophins. Fig NGF family of neurotrophins. Discussion Origin of cNF The origin of pNF and cNF in NF1 patients has been attributed to an increased probability of aberrant hyperproliferation by nSC due to a nSC-specific spontaneous monoallelic to biallelic loss-of-function mutation of NF1 resulting in a depletion of neurofibromin. Potential SC precursors.

Mast cells. TrpA1 and TrpV1. What triggers the onset of pre-cNF and the evolution of cNF? Supporting information. S1 Text. Supplemental text. S1 Fig. Secondary antibody labeling and autofluorescence. S2 Fig. Mast cells MC. S3 Fig. Compartmentalizing Cells and Sensory Corpuscles.

References 1. Adv Anat Pathol. Riccardi VM. Neurofibromatosis: Phenotype, Natural History and Pathogenesis. Baltimore: Johns Hopkins University Press; View Article Google Scholar 4. Tumor microenvironment and neurofibromatosis type I: connecting the GAPs. SB and neurofibromin immunostaining and X-inactivation patterns of laser microdissected cells indicate a multicellular origin of some NF1-associated neurofibromas.

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Tumor suppressor mutations and growth factor signaling in the pathogenesis of NF1-associated peripheral nerve sheath tumors: II. The role of dysregulated growth factor signaling. J Neuropathol Exp Neurol. Benign neurofibromas in type 1 neurofibromatosis NF1 show somatic deletions of the NF1 gene. Nat Genet.

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Adaptations of synaptic form in an aberrant projection to the avian cochlear nucleus.

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Differential hypertrophy and atrophy among all types of cutaneous innervation in the glabrous skin of the monkey hand during aging and naturally occurring type 2 diabetes. Barohn RJ. Intraepidermal nerve fiber assessment: a new window on peripheral neuropathy. Arch Neurol. Skin biopsy for the diagnosis of peripheral neuropathy. HIS [pii] pmid Epidermal nerve fiber quantification in the assessment of diabetic neuropathy. Acta Histochem. Evidence of focal small-fiber axonal degeneration in complex regional pain syndrome-I reflex sympathetic dystrophy.

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    Jacob C. Transcriptional control of neural crest specification into peripheral glia. Jessen KR, Mirsky R. Unable to display preview. Download preview PDF. Skip to main content. Advertisement Hide. Further studies on the aberrant crossed visual corticotectal pathway in rats. Authors Authors and affiliations L. Jen R. Lund J. This is a preview of subscription content, log in to check access. Baisinger, J. Exp Neurol 54 , — Google Scholar. Bunt, A. Brain Res 73 , — Google Scholar. Colman, D. Anat Rec , Google Scholar. Fink, R. Brain Res 4 , — Google Scholar. Frost, D. Gilbert, C. J Comp Neurol , 81— Google Scholar.

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