Immunological relationships of NGF, BDNF, and NT-3: recognition and functional inhibition by antibodies to NGF

Murphy, RA; Acheson, Ann; Hodges, Robert S.; Haskins, Julie; Richards, Cheryl; Reklow, E.; Chlumecky, Vera; Barker, P. A.; Alderson, RF; Lindsay, R. M.

doi:10.1523/jneurosci.13-07-02853.1993

Cited by 53 publications

(31 citation statements)

References 44 publications

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“…ELISAs have shown that our polyclonal antibody recognizes NT-3, although to a significantly lesser extent than NGF and, to an even lesser extent, BDNF (Murphy et al, 1993), but in in vitro survival assays it blocks only the biological activity of NGF and not that of personal communication). In preliminary in vitro mouse dorsal root ganglia studies, our anti-NGF had a small effect on sprouting induced by NT-3, whereas BDNF-induced sprouting was unaffected ( Van der Zee et al, 1995).…”

Section: Preparation and Characterization Of Ngf And Its Antiserummentioning

confidence: 85%

Ceramide Is Responsible for the Failure of Compensatory Nerve Sprouting in Apolipoprotein E Knock-Out Mice

Maysinger¹,

Holmes²,

Han³

et al. 2008

J. Neurosci.

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Apolipoprotein E (apoE) is a key transporter of the cholesterol and phospholipids required for membrane synthesis and nerve growth. We now report a virtual absence in apoE knock-out (KO) mice of normal nerve growth factor (NGF)-driven compensatory sprouting of undamaged cutaneous nociceptive nerves. In contrast, NGF-independent regeneration of crushed axons was unaffected. Essentially similar results came from aged wild-type mice. In apoE KO mice, the endogenous sprouting stimulus was suspect, because NGF administration induced normal sprouting; nevertheless, NGF increased normally in denervated skin, transported normally in the axons, and led to phosphorylation of trkA, erk1, and erk2. However, sprouting was restored in apoE KO mice (although not in aged mice) by fumonisin B1, an inhibitor of ceramide synthesis. A shotgun analysis revealed a wide array of changes in individual ceramide species in DRG neurons of apoE KO mice, and the changes for ceramide species OH_N15:0 made it a candidate inhibitor of sprouting (increased in apoE KO mice and normalized by fumonisin B1). Nevertheless, the unknown effects of individual ceramide species on sprouting, as well as the variability of their changed levels in apoE KO mice and how these were affected by fumonisin B1, support a different conclusion. We suggest that absence of apoE expression alters the balance among ceramide species to one that collectively inhibits compensatory sprouting, whereas fumonisin B1 establishes a new balance that allows sprouting. Nontoxic ceramide modulators might usefully promote sprouting and circuitry repair in neurodegenerative disorders in which ceramide species are perturbed, adding to the benefits of reducing ceramideinduced neuronal apoptosis.

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Section: Preparation and Characterization Of Ngf And Its Antiserummentioning

confidence: 85%

Ceramide Is Responsible for the Failure of Compensatory Nerve Sprouting in Apolipoprotein E Knock-Out Mice

Maysinger¹,

Holmes²,

Han³

et al. 2008

J. Neurosci.

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“…Fortunately, our NGF antibody readily cross-reacts with NT3 [22] and immunoprecipitates both proNT3 and NT3. As shown in Fig.…”

Section: Processing Of Pront3mentioning

confidence: 99%

Cellular processing of the neurotrophin precursors of NT3 and BDNF by the mammalian proprotein convertases

et al. 1996

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In order to define the enzymes responsible for the maturation of the precursors of brain-derived neurotrophic factor (proBDNF) and neurotrophin-3 (proNT3), we have analysed their biosynthesis and intracellular processing by the proprotein convertases furin, PC1, PC2, PACE4, PC5 and its isoform PC5/6-B. In these studies, we utilized a vaccinia virus expression system in either BSC40 or the furin activity-deficient LoVo cells. Results demonstrated that in both cells furin and, to a lesser extent, PACE4 and PC516-B effectively process proBDNF and proNT3. Furthermore, we have determined that human proNT3 is sulfated, suggesting that processing of proNT3 occurs following the arrival of the precursor to the Trans Golgi Network.

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“…Our results indicate NGF-like immunoreactivity in mast cells of mesenchymal adult rodent tissues or RPMCs. Although some cross-reactivity of the polyclonal antibody toward other neurotrophins cannot be excluded (38) (7,8). Mast cells could, by releasing cytokines such as tumor necrosis factor, also indirectly upregulate NGF production in surrounding cells (35).…”

Section: Sympathetic (E10) and Drg (E8) Neurons Were Cultured 24mentioning

confidence: 99%

Mast cells synthesize, store, and release nerve growth factor.

Leon

Buriani

Toso

et al. 1994

Proc. Natl. Acad. Sci. U.S.A.

584

284

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Mast cells and nerve growth factor (NGF) have both been reported to be involved in neuroimmune interactions and tissue inflammation. In many peripheral tissues, mast cells interact with the innervating fibers. Changes in the behaviors of both of these elements occur after tissue injury/inflammation. As such conditions are typically associated with rapid mast cell activation and NGF accumulation in inflammatory exudates, we hypothesized that mast cells may be capable of producing NGF. Here we report that (i) NGF mRNA is expressed in adult rat peritoneal mast cells; (ii) anti-NGF antibodies clearly stain vesicular compartments of purified mast cells and mast cells in histological sections of adult rodent mesenchymal tissues; and (iii) medium conditioned by peritoneal mast cells contains biologically active NGF. Mast cells thus represent a newly recognized source of NGF. The known actions of NGF on peripheral nerve fibers and immune cells suggest that mast cell-derived NGF may control adaptive/reactive responses of the nervous and immune systems toward noxious tissue perturbations. Conversely, alterations in normal mast cell behaviors may provoke maladaptive neuroimmune tissue responses whose consequences could have profound implications in inflammatory disease states, including those of an autoimmune nature.

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Immunological relationships of NGF, BDNF, and NT-3: recognition and functional inhibition by antibodies to NGF

Cited by 53 publications

References 44 publications

Ceramide Is Responsible for the Failure of Compensatory Nerve Sprouting in Apolipoprotein E Knock-Out Mice

Ceramide Is Responsible for the Failure of Compensatory Nerve Sprouting in Apolipoprotein E Knock-Out Mice

Cellular processing of the neurotrophin precursors of NT3 and BDNF by the mammalian proprotein convertases

Mast cells synthesize, store, and release nerve growth factor.

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