Distribution of TGF-β, the TGF-β type I receptor and the R-II receptor in peripheral nerves and mechanoreceptors; observations on changes after traumatic injury

Stark, Birgit; Carlstedt, Thomas; Risling, Mårten

doi:10.1016/s0006-8993(01)02757-3

Cited by 31 publications

(18 citation statements)

References 39 publications

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“…On the other hand, we do not know why type I collagen was upregulated in all the DRGs, except for the ipsilateral L5 DRG, of ligated animals ( Table 2). Although we failed to observe transforming growth factor (TGF)-␤ on our gels, TGF-␤ is secreted after nerve injury by injured DRG cells and axons (122,130), and it modulates the expression of extracellular proteins including type I collagen (135). In addition, nerve ligation in this study upregulated a number of proteins known to regulate the expression and/or functions of extracellular matrix-associated proteins (30,60,113,139).…”

Section: Resultscontrasting

confidence: 52%

Proteomics study of neuropathic and nonneuropathic dorsal root ganglia: altered protein regulation following segmental spinal nerve ligation injury

Komori

Takemori

Kim

et al. 2007

Physiological Genomics

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Peripheral nerve injury is often followed by the development of severe neuropathic pain. Nerve degeneration accompanied by inflammatory mediators is thought to play a role in generation of neuropathic pain. Neuronal cell death follows axonal degeneration, devastating a vast number of molecules in injured neurons and the neighboring cells. Because we have little understanding of the cellular and molecular mechanisms underlying neuronal cell death triggered by nerve injury, we conducted a proteomics study of rat 4th and 5th lumbar (L4 and L5) dorsal root ganglion (DRG) after L5 spinal nerve ligation. DRG proteins were displayed on two-dimensional gels and analyzed through quantitative densitometry, statistical validation of the quantitative data, and peptide mass fingerprinting for protein identification. Among approximately 1,300 protein spots detected on each gel, we discovered 67 proteins that were tightly regulated by nerve ligation. We find that the injury to primary sensory neurons turned on multiple cellular mechanisms critical for the structural and functional integrity of neurons and for the defense against oxidative damage. Our data indicate that the regulation of metabolic enzymes was carefully orchestrated to meet the altered energy requirement of the DRG cells. Our data also demonstrate that ligation of the L5 spinal nerve led to the upregulation in the L4 DRG of the proteins that are highly expressed in embryonic sensory neurons. To understand the molecular mechanisms underlying neuropathic pain, we need to comprehend such dynamic aspect of protein modulations that follow nerve injury.

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Section: Resultscontrasting

confidence: 52%

Proteomics study of neuropathic and nonneuropathic dorsal root ganglia: altered protein regulation following segmental spinal nerve ligation injury

Komori

Takemori

Kim

et al. 2007

Physiological Genomics

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“…Indeed, other studies showed that neuropeptides released by cutaneous nerves, such as substance P, vasoactive intestinal peptide, and so matostatin can induce mast cells to release inflammatory mediators, such as histamine, tumor necrosis factor (TNF), and other inflammatory mediators (63–68). Afferent nerves express specific receptors for neuropeptides (69), prostaglandins (70), histamine (71), proteases (72), neurotrophins (73), and cytokines (74, 75). Levels of IL-13 in the skin samples from Tg(+)/ c-Kit +/+ and Tg(+)/ Kit W-s/W-sh were comparable indicating that mast cell deficiency in K5-tTA-IL-13 mice did not affect the expression of theIL-13transgene and that changes in diminished TRPA1 expression and reduced AD severity in mast cell deficient Tg(+) mice were not caused by inhibition of the IL-13 transgene (Supplemental Figure 3a).…”

Section: Discussionmentioning

confidence: 99%

TRPA1-Dependent Pruritus in IL-13–Induced Chronic Atopic Dermatitis

et al. 2013

The Journal of Immunology

173

172

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Chronic debilitating pruritus is a cardinal feature of a topic dermatitis (AD). Little is known about the underlying mechanisms. Antihistamines lack efficacy in treating itch in AD, suggesting the existence of histamine-independent itch pathways in AD. Transient receptor potential ankyrin 1 (TRPA1) is essential in the signaling pathways that promote histamine-independent itch. In the present study, we tested the hypothesis that TRPA1-dependent neural pathways play a key role in chronic itch in AD using an IL-13 transgenic mouse model of AD. In these mice, IL-13 causes chronic AD characterized by intensive chronic itch associated with markedly enhanced growth of dermal neuropeptide-secreting afferent nerve fibers and enhanced expression of TRPA1 in dermal sensory nerve fibers, their dorsal root ganglia, and mast cells. Inhibition of TRPA1 with a specific antagonist in these mice selectively attenuated itch-evoked scratching. Genetic deletion of mast cells in these mice led to significantly diminished itch-scratching behaviors and reduced TRPA1 expression in dermal neuropeptide containing afferents in the AD skin. Interestingly, IL-13 strongly stimulates TRPA1 expression, which is functional in calcium mobilization in mast cells. In accordance with these observations in the AD mice, TRPA1 expression was highly enhanced in the dermal afferent nerves, mast cells, and the epidermis in the lesional skin biopsies from patients with AD, but not in the skin from normal subjects. These studies demonstrate a novel neural mechanism underlying chronic itch in AD and highlight the complex interactions among TRPA1+ dermal afferent nerves and TRPA1+ mast cells in a Th2-dominated inflammatory environment.

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“…This growth factor is involved in the induction of Schwann cell proliferation, production of extracellular matrix, and regulation of the synthesis of cell adhesion molecules (see Unsicker and Strelau, 2000). Stark et al (2001b) detected TGF-b, the TGF-b receptors RI and RII, in peripheral nerves and mechanoreceptors, localized in the inner-core lamellar cells of cat Pacinian corpuscles and the lamellar cells of Meissner corpuscles. The function of these molecules in mechanoreceptors remains to be elucidated.…”

Section: Growth Factor Other Thanmentioning

confidence: 95%

The Meissner and Pacinian sensory corpuscles revisited new data from the last decade

Vega

García‐Suárez

Montano

et al. 2008

Microscopy Res & Technique

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This article reviews the biochemical, physiological, and experimental data cumulated during the last decade on the Meissner and Pacinian corpuscles. It includes information about (i) the localization of molecules recently detected in sensory corpuscles; (ii) the unsolved problem of the accessory fibers in sensory corpuscles and the occurrence of myelin within them; (iii) the development of sensory corpuscles, especially their neuronal and growth factor dependency; (iv) the composition and functional significance of the extracellular matrix as an essential part of the mechanisms involved in the genesis of the stimuli generated in sensory corpuscles; (v) the molecular basis of mechanotransduction; (vi) a miscellaneous section containing sparse new data on the protein composition of sensory corpuscles, as well as in the proteins involved in live-death cell decisions; (vii) the changes in sensory corpuscles as a consequence of aging, the central, or peripheral nervous system injury; and finally, (viii) the special interest of Meissner corpuscles and Pacinian corpuscles for pathologists for the diagnosis of some peripheral neuropathies and neurodegenerative diseases.

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Distribution of TGF-β, the TGF-β type I receptor and the R-II receptor in peripheral nerves and mechanoreceptors; observations on changes after traumatic injury

Cited by 31 publications

References 39 publications

Proteomics study of neuropathic and nonneuropathic dorsal root ganglia: altered protein regulation following segmental spinal nerve ligation injury

Proteomics study of neuropathic and nonneuropathic dorsal root ganglia: altered protein regulation following segmental spinal nerve ligation injury

TRPA1-Dependent Pruritus in IL-13–Induced Chronic Atopic Dermatitis

The Meissner and Pacinian sensory corpuscles revisited new data from the last decade

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