An Update on Wound Healing and the Nervous System

Hanna, Kasandra R.; Katz, Adam J.

doi:10.1097/sap.0b013e31822284de

Cited by 11 publications

(8 citation statements)

References 42 publications

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“…Based on these, we have predicted that cell-environment interactions and intracellular damage processing activities represent two large classes of signals that may induce the neural activities in both TNBC and NTNBC, with TNBC having substantially more interactions between neural and non-neural functions than in NTNBC. Furthermore, we have provided evidence regarding how neural functions might have driven different immune responses in the two subtypes of breast cancer, knowing the leading roles of neural functions in organ development and tissue repair, as well as in modulating immunity response and cell proliferation [43][44][45][46][47][48] . Figure 5 summarizes the cross-talks between different neural and non-neural functions in TNBC and NTNBC.…”

Section: Discussionmentioning

confidence: 99%

“…Bioinformatics techniques provide novel angles through systematic comparative analyses of gene-expression data of cancers of different subtypes. It has been widely accepted that neural functions are indispensable in tissue repair 43,[45][46][47] . For example, tissue repair in patients with nerve damages or spinal cord www.nature.com/scientificreports www.nature.com/scientificreports/ injury tends to be slow 35 .…”

Section: Discussionmentioning

confidence: 99%

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Neural Functions Play Different Roles in Triple Negative Breast Cancer (TNBC) and non-TNBC

Tan

Huang

et al. 2020

Sci Rep

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Triple negative breast cancer (TNBC) represents the most malignant subtype of breast cancer, and yet our understanding about its unique biology remains elusive. We have conducted a comparative computational analysis of transcriptomic data of TNBC and non-TNBC (NTNBC) tissue samples from the TCGA database, focused on genes involved in neural functions. Our main discoveries are: (1) while both subtypes involve neural functions, TNBC has substantially more up-regulated neural genes than NTNBC, suggesting that TNBC is more complex than NTNBC; (2) non-neural functions related to cellmicroenvironment interactions and intracellular damage processing are key inducers of the neural genes in both TNBC and NTNBC, but the inducer-responder relationships are different in the two cancer subtypes; (3) key neural functions such as neural crest formation are predicted to enhance adaptive immunity in TNBC while glia development, along with a few other neural functions, induce both innate and adaptive immunity in NTNBC. These results reveal key differences in the biology between the two cancer subtypes, particularly in terms of the roles that neural functions play. Our findings may open new doors for further investigation of the distinct biology of TNBC vs. NTNBC.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Neural Functions Play Different Roles in Triple Negative Breast Cancer (TNBC) and non-TNBC

Tan

Huang

et al. 2020

Sci Rep

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“…However, as disruption of versican, the extracellular matrix produced by the subset of nociceptors that mediates hyperalgesic priming (Bogen et al ., ; Joseph & Levine, ), attenuates the prolongation of the PGE 2 ‐induced hyperalgesia, suggesting that the elements involved in this signaling pathway are located in the terminal of the sensory neuron, it is possible that its impact on the development of changes in the nociceptor is even stronger and can, therefore, also contribute to the transition from acute to chronic pain. Another possible contribution could be in the role of the peripheral nervous system in terms of wound healing (Brain, ; Schaffer et al ., ; Scott et al ., ; Hanna & Katz, ) and its other trophic influences on the tissue it innervates (Ansel et al ., ; Peters et al ., ; Jarvikallio et al ., ; Roosterman et al ., ; Saraceno et al ., ). The elucidation of these other influences of the cAMP–adenosine extracellular mechanisms remains to be established.…”

Section: Discussionmentioning

confidence: 99%

Role of a novel nociceptor autocrine mechanism in chronic pain

Ferrari

Levine

2013

Eur J of Neuroscience

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We have previously shown, in the rat, that neuropathic and inflammatory events produce a neuroplastic change in nociceptor function whereby a subsequent exposure to a proinflammatory mediator (e.g. prostaglandin E2 ; PGE2 ) produces markedly prolonged mechanical hyperalgesia. While the initial approximately 30 min of this prolonged PGE2 hyperalgesia remains PKA-dependent, it subsequently switches to become dependent on protein kinase C epsilon (PKCε). In this study we tested the hypothesis that the delayed onset, PKCε-mediated, component of PGE2 hyperalgesia is generated by the active release of a nucleotide from the peripheral terminal of the primed nociceptor and this nucleotide is then metabolized to produce adenosine, which acts on a Gi-coupled A1 adenosine receptor on the nociceptor to generate PKCε-dependent hyperalgesia. We report that inhibitors of ATP-binding cassette transporters, of ecto-5'-phosphodiesterase and ecto-5'nucleotidase (enzymes involved in the metabolism of cyclic nucleotides to adenosine) and of A1 adenosine receptors each eliminated the late, but not the early, phase of PGE2 -induced hyperalgesia in primed animals. A second model of chronic pain induced by transient attenuation of G-protein-coupled receptor kinase 2, in which the prolongation of PGE2 hyperalgesia is not PKCε-dependent, was not attenuated by inhibitors of any of these mechanisms. Based on these results we propose a contribution of an autocrine mechanism, in the peripheral terminal of the nociceptor, in the hyperalgesic priming model of chronic pain.

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“…Nevertheless, the muscle damage itself may promote the signaling activities to trigger regeneration of the myometrium. The synthesis and release of signaling molecules, initiated by neurotransmitters and neurofibres, after the cellular damage, can prompt itself the cell activation, inducing muscle regeneration and healing [9]. After the muscle damage, the biological "injury-repair-regeneration" sequence leads to complete functional recovery during the days or weeks after the initial injury [10].…”

Section: Physiology Of Uterine Muscle Repairmentioning

confidence: 99%

Myoma pseudocapsule - a biological and surgical structure to respect during myomectomy

Tinelli¹,

Sparić

2020

Srp Arh Celok Lek

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Uterine fibroids affect almost one in two patients, causing many pelvic problems and requiring pharmacologic and surgical treatment. For many years, the importance of the fibroid was emphasized as uterine pathology, without focusing on the complex myometrial biology peripheral to fibroid. Moreover, the traditional surgical technique in fibroid removal has not been investigated for years. In recent years, on the contrary, morphological, neuroendocrine and anatomical studies have demonstrated the importance of a biological and surgical structure surrounding myoma, rich in neurotransmitters and neurofibres, the myoma pseudocapsule. This structure is formed in the womb peripheral to fibroid onset, it separates the fibroid from the myometrium and acts as a tissue regenerator after the removal of the fibroid from the uterus. The translation of scientific research on pseudocapsules into surgical practice has allowed us to identify new techniques of myomectomy, removing the myoma inside the pseudocapsule and promoting the pseudocapsules sparing surgery. All this to favor the subsequent biological process of uterine scarring and healing, by activating the neurotransmitters and neurofibres present in the myometrial fovea. The correct healing after fibroid removal restores the uterine anatomy, with a positive impact on subsequent reproductive function, reducing problems related to the muscle scar.

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An Update on Wound Healing and the Nervous System

Cited by 11 publications

References 42 publications

Neural Functions Play Different Roles in Triple Negative Breast Cancer (TNBC) and non-TNBC

Neural Functions Play Different Roles in Triple Negative Breast Cancer (TNBC) and non-TNBC

Role of a novel nociceptor autocrine mechanism in chronic pain

Myoma pseudocapsule - a biological and surgical structure to respect during myomectomy

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