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      Therapeutics and Clinical Risk Management (submit here)

      This international, peer-reviewed Open Access journal by Dove Medical Press focuses on reporting of clinical studies, outcomes and safety in all therapeutic areas and surgical intervention areas. Sign up for email alerts here.

      34,006 Monthly downloads/views I 2.755 Impact Factor I 4.5 CiteScore I 1.0 Source Normalized Impact per Paper (SNIP) I 0.598 Scimago Journal & Country Rank (SJR)

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      The expressions of NGF and VEGF in the fracture tissues are closely associated with accelerated clavicle fracture healing in patients with traumatic brain injury

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          Abstract

          Background

          Angiogenesis and bone formation are vital for fracture healing. Nerve growth factor (NGF) not only promotes neuronal survival but also enhances the proliferation and differentiation of osteoblasts. Vascular endothelial growth factor (VEGF) plays an important role in angiogenesis. However, the potential correlation of NGF and VEGF levels with fracture healing in patients with traumatic brain injury (TBI) remains unclear.

          Methods

          This study enrolled 22 patients with clavicle fracture and concomitant TBI (CFT group) and 25 patients with clavicle fracture alone (CF group). Serum NGF levels were measured with ELISA. The expressions of NGF, VEGF, and CD31 in callus tissues were measured with immunohistochemistry.

          Results

          The fracture healing time in CFT group (82.22±13.61 days) was significantly shorter than that in CF group (127±25.05 days; P<0.001). The expression of CD31, marker of blood vessels, in callus tissues of CFT group was higher compared with that of CF group. Serum NGF levels and the expression of NGF in callus tissues of CFT group were higher than those in CF group ( P<0.01). The expressions of CD31, NGF, and VEGF are correlated with shorter fracture healing time.

          Conclusion

          The formation of blood vessels was increased in CFT group compared with CF group. NGF and VEGF levels were higher in CFT group than in CF group and correlated with shorter fracture healing time. Accelerated fracture healing in patients with TBI may be due to NGF- and VEGF-mediated angiogenesis at the fracture site.

          Most cited references30

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          Roles of VEGF-A signalling in development, regeneration, and tumours.

          Ken-ichi Matsumoto, Masatsugu Ema (2014)
          Angiogenesis, the formation of new networks of blood vessels, has essential roles in embryonic development, organ homeostasis and disease progression. Several signalling molecules, such as vascular endothelial growth factors (VEGFs), fibroblast growth factors (FGFs), transforming growth factor (TGF)-β and angiopoietin-1 and 2, are known to be key regulators of blood vessel development and network patterning. Among these, the roles of VEGF-A and its receptors in vessel morphogenesis are understood best. VEGF-A signalling plays a crucial role in embryonic development through the regulation of angiogenesis. VEGF-A regulates most of the endothelial response, such as the proliferation and migration of endothelial cells (ECs), vascular permeability and the selection of tip and stalk cells. VEGF-A signalling also regulates organ homeostasis in adults. If an organ is exposed to severe injury, VEGF-A induces the release of paracrine factors from ECs, which increase the rate of regeneration of the organ. VEGF-A signalling also has an important role in the progression of angiogenesis-related diseases, especially cancer. Consequently, many agents that block VEGF-A have been developed and reported as useful tools for the inhibition of the growth and metastatic spread of tumours. Here, we summarize recent reports of the multiple functions of VEGF-A signalling during development, organ regeneration and tumour progression.
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            The Role of the Immune Cells in Fracture Healing

            Gurpreet Baht, Linda Vi, Benjamin Alman (2018)
            Purpose of review Bone fracture healing is a complex physiological process relying on numerous cell types and signals. Inflammatory factors secreted by immune cells help to control recruitment, proliferation, differentiation, and activation of hematopoietic and mesenchymal cells. Within this review we will discuss the functional role of immune cells as it pertains to bone fracture healing. In doing so, we will outline the cytokines secreted and their effects within the healing fracture callus. Recent findings Macrophages have been found to play an important role in fracture healing. These immune cells signal to other cells of the fracture callus, modulating bone healing. Summary Cytokines and cellular signals within fracture healing continue to be studied. The findings from this work have helped to reinforce the importance of osteoimmunity in bone fracture healing. Owing to these efforts, immunomodulation is emerging as a potential therapeutic target to improve bone fracture healing.
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              NGF and Its Receptors in the Regulation of Inflammatory Response

              Gaetana Minnone, Fabrizio De Benedetti, Luisa Bracci-Laudiero (2017)
              There is growing interest in the complex relationship between the nervous and immune systems and how its alteration can affect homeostasis and result in the development of inflammatory diseases. A key mediator in cross-talk between the two systems is nerve growth factor (NGF), which can influence both neuronal cell function and immune cell activity. The up-regulation of NGF described in inflamed tissues of many diseases can regulate innervation and neuronal activity of peripheral neurons, inducing the release of immune-active neuropeptides and neurotransmitters, but can also directly influence innate and adaptive immune responses. Expression of the NGF receptors tropomyosin receptor kinase A (TrkA) and p75 neurotrophin receptor (p75NTR) is dynamically regulated in immune cells, suggesting a varying requirement for NGF depending on their state of differentiation and functional activity. NGF has a variety of effects that can be either pro-inflammatory or anti-inflammatory. This apparent contradiction can be explained by considering NGF as part of an endogenous mechanism that, while activating immune responses, also activates pathways necessary to dampen the inflammatory response and limit tissue damage. Decreases in TrkA expression, such as that recently demonstrated in immune cells of arthritis patients, might prevent the activation by NGF of regulatory feed-back mechanisms, thus contributing to the development and maintenance of chronic inflammation.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Ther Clin Risk Manag
                Journal ID (iso-abbrev): Ther Clin Risk Manag
                Journal ID (publisher-id): Therapeutics and Clinical Risk Management
                Title: Therapeutics and Clinical Risk Management
                Publisher: Dove Medical Press
                ISSN (Print): 1176-6336
                ISSN (Electronic): 1178-203X
                Publication date Collection: 2018
                Publication date (Electronic): 21 November 2018
                Volume: 14
                Pages: 2315-2322
                Affiliations
                [1 ]Department of Orthopedics, Liuzhou General Hospital, Liuzhou 545006, Guangxi, China, zr7971@ 123456126.com
                [2 ]The Department of Orthopedics, The Affiliated Liuzhou General Hospital of Guangxi University of Technology, Liuzhou 545006, Guangxi, China, zr7971@ 123456126.com
                Author notes
                Correspondence: Ran Zhang, Department of Orthopedics, Liuzhou General Hospital, 8 Wenchang Rd, Liuzhou 545006, Guangxi, China, Tel +86 138 7728 7971, Email zr7971@ 123456126.com
                Article
                Publisher ID: tcrm-14-2315
                DOI: 10.2147/TCRM.S182325
                PMC ID: 6254501
                PubMed ID: 30538487
                SO-VID: d3c0bb00-20e7-4587-9c9d-a063c69d8ddf
                Copyright statement: © 2018 Zhang et al. This work is published and licensed by Dove Medical Press Limited
                License:

                The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

                History
                Categories
                Subject: Original Research

                ScienceOpen disciplines: Medicine
                Keywords: traumatic brain injury,fracture healing,clavicle fracture,ngf,vegf,angiogenesis
                Data availability:
                ScienceOpen disciplines: Medicine
                Keywords: traumatic brain injury, fracture healing, clavicle fracture, ngf, vegf, angiogenesis

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