The influence of traumatic spinal cord injury on expression of transforming growth factor-(TGF)-b1 and platelet-derived growth factor (PDGF)-A in cutaneous wound healing in rats

Abstract Background Collagen is the most abundant structural protein in the mammalian connective tissue and represents approximately 30% of animal protein. The current study evaluated the potential capacity of collagen extract derived from Nile tilapia skin in improving the cutaneous wound healing in rats and investigated the underlying possible mechanisms. A rat model was used, and the experimental design included a control group (CG) and the tilapia collagen treated group (TCG). Full-thickness wounds were conducted on the back of all the rats under general anesthesia, then the tilapia collagen extract was applied topically on the wound area of TCG. Wound areas of the two experimental groups were measured on days 0, 3, 6, 9, 12, and 15 post-wounding. The stages of the wound granulation tissues were detected by histopathologic examination and the expression of vascular endothelial growth factor (VEGF), and transforming growth factor (TGF-ß1) were investigated using immunohistochemistry. Moreover, relative gene expression analysis of transforming growth factor-beta (TGF-ß1), basic fibroblast growth factor (bFGF), and alpha-smooth muscle actin (α-SMA) were quantified by real-time qPCR. Results The histopathological assessment showed noticeable signs of skin healing in TCG compared to CG. Immunohistochemistry results revealed remarkable enhancement in the expression levels of VEGF and TGF-β1 in TCG. Furthermore, TCG exhibited marked upregulation in the VEGF, bFGF, and α-SMA genes expression. These findings suggested that the topical application of Nile tilapia collagen extract can promote the cutaneous wound healing process in rats, which could be attributed to its stimulating effect on recruiting and activating macrophages to produce chemotactic growth factors, fibroblast proliferation, and angiogenesis. Conclusions The collagen extract could, therefore, be a potential biomaterial for cutaneous wound healing therapeutics.

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Transforming Growth Factor Transforms Astrocytes to a Growth-Supportive Phenotype after Spinal Cord Injury

Journal of Neuroscience ◽

10.1523/jneurosci.3441-11.2011 ◽

2011 ◽

Vol 31 (42) ◽

pp. 15173-15187 ◽

Cited By ~ 47

Author(s):

R. E. White ◽

M. Rao ◽

J. C. Gensel ◽

D. M. McTigue ◽

B. K. Kaspar ◽

...

Keyword(s):

Spinal Cord ◽

Spinal Cord Injury ◽

Growth Factor ◽

Transforming Growth Factor ◽

Cord Injury

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Transforming Growth Factor Beta Signaling in Cutaneous Wound Healing: Lessons Learned from Animal Studies

Advances in Wound Care ◽

10.1089/wound.2012.0419 ◽

2013 ◽

Vol 2 (5) ◽

pp. 225-237 ◽

Cited By ~ 52

Author(s):

Kenneth W. Finnson ◽

Praveen R. Arany ◽

Anie Philip

Keyword(s):

Wound Healing ◽

Growth Factor ◽

Transforming Growth Factor Beta ◽

Animal Studies ◽

Transforming Growth Factor ◽

Lessons Learned ◽

Cutaneous Wound Healing ◽

Cutaneous Wound ◽

Growth Factor Beta

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The role of thrombospondin-1 and transforming growth factor-β after spinal cord injury in the rat

Journal of Clinical Neuroscience ◽

10.1016/j.jocn.2008.09.014 ◽

2009 ◽

Vol 16 (6) ◽

pp. 818-821 ◽

Cited By ~ 19

Author(s):

Xianghua Wang ◽

Weiping Chen ◽

Wangmi Liu ◽

Jiayan Wu ◽

Yanqi Shao ◽

...

Keyword(s):

Spinal Cord ◽

Spinal Cord Injury ◽

Growth Factor ◽

Transforming Growth Factor ◽

Transforming Growth Factor Β ◽

Cord Injury ◽

Thrombospondin 1

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WOUND-HEALING PROPERTIES OF TRANSFORMING GROWTH FACTOR β (TGF-β) INDUCIBLE EARLY GENE 1 (TIEG1) KNOCKOUT MICE

Journal of Musculoskeletal Research ◽

10.1142/s0218957708002012 ◽

2008 ◽

Vol 11 (02) ◽

pp. 63-69 ◽

Cited By ~ 8

Author(s):

Manabu Taguchi ◽

Steven L. Moran ◽

Mark E. Zobitz ◽

Chunfeng Zhao ◽

Malayannan Subramaniam ◽

...

Keyword(s):

Wound Healing ◽

Growth Factor ◽

Transforming Growth Factor Beta ◽

Knockout Mice ◽

Transforming Growth Factor ◽

Breaking Strength ◽

Healing Process ◽

Early Gene ◽

Cutaneous Wound Healing ◽

Cutaneous Wound

Transforming growth factor beta (TGF-β) has a broad effect on wound healing, but many questions remain about the regulation of TGF-β during the healing process. TGF-β inducible early gene 1 (TIEG1) is a primary response gene for TGF-β that controls the activities of the TGF-β/Smad pathway, the primary TGF-β signaling pathway. The purpose of this study was to investigate the role of TIEG1 in cutaneous wound healing using TIEG1 knockout mice. The wound healing in TIEG1 knockout mice and wild-type controls was evaluated by wound breaking strength, Western blot, and histology at postoperative days 3, 7, and 14. Although re-epithelialization of both groups was similarly complete at day 7, the TIEG1 knockout mice had a significantly lower wound breaking strength than the controls at postoperative day 14. These results suggest that TIEG1 expression may be an important factor involved in the initiation and support of normal cutaneous wound healing.

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Dynamics of biomarkers across the stages of traumatic spinal cord injury - implications for neural plasticity and repair

Restorative Neurology and Neuroscience ◽

10.3233/rnn-211169 ◽

2021 ◽

pp. 1-28

Author(s):

Tatjana. Begenisic ◽

Chiara. Pavese ◽

Beatrice. Aiachini ◽

Antonio. Nardone ◽

Daniela. Rossi

Keyword(s):

Spinal Cord ◽

Spinal Cord Injury ◽

Growth Factor ◽

Neural Plasticity ◽

Functional Improvement ◽

Traumatic Spinal Cord Injury ◽

Altered Expression ◽

Pubmed Database ◽

Cord Injury ◽

Selection Of

Background: Traumatic spinal cord injury (SCI) is a complex medical condition causing significant physical disability and psychological distress. While the adult spinal cord is characterized by poor regenerative potential, some recovery of neurological function is still possible through activation of neural plasticity mechanisms. We still have limited knowledge about the activation of these mechanisms in the different stages after human SCI. Objective: In this review, we discuss the potential role of biomarkers of SCI as indicators of the plasticity mechanisms at work during the different phases of SCI. Methods: An extensive review of literature related to SCI pathophysiology, neural plasticity and humoral biomarkers was conducted by consulting the PubMed database. Research and review articles from SCI animal models and SCI clinical trials published in English until January 2021 were reviewed. The selection of candidates for humoral biomarkers of plasticity after SCI was based on the following criteria: 1) strong evidence supporting involvement in neural plasticity (mandatory); 2) evidence supporting altered expression after SCI (optional). Results: Based on selected findings, we identified two main groups of potential humoral biomarkers of neural plasticity after SCI: 1) neurotrophic factors including: Brain derived neurotrophic factor (BDNF), Nerve growth factor (NGF), Neurotrofin-3 (NT-3), and Insulin-like growth factor 1 (IGF-1); 2) other factors including: Tumor necrosis factor-alpha (TNF-α), Matrix Metalloproteinases (MMPs), and MicroRNAs (miRNAs). Plasticity changes associated with these biomarkers often can be both adaptive (promoting functional improvement) and maladaptive. This dual role seems to be influenced by their concentrations and time-window during SCI. Conclusions: Further studies of dynamics of biomarkers across the stages of SCI are necessary to elucidate the way in which they reflect the remodeling of neural pathways. A better knowledge about the mechanisms underlying plasticity could guide the selection of more appropriate therapeutic strategies to enhance positive spinal network reorganization.

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