Chondroitin Sulfate in Palatal Wound Healing

2004 ◽  
Vol 83 (11) ◽  
pp. 880-885 ◽  
Author(s):  
X.H. Zou ◽  
W.C. Foong ◽  
T. Cao ◽  
B.H. Bay ◽  
H.W. Ouyang ◽  
...  

Chondroitin sulfate is up-regulated in granulation tissue during wound healing. To investigate the role of chondroitin sulfate in the wound-healing process after surgical repair of cleft palate, we isolated and cultured rabbit palatal fibroblasts. Treatment with chondroitin-6-sulfate resulted in a dose-dependent increase in cell adhesion and cell proliferation, whereas the reverse effects were seen after chondroitinase degradation of chondroitin sulfate. The biological actions of chondroitin sulfate appeared to be dependent on the presence and position of sulfate groups. Inhibition of glycosaminoglycan sulfation by chlorate treatment led to reduced cell adhesion and cell proliferation and a slower rate of wound closure in vitro. Furthermore, exposure to chondroitin-4-sulfate resulted in a dose-dependent reduction in cell adhesion. Together, these results show that chondroitin sulfate is involved in palatal wound healing.

2021 ◽  
Vol 165 ◽  
pp. 39
Author(s):  
Francesca Lombardi ◽  
Silvano Santini ◽  
Paola Palumbo ◽  
Valeria Cordone ◽  
Virginio Bignotti ◽  
...  

2020 ◽  
Author(s):  
Daisuke Ito ◽  
Hiroyasu Ito ◽  
Takayasu Ideta ◽  
Ayumu Kanbe ◽  
Soranobu Ninomiya ◽  
...  

Abstract Background The skin wound healing process is regulated by various cytokines, chemokines, and growth factors. Recent reports have demonstrated that spermine/spermidine (SPD) promote wound healing through urokinase-type plasminogen activator (uPA)/uPA receptor (uPAR) signaling in vitro. Here, we investigated whether the systemic and topical administration of SPD would accelerate the skin wound-repair process in vivo.Methods A skin wound repair model was established using C57BL/6 J mice. SPD was mixed with white petrolatum for topical administration. For systemic administration, SPD mixed with drinking water was orally administered. Changes in wound size over time were calculated using digital photography.Results Systemic and topical SPD treatment significantly accelerated skin wound healing. The administration of SPD promoted the uPA/uPAR pathway in wound sites. Moreover, topical treatment with SPD enhanced the expression of IL-6 and TNF-α in wound sites. Scratch and cell proliferation assays revealed that SPD administration accelerated scratch wound closure and cell proliferation in vitro.Conclusion These results indicate that treatment with SPD promotes skin wound healing through activation of the uPA/uPAR pathway and induction of the inflammatory response in wound sites. The administration of SPD might contribute to new effective treatments to accelerate skin wound healing.


2021 ◽  
Author(s):  
Mary Yinghua Zhang ◽  
Shuyi Fang ◽  
Hongyu Gao ◽  
Xiaoli Zhang ◽  
Dongsheng Gu ◽  
...  

ABSTRACTWe report our discovery of an important player in the development of skin fibrosis, a hallmark of scleroderma. Scleroderma is a fibrotic disease, affecting 70,000 to 150,000 Americans. Fibrosis is a pathological wound healing process that produces an excessive extracellular matrix to interfere with normal organ function. Fibrosis contributes to nearly half of human mortality. Scleroderma has heterogeneous phenotypes, unpredictable outcomes, no validated biomarkers, and no effective treatment. Thus, strategies to slow down scleroderma progression represent an urgent medical need. While a pathological wound healing process like fibrosis leaves scars and weakens organ function, oral mucosa wound healing is a scarless process. After re-analyses of gene expression datasets from oral mucosa wound healing and skin fibrosis, we discovered that several pathways constitutively activated in skin fibrosis are transiently induced during oral mucosa wound healing process, particularly the amphiregulin (Areg) gene. Areg expression is upregulated ~10 folds 24hrs after oral mucosa wound but reduced to the basal level 3 days later. During bleomycin-induced skin fibrosis, a commonly used mouse model for skin fibrosis, Areg is up-regulated throughout the fibrogenesis and is associated with elevated cell proliferation in the dermis. To demonstrate the role of Areg for skin fibrosis, we used mice with Areg knockout, and found that Areg deficiency essentially prevents bleomycin-induced skin fibrosis. We further determined that bleomycin-induced cell proliferation in the dermis was not observed in the Areg null mice. Furthermore, we found that inhibiting MEK, a downstream signaling effector of Areg, by selumetinib also effectively blocked bleomycin-based skin fibrosis model. Based on these results, we concluded that the Areg-EGFR-MEK signaling axis is critical for skin fibrosis development. Blocking this signaling axis may be effective in treating scleroderma.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Mary Yinghua Zhang ◽  
Shuyi Fang ◽  
Hongyu Gao ◽  
Xiaoli Zhang ◽  
Dongsheng Gu ◽  
...  

AbstractWe report our discovery of an important player in the development of skin fibrosis, a hallmark of scleroderma. Scleroderma is a fibrotic disease, affecting 70,000 to 150,000 Americans. Fibrosis is a pathological wound healing process that produces an excessive extracellular matrix to interfere with normal organ function. Fibrosis contributes to nearly half of human mortality. Scleroderma has heterogeneous phenotypes, unpredictable outcomes, no validated biomarkers, and no effective treatment. Thus, strategies to slow down scleroderma progression represent an urgent medical need. While a pathological wound healing process like fibrosis leaves scars and weakens organ function, oral mucosa wound healing is a scarless process. After re-analyses of gene expression datasets from oral mucosa wound healing and skin fibrosis, we discovered that several pathways constitutively activated in skin fibrosis are transiently induced during oral mucosa wound healing process, particularly the amphiregulin (Areg) gene. Areg expression is upregulated ~ 10 folds 24hrs after oral mucosa wound but reduced to the basal level 3 days later. During bleomycin-induced skin fibrosis, a commonly used mouse model for skin fibrosis, Areg is up-regulated throughout the fibrogenesis and is associated with elevated cell proliferation in the dermis. To demonstrate the role of Areg for skin fibrosis, we used mice with Areg knockout, and found that Areg deficiency essentially prevents bleomycin-induced skin fibrosis. We further determined that bleomycin-induced cell proliferation in the dermis was not observed in the Areg null mice. Furthermore, we found that inhibiting MEK, a downstream signaling effector of Areg, by selumetinib also effectively blocked bleomycin-based skin fibrosis model. Based on these results, we concluded that the Areg-EGFR-MEK signaling axis is critical for skin fibrosis development. Blocking this signaling axis may be effective in treating scleroderma.


Pharmaceutics ◽  
2019 ◽  
Vol 11 (12) ◽  
pp. 631 ◽  
Author(s):  
Paola Franco ◽  
Raffaella Belvedere ◽  
Emanuela Pessolano ◽  
Sara Liparoti ◽  
Roberto Pantani ◽  
...  

In this work, a one-shot process for the simultaneous foaming of polycaprolactone (PCL) and impregnation of mesoglycan (MSG) into the porous structure was successfully attempted. Supercritical carbon dioxide plays the role of the foaming agent with respect to PCL and of the solvent with respect to MSG. The main objective is to produce an innovative topical device for application on skin lesions, promoting prolonged pro-resolving effects. The obtained device offers a protective barrier to ensure a favorable and sterilized environment for the wound healing process. The impregnation kinetics revealed that a pressure of 17 MPa, a temperature of 35 °C, and a time of impregnation of 24 h assured a proper foaming of PCL in addition to the impregnation of the maximum amount of MSG; i.e., 0.22 mgMSG/mgPCL. After a preliminary study conducted on PCL granules used as brought, the MSG impregnation was performed at the optimized process conditions also on a PCL film, produced by compression molding, with the final goal of producing medical patches. Comparing the dissolution profiles in phosphate buffered saline solution (PBS) of pure MSG and MSG impregnated on foamed PCL, it was demonstrated that the release of MSG was significantly prolonged up to 70 times. Next, we performed functional assays of in vitro wound healing, cell invasion, and angiogenesis to evaluate the biological effects of the PCL-derived MSG. Interestingly, we found the ability of this composite system to promote the activation of human keratinocytes, fibroblasts, and endothelial cells, as the main actors of tissue regeneration, confirming what we previously showed for the MSG alone.


2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Daisuke Ito ◽  
Hiroyasu Ito ◽  
Takayasu Ideta ◽  
Ayumu Kanbe ◽  
Soranobu Ninomiya ◽  
...  

Abstract Background The skin wound healing process is regulated by various cytokines, chemokines, and growth factors. Recent reports have demonstrated that spermine/spermidine (SPD) promote wound healing through urokinase-type plasminogen activator (uPA)/uPA receptor (uPAR) signaling in vitro. Here, we investigated whether the systemic and topical administration of SPD would accelerate the skin wound-repair process in vivo. Methods A skin wound repair model was established using C57BL/6 J mice. SPD was mixed with white petrolatum for topical administration. For systemic administration, SPD mixed with drinking water was orally administered. Changes in wound size over time were calculated using digital photography. Results Systemic and topical SPD treatment significantly accelerated skin wound healing. The administration of SPD promoted the uPA/uPAR pathway in wound sites. Moreover, topical treatment with SPD enhanced the expression of IL-6 and TNF-α in wound sites. Scratch and cell proliferation assays revealed that SPD administration accelerated scratch wound closure and cell proliferation in vitro. Conclusion These results indicate that treatment with SPD promotes skin wound healing through activation of the uPA/uPAR pathway and induction of the inflammatory response in wound sites. The administration of SPD might contribute to new effective treatments to accelerate skin wound healing.


Author(s):  
Nermin Topaloglu Avsar ◽  
Ufuk Balkaya ◽  
Ziysan Buse Yarali Cevik

Photobiomodulation is a practical and noninvasive treatment that triggers cell proliferation, cell differentiation, wound healing, new tissue formation, inflammation and pain reduction with low-level light therapy. Light-emitting diodes (LEDs) are energy-saving, affordable and safe alternatives to laser devices which are recently preferred in photobiomodulation. Although the wavelengths between 600-700 nm are most preferred ones, there is a lack of practical optical systems which study this mechanism in vitro with different wavelengths simultaneously. In this study, a portable and remotely controlled multicolor LED-based system was designed and tested on the wound healing process of human keratinocytes by irradiating the cells homogenously with 3 different wavelengths (460-475 nm as blue, 515-535 nm as green, and 585-595 nm as orange) on different experimental groups at the same time. Its proliferative and wound healing effect was evaluated with cell viability (MTT) analysis and cell migration (scratch) assay, respectively. It was observed that orange-LEDs were designated as the most triggering wavelength in terms of cell proliferation. Also, it was revealed with this device that different wavelengths can reach the intended accelerated wound healing process, so this optical system will be an advantageous design for future practical photobiomodulation studies in vitro.


2021 ◽  
Vol 7 (2) ◽  
pp. 295-298
Author(s):  
Jana Markhoff ◽  
Andreas Brietzke ◽  
Niels Grabow

Abstract In vitro wound healing assays are a suitable application to verify the efficiency of pharmaceuticals or growth factors that will be incorporated in or immobilized to e.g. electrospun biomaterials for wound dressings or other biological devices in advance. Thereby, various factors like culture conditions or cell density influence the specific cell proliferation. Hence, to establish a wound healing assay for various cell types, a stepwise adaptation of cell numbers was done for better estimation and comparison of cell density for the validation of the influence of drugs on the wound healing process. Cell proliferation of different tissue relevant cell types was evaluated by impedance measurements and live cell imaging. Cell numbers could be successfully adapted for assay specific cell densities. In general, a universal comparison of biological or chemical materials and agents in vitro may require the creation of appropriate ISO or OECD standards for a consistent and cell specific adaptation or demand of initial cell density.


2021 ◽  
Author(s):  
Nermin Topaloglu ◽  
Ufuk Balkaya ◽  
Ziyşan Buse Yaralı Çevik

Abstract Photobiomodulation is a practical and non-invasive treatment that triggers cell proliferation, cell differentiation, wound healing, new tissue formation, inflammation and pain reduction with low-level light therapy. Light-emitting diodes (LEDs) are energy-saving, affordable and safe alternatives to laser devices which are recently preferred in photobiomodulation. Although the wavelengths between 600-700 nm are most preferred ones, there is a lack of practical optical systems which study this mechanism in vitro with different wavelengths simultaneously. In this study, a portable and remotely controlled multicolor LED-based system was designed and tested on the wound healing process of human keratinocytes by irradiating the cells homogenously with 3 different wavelengths (460-475 nm as blue, 515-535 nm as green, and 585-595 nm as orange) on different experimental groups at the same time. Its proliferative and wound healing effect was evaluated with cell viability (MTT) analysis and cell migration (scratch) assay, respectively. It was observed that orange-LEDs were designated as the most triggering wavelength in terms of cell proliferation. Also, it was revealed with this device that different wavelengths can reach the intended accelerated wound healing process, so this optical system will be an advantageous design for future practical photobiomodulation studies in vitro.


2021 ◽  
Author(s):  
Nermin Topaloglu ◽  
Ufuk Balkaya ◽  
Ziyşan Buse Yaralı Çevik

Abstract Photobiomodulation is a practical and non-invasive treatment that triggers cell proliferation, cell differentiation, wound healing, new tissue formation, inflammation and pain reduction with low-level light therapy. Light-emitting diodes (LEDs) are energy-saving, affordable and safe alternatives to laser devices which are recently preferred in photobiomodulation. Although the wavelengths between 600–700 nm are most preferred ones, there is a lack of practical optical systems which study this mechanism in vitro with different wavelengths simultaneously. In this study, a portable and remotely controlled multicolor LED-based system was designed and tested on the wound healing process of human keratinocytes by irradiating the cells homogenously with 3 different wavelengths (460–475 nm as blue, 515–535 nm as green, and 585–595 nm as orange) on different experimental groups at the same time. Its proliferative and wound healing effect was evaluated with cell viability (MTT) analysis and cell migration (scratch) assay, respectively. It was observed that orange-LEDs were designated as the most triggering wavelength in terms of cell proliferation. Also, it was revealed with this device that different wavelengths can reach the intended accelerated wound healing process, so this optical system will be an advantageous design for future practical photobiomodulation studies in vitro.


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