N2 non-thermal atmospheric pressure plasma promotes wound healing in vitro and in vivo: Potential modulation of adhesion molecules and matrix metalloproteinase-9

2017 ◽  
Vol 26 (2) ◽  
pp. 163-170 ◽  
Author(s):  
Sung Un Kang ◽  
Jae Won Choi ◽  
Jae Won Chang ◽  
Kang il Kim ◽  
Yeon Soo Kim ◽  
...  
2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Guohua Yuan ◽  
Lei Chen ◽  
Junsheng Feng ◽  
Guobin Yang ◽  
Qingwen Ni ◽  
...  

2013 ◽  
Vol 31 (15_suppl) ◽  
pp. e22103-e22103
Author(s):  
Yang Xu ◽  
Bo Hu ◽  
Robert Anders ◽  
Anirban Maitra ◽  
Jia Fan

e22103 Background: Curcumin regulates the expression and secretion of MMPs, and has potent anti-cancer properties in several human cancer cell lines and animal carcinogenesis models. In this study we try to investigate the effects of polymeric nanoparticle encapsulated formulation of curcumin– nanocurcumin (NC) on Hepatocellular carcinoma (HCC) in vitro and in vivo. Methods: The effects of NC alone and in combination with sorafenib (SO) were investigated on HCC cell lines, Huh7 and MHCCLM3 in vitro by using proliferation and invasion assay, western blot, qRT-PCR, enzyme-linked immunosorbent assay and immunohistochemistry staining, and the subcutaneous and orthotopic HCC xenograft nude mice models (MHCCLM3) were used to evaluate primary tumor growth and metastasis after treatments. Results: NC alone (or combined with SO)inhibited HCC cell proliferation (p<0.05) and invasion in vitro (p<0.01), and remarkably decreased both the subcutaneous and orthotopic primary tumor growth and lung metastases in vivo. NC and/or SO could down-regulating the expressions of Matrix Metalloproteinase-9 (MMP9), p-ERK1 and NF-kB/p65 (p<0.05). Conclusions: NC showed potent anti-invasion and metastasis properties in HCC via NF-κB mediated MMP9 down-regulation, which may provide a new strategy to the treatment of HCC patients and prevention of tumor recurrence after operation.


Viruses ◽  
2015 ◽  
Vol 7 (8) ◽  
pp. 4230-4253 ◽  
Author(s):  
Michele Kong ◽  
Richard Whitley ◽  
Ning Peng ◽  
Robert Oster ◽  
Trenton Schoeb ◽  
...  

2011 ◽  
Vol 317 (10) ◽  
pp. 1454-1464 ◽  
Author(s):  
Gilson C.N. Franco ◽  
Mikihito Kajiya ◽  
Tadashi Nakanishi ◽  
Kouji Ohta ◽  
Pedro L. Rosalen ◽  
...  

2021 ◽  
Vol 68 (4) ◽  
pp. 364-369
Author(s):  
Ha-Eun Lee ◽  
Joon-Young Kim ◽  
Soon-Wuk Jeong ◽  
Seung-Yeol Nah

AbstractIt has been shown that gintonin, isolated from Panax ginseng, can promote rapid corneal wound healing. We aimed to elucidate the underlying mechanism and investigated whether gintonin affects the concentration of the extracellular matrix remodelling factor matrix metalloproteinase-9 (MMP-9) in tears during rabbit corneal wound healing in vivo. Twelve eyes (six rabbits) were divided equally into three groups. All eyes underwent corneal de-epithelialisation. The control group received Tearin Free sodium hyaluronate 0.1%, the solcoseryl group received solcoseryl-120 concentrate, and the gintonin group received 2.5 mg gintonin in sodium hyaluronate 0.1%. All preparations were administered for 5 days and the concentration of MMP-9 was measured in tears via ELISA on days 0, 1, and 5. MMP-9 concentrations in all groups were increased at day 1 and reduced at day 5. Of note, we found a significant change over the time frame for the gintonin group (P < 0.05) but not for the control or solcoseryl groups (P > 0.05) Moreover, increased MMP-9 levels between days 0 and 1, and their reduction between days 1 and 5, were significant in the gintonin group compared to those in the other groups (P < 0.05); however, and once more, these changes were not significant between the control and solcoseryl groups (P > 0.05). In conclusion, gintonin increases the concentration of MMP-9 rapidly within a day of injury, and decreasing it thereafter.


2012 ◽  
Vol 302 (10) ◽  
pp. H1953-H1964 ◽  
Author(s):  
Jason A. Scott ◽  
Litao Xie ◽  
Hui Li ◽  
Weiwei Li ◽  
Julie B. He ◽  
...  

The multifunctional CaMKII has been implicated in vascular smooth muscle cell (VSMC) migration, but little is known regarding its downstream targets that mediate migration. Here, we examined whether CaMKII regulates migration through modulation of matrix metalloproteinase 9 (MMP9). Using CaMKIIδ−/−mice as a model system, we evaluated migration and MMP9 regulation in vitro and in vivo. After ligation of the common carotid artery, CaMKII was activated in the neointima as determined by oxidation and autophosphorylation. We found that MMP9 was robustly expressed in the neointima and adventitia of carotid-ligated wild-type (WT) mice but was barely detectable in CaMKIIδ−/−mice. The perimeter of the external elastic lamina, a correlate of migration-related outward remodeling, was increased in WT but not in CaMKIIδ−/−mice. Migration induced by serum, platelet-derived growth factor, and tumor necrosis factor-α (TNF-α) was significantly decreased in CaMKIIδ−/−as compared with WT VSMCs, but migration was rescued with adenoviral overexpression of MMP9 in CaMKIIδ−/−VSMCs. Likewise, overexpression of CaMKIIδ in CaMKIIδ−/−VSMCs increased migration, whereas an oxidation-resistant mutant of CaMKIIδ did not. TNF-α strongly induced CaMKII oxidation and autophosphorylation as well as MMP9 activity, mRNA, and protein levels in WT, but not in CaMKIIδ−/−VSMC. Surprisingly, TNF-α strongly induced MMP9 promoter activity in WT and CaMKIIδ−/−VSMC. However, the MMP9 mRNA stability was significantly decreased in CaMKIIδ−/−VSMC. Our data demonstrate that CaMKII promotes VSMC migration through posttranscriptional regulation of MMP9 and suggest that CaMKII effects on MMP9 expression may be a therapeutic pathway in vascular injury.


Blood ◽  
2012 ◽  
Vol 120 (18) ◽  
pp. 3741-3749 ◽  
Author(s):  
Sabina Adhikary ◽  
Virginia P. Kocieda ◽  
Jui-Hung Yen ◽  
Ronald F. Tuma ◽  
Doina Ganea

Abstract Administration of cannabinoid receptor 2 (CB2R) agonists in inflammatory and autoimmune disease and CNS injury models results in significant attenuation of clinical disease, and reduction of inflammatory mediators. Previous studies reported that CB2R signaling also reduces leukocyte migration. Migration of dendritic cells (DCs) to various sites is required for their activation and for the initiation of adaptive immune responses. Here, we report for the first time that CB2R signaling affects DC migration in vitro and in vivo, primarily through the inhibition of matrix metalloproteinase 9 (MMP-9) expression. Reduced MMP-9 production by DCs results in decreased migration to draining lymph nodes in vivo and in vitro in the matrigel migration assay. The effect on Mmp-9 expression is mediated through CB2R, resulting in reduction in cAMP levels, subsequent decrease in ERK activation, and reduced binding of c-Fos and c-Jun to Mmp-9 promoter activator protein 1 sites. We postulate that, by dampening production of MMP-9 and subsequent MMP-9–dependent DC migration, cannabinoids contribute to resolve acute inflammation and to reestablish homeostasis. Selective CB2R agonists might be valuable future therapeutic agents for the treatment of chronic inflammatory conditions by targeting activated immune cells, including DCs.


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