Suppression of TNF-alpha-induced MMP-9 expression by a cell-permeable superoxide dismutase in keratinocytes

Song, Ha Yong; Ju, Sung Mi; Goh, Ah Ra; Kwon, Dong-Joo; Choi, Soo Young; Park, Jinseu

doi:10.5483/bmbrep.2011.44.7.462

Cited by 20 publications

(17 citation statements)

References 24 publications

(43 reference statements)

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“…Clear bands appear on the Coomassie stained blue background in areas of gelatinolytic activity. Gels were scanned and images were processed by extraction of the blue channel signal, converting it to black and white, and inverting it for quantification of gelatinolytic activities from the integrated optical density (28).…”

Section: Measurementmentioning

confidence: 99%

Inhibition of migration and invasion of LNCaP human prostate carcinoma cells by cordycepin through inactivation of Akt

Jeong

Jin²,

Park³

et al. 2012

Int J Oncol

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Abstract. Cordycepin (3'-deoxyadenosine), a major bioactive compound of Cordyceps militaris, has many pharmacological actions, such as anti-inflammatory and anticancer activities. In this study, the relationship between inhibition of cell motility and anti-invasive activity by cordycepin in LNCaP human prostate carcinoma cells was investigated. Within the concentration range that was not cytotoxic, cordycepin time-dependently inhibited cell motility and invasiveness of LNCaP cells. The inhibitory effects of cordycepin on cell invasiveness were associated with tightening of tight junctions (TJs), which was demonstrated by an increase in transepithelial electrical resistance (TER). Immunoblotting indicated that cordycepin decreases levels of claudin proteins, which are major components of TJs that play a key role in control and selectivity of paracellular transport. Furthermore, cordycepin inhibited the expression and activity of matrix metalloproteinase (MMP)-2 and MMP-9, and simultaneously increased levels of tissue inhibitor of metalloproteinase (TIMP)-1 and TIMP-2. These effects were related to inactivation of the phosphoinositide 3-kinase (PI3K)/Akt pathway in LNCaP cells. These findings suggest that cordycepin inhibits the migration and invasion of LNCaP cells by downregulating the activity of TJs and MMPs, possibly in association with suppression of Akt activation.

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Section: Measurementmentioning

confidence: 99%

Inhibition of migration and invasion of LNCaP human prostate carcinoma cells by cordycepin through inactivation of Akt

Jeong

Jin²,

Park³

et al. 2012

Int J Oncol

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“…As a by-product of OXPHOS, mitochondria produce ROS, in the form of superoxide, as electrons leak from the electron transport chain 47 . Studies have revealed that ROS can function as a signalling molecule to regulate the transcription and functional activity of various inflammatory mediators, including MMPs 14,15,48 . We have previously shown that the paralog of Irg1l, Irg1, is required within the mitochondria of activated macrophages for enhanced utilization of fatty acids that fuels mROS production 7 .…”

Section: Mouse Epidermal Cells Upregulate Irg1 During Inflammationmentioning

confidence: 99%

“…Both the expression and activity of MMPs has been shown to be directly regulated by mROS 14 . Furthermore, tumour necrosis factor alpha (TNF-a)-driven MMP9 expression within human keratinocytes is ROS-dependent 15 . Collectively, these data suggest mROS production within keratinocytes may promote leukocyte migration through regulation of MMP activity.…”

mentioning

confidence: 99%

Epidermal cells help coordinate leukocyte migration during inflammation through fatty acid-fuelled matrix metalloproteinase production

et al. 2014

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In addition to satisfying the metabolic demands of cells, mitochondrial metabolism helps regulate immune cell function. To date, such cell-intrinsic metabolic-immunologic cross-talk has only been described operating in cells of the immune system. Here we show that epidermal cells utilize fatty acid b-oxidation to fuel their contribution to the immune response during cutaneous inflammation. By live imaging metabolic and immunological processes within intact zebrafish embryos during cutaneous inflammation, we uncover a mechanism where elevated b-oxidation-fuelled mitochondria-derived reactive oxygen species within epidermal cells helps guide matrix metalloproteinase-driven leukocyte recruitment. This mechanism requires the activity of a zebrafish homologue of the mammalian mitochondrial enzyme, Immunoresponsive gene 1. This study describes the first example of metabolic reprogramming operating within a non-immune cell type to help control its contribution to the immune response. Targeting of this metabolic-immunologic interface within keratinocytes may prove useful in treating inflammatory dermatoses.

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“…For example, following heatshock stimulation, MMP9 expression within human keratinocytes has been shown to be dependent on mROS (a mitochondrial output of FA -oxidation) [29] . Redoxdependent mechanisms also contribute to MMP9 production within TNF--stimulated human keratinocytes [30] . Given the immunoregulatory activities of MMP9, that include directing immune cell trafficking, these data suggest a possible role for FA -oxidation-fueled mROSdriven MMP9 production within keratinocytes in regulating immune cell activity within the inflamed skin ( Figure 1A).…”

Section: A New Immunometabolic Role For Epidermal Cells During Cutanementioning

confidence: 99%

Live imaging epidermal cell metabolism during inflammation: a new immunometabolic role for epidermal keratinocytes?

Hall

Crosier

2014

Inflamm Cell Signal

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Until recently, immunity and metabolism have existed as two distinct fields of research. Primarily driven by research into obesity-associated inflammation it is now clear that immunity and metabolism functionally intersect at specific nodes. This new field of research called immunometabolism seeks to understand how immune cell function is influenced by adaptive changes in metabolic processes. The concept of metabolic reprogramming, as a mechanism to guide the immune response, has primarily focused on how an immune cell's metabolic mode can directly influence its activity. Whether non-hematopoietic cells, that also help orchestrate inflammation, utilize a similar mechanism to drive their immune activity is poorly understood. Due to their strategic location at the interface between the host and the environment, epidermal keratinocytes are highly adaptive cells that must respond to external stimuli by communicating to immune cells in the skin to generate an appropriate response. As such, keratinocytes are an important non-hematopoietic component of the immune system that function to maintain homeostasis, in part, by controlling inflammation within the skin. By live imaging epidermal cell metabolism during inflammation we have recently identified a new mechanism through which adaptive cell-intrinsic changes in epidermal cell metabolism helps direct their immune response. During inflammation, epidermal cells elevate mitochondrial uptake of fatty acids (FAs) that, following -oxidation, helps fuel matrix metalloproteinase production and leukocyte recruitment. We believe this represents the first example of metabolic reprogramming operating within a non-immune cell type to help orchestrate inflammation. Our results suggest that targeting the metabolic-immunological interface, at the level of the epidermal cell, may represent a new therapeutic strategy to alleviate inflammation that is associated with chronic skin diseases.To cite this article: Dingzhi Wang, et al. PPAR and PGE2 signaling pathways communicate and connect inflammation to colorectal cancer.

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Suppression of TNF-alpha-induced MMP-9 expression by a cell-permeable superoxide dismutase in keratinocytes

Cited by 20 publications

References 24 publications

Inhibition of migration and invasion of LNCaP human prostate carcinoma cells by cordycepin through inactivation of Akt

Inhibition of migration and invasion of LNCaP human prostate carcinoma cells by cordycepin through inactivation of Akt

Epidermal cells help coordinate leukocyte migration during inflammation through fatty acid-fuelled matrix metalloproteinase production

Live imaging epidermal cell metabolism during inflammation: a new immunometabolic role for epidermal keratinocytes?

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