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Non-thermal atmospheric-pressure plasma possible application in wound healing.

Haertel B, von Woedtke T, Weltmann KD, Lindequist U - Biomol Ther (Seoul) (2014)

Bottom Line: Therefore, it cannot be equated with plasma from blood; it is not biological in nature.This review emphasizes plasma effects on wound healing.We summarize the effects of plasma on eukaryotic cells, especially on keratinocytes in terms of viability, proliferation, DNA, adhesion molecules and angiogenesis together with the role of reactive oxygen species and other components of plasma.

View Article: PubMed Central - PubMed

Affiliation: Department of Pharmaceutical Biology, Institute of Pharmacy, Ernst-Moritz-Arndt University of Greifswald, D17489 Greifswald, Germany.

ABSTRACT
Non-thermal atmospheric-pressure plasma, also named cold plasma, is defined as a partly ionized gas. Therefore, it cannot be equated with plasma from blood; it is not biological in nature. Non-thermal atmospheric-pressure plasma is a new innovative approach in medicine not only for the treatment of wounds, but with a wide-range of other applications, as e.g. topical treatment of other skin diseases with microbial involvement or treatment of cancer diseases. This review emphasizes plasma effects on wound healing. Non-thermal atmospheric-pressure plasma can support wound healing by its antiseptic effects, by stimulation of proliferation and migration of wound relating skin cells, by activation or inhibition of integrin receptors on the cell surface or by its pro-angiogenic effect. We summarize the effects of plasma on eukaryotic cells, especially on keratinocytes in terms of viability, proliferation, DNA, adhesion molecules and angiogenesis together with the role of reactive oxygen species and other components of plasma. The outcome of first clinical trials regarding wound healing is pointed out.

No MeSH data available.


Related in: MedlinePlus

Cell cycle analysis of HaCaT keratinocytes which stayed either untreated (A) or were treated with the kINPen 09 for 60s (B), surface DBD for 120 s (C) or volume DBD for 20 s (D). Analysis was done 24 h after exposure to plasma. Representative histograms with indication of the percentage of cells detected in the G1 and G2/M phase are shown. Plasma treatment induced independent of the plasma source used a typical G2/M.
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f5-bt-22-477: Cell cycle analysis of HaCaT keratinocytes which stayed either untreated (A) or were treated with the kINPen 09 for 60s (B), surface DBD for 120 s (C) or volume DBD for 20 s (D). Analysis was done 24 h after exposure to plasma. Representative histograms with indication of the percentage of cells detected in the G1 and G2/M phase are shown. Plasma treatment induced independent of the plasma source used a typical G2/M.

Mentions: Cell cycle analyses after plasma treatment give additional indication for influences on DNA. In HaCaT keratinocytes a G2/M phase arrest was detected after treating the cells with plasma. All plasma sources used induced comparable effects, however, in dependence on the plasma source with different plasma treatment times (Blackert et al., 2013; Straβenburg et al., 2013; Straβenburg, 2014; Wende et al., 2014). Representative examples for a G2/M arrest of HaCaT keratinocytes are shown in Fig. 5. HaCaT cells remained untreated (Fig. 5A), were either treated with the kINPen 09 for 60s (Fig. 5B), SDBD for 120 s (Fig. 5C) or V-DBD for 20 s (Fig. 5D). G2/M arrest seems to be a typical sign after a given plasma treatment, since also others observed such a phenomenon not only in keratinocytes (Volotskova et al., 2012a) but particularly in different types of cancer cells (Vandamme et al., 2012; Volotskova et al., 2012a; Arndt et al., 2013; Köritzer et al., 2013). A cell cycle arrest in the G2/M phase gives cells time for DNA repair. Oxidative DNA damages will be detected, deleted and replaced by the DNA base excision repair (BER) pathway. In preliminary studies with HaCaT keratinocytes we looked for two enzymes (Ogg1 and APE-1) belonging to this repair pathway. By using the western blot technique, Ogg1, responsible for excision of 8-hydroxy-2′-deoxyguanosine, was found to be enhanced after kINPen 09 treatment of HaCaT cells (Kurth, 2013). These results are underlined by Brun et al. (2012) who demonstrated an increase of Ogg1 2 to 24h after a 2 min plasma treatment. In contrast, the repair enzyme APE-1 (apurinic/apyrimidinic endonuclease-1) was found to be reduced in HaCaT cells after kINPen 09 treatment (Kurth, 2013). This enzyme is the major human repair enzyme for abasic sites and incises the phosphodiester backbone 5′ to the lesion to initiate a cascade of events aimed at removing the AP moiety and maintaining genetic integrity (Hadi et al., 2000). Up to now it is not clear whether the repair mechanism stops after deleting of 8-hydroxy-2′-deoxyguanosine by Ogg1.


Non-thermal atmospheric-pressure plasma possible application in wound healing.

Haertel B, von Woedtke T, Weltmann KD, Lindequist U - Biomol Ther (Seoul) (2014)

Cell cycle analysis of HaCaT keratinocytes which stayed either untreated (A) or were treated with the kINPen 09 for 60s (B), surface DBD for 120 s (C) or volume DBD for 20 s (D). Analysis was done 24 h after exposure to plasma. Representative histograms with indication of the percentage of cells detected in the G1 and G2/M phase are shown. Plasma treatment induced independent of the plasma source used a typical G2/M.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4256026&req=5

f5-bt-22-477: Cell cycle analysis of HaCaT keratinocytes which stayed either untreated (A) or were treated with the kINPen 09 for 60s (B), surface DBD for 120 s (C) or volume DBD for 20 s (D). Analysis was done 24 h after exposure to plasma. Representative histograms with indication of the percentage of cells detected in the G1 and G2/M phase are shown. Plasma treatment induced independent of the plasma source used a typical G2/M.
Mentions: Cell cycle analyses after plasma treatment give additional indication for influences on DNA. In HaCaT keratinocytes a G2/M phase arrest was detected after treating the cells with plasma. All plasma sources used induced comparable effects, however, in dependence on the plasma source with different plasma treatment times (Blackert et al., 2013; Straβenburg et al., 2013; Straβenburg, 2014; Wende et al., 2014). Representative examples for a G2/M arrest of HaCaT keratinocytes are shown in Fig. 5. HaCaT cells remained untreated (Fig. 5A), were either treated with the kINPen 09 for 60s (Fig. 5B), SDBD for 120 s (Fig. 5C) or V-DBD for 20 s (Fig. 5D). G2/M arrest seems to be a typical sign after a given plasma treatment, since also others observed such a phenomenon not only in keratinocytes (Volotskova et al., 2012a) but particularly in different types of cancer cells (Vandamme et al., 2012; Volotskova et al., 2012a; Arndt et al., 2013; Köritzer et al., 2013). A cell cycle arrest in the G2/M phase gives cells time for DNA repair. Oxidative DNA damages will be detected, deleted and replaced by the DNA base excision repair (BER) pathway. In preliminary studies with HaCaT keratinocytes we looked for two enzymes (Ogg1 and APE-1) belonging to this repair pathway. By using the western blot technique, Ogg1, responsible for excision of 8-hydroxy-2′-deoxyguanosine, was found to be enhanced after kINPen 09 treatment of HaCaT cells (Kurth, 2013). These results are underlined by Brun et al. (2012) who demonstrated an increase of Ogg1 2 to 24h after a 2 min plasma treatment. In contrast, the repair enzyme APE-1 (apurinic/apyrimidinic endonuclease-1) was found to be reduced in HaCaT cells after kINPen 09 treatment (Kurth, 2013). This enzyme is the major human repair enzyme for abasic sites and incises the phosphodiester backbone 5′ to the lesion to initiate a cascade of events aimed at removing the AP moiety and maintaining genetic integrity (Hadi et al., 2000). Up to now it is not clear whether the repair mechanism stops after deleting of 8-hydroxy-2′-deoxyguanosine by Ogg1.

Bottom Line: Therefore, it cannot be equated with plasma from blood; it is not biological in nature.This review emphasizes plasma effects on wound healing.We summarize the effects of plasma on eukaryotic cells, especially on keratinocytes in terms of viability, proliferation, DNA, adhesion molecules and angiogenesis together with the role of reactive oxygen species and other components of plasma.

View Article: PubMed Central - PubMed

Affiliation: Department of Pharmaceutical Biology, Institute of Pharmacy, Ernst-Moritz-Arndt University of Greifswald, D17489 Greifswald, Germany.

ABSTRACT
Non-thermal atmospheric-pressure plasma, also named cold plasma, is defined as a partly ionized gas. Therefore, it cannot be equated with plasma from blood; it is not biological in nature. Non-thermal atmospheric-pressure plasma is a new innovative approach in medicine not only for the treatment of wounds, but with a wide-range of other applications, as e.g. topical treatment of other skin diseases with microbial involvement or treatment of cancer diseases. This review emphasizes plasma effects on wound healing. Non-thermal atmospheric-pressure plasma can support wound healing by its antiseptic effects, by stimulation of proliferation and migration of wound relating skin cells, by activation or inhibition of integrin receptors on the cell surface or by its pro-angiogenic effect. We summarize the effects of plasma on eukaryotic cells, especially on keratinocytes in terms of viability, proliferation, DNA, adhesion molecules and angiogenesis together with the role of reactive oxygen species and other components of plasma. The outcome of first clinical trials regarding wound healing is pointed out.

No MeSH data available.


Related in: MedlinePlus