Staphylococcus aureus impairs cutaneous wound healing by activating the expression of a gap junction protein, connexin-43 in keratinocytes

Abstract Chronic wounds have been considered as major medical problems that may result in expensive healthcare. One of the common causes of chronic wounds is bacterial contamination that leads to persistent inflammation and unbalanced host cell immune responses. Among the bacterial strains that have...
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Autor*in:	Xu, Wei [verfasserIn] Dielubanza, Elodi [verfasserIn] Maisel, Amanda [verfasserIn] Leung, Kai [verfasserIn] Mustoe, Thomas [verfasserIn] Hong, Seok [verfasserIn] Galiano, Robert [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2020

Schlagwörter:	Skin wound repair Connexin 43 Re-epithelialization

Übergeordnetes Werk:	Enthalten in: Cellular and molecular life sciences - Cham (ZG) : Springer International Publishing AG, 1997, 78(2020), 3 vom: 14. Mai, Seite 935-947
Übergeordnetes Werk:	volume:78 ; year:2020 ; number:3 ; day:14 ; month:05 ; pages:935-947

Links:	Volltext

DOI / URN:	10.1007/s00018-020-03545-4

Katalog-ID:	SPR04326042X

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520			\|a Abstract Chronic wounds have been considered as major medical problems that may result in expensive healthcare. One of the common causes of chronic wounds is bacterial contamination that leads to persistent inflammation and unbalanced host cell immune responses. Among the bacterial strains that have been identified from chronic wounds, Staphylococcus aureus is the most common strain. We previously observed that S. aureus impaired mouse cutaneous wound healing by delaying re-epithelialization. Here, we investigated the mechanism of delayed re-epithelialization caused by S. aureus infection. With the presence of S. aureus exudate, the migration of in vitro cultured human keratinocytes was significantly inhibited and connexin-43 (Cx43) was upregulated. Inhibition of keratinocyte migration by S. aureus exudate disappeared in keratinocytes where the expression of Cx43 knocked down. Protein kinase phosphorylation array showed that phosphorylation of Akt-S473 was upregulated by S. aureus exudate. In vivo study of Cx43 in S. aureus-infected murine splinted cutaneous wound model showed upregulation of Cx43 in the migrating epithelial edge by S. aureus infection. Treatment with a PI3K/Akt inhibitor reduced Cx43 expression and overcame the wound closure impairment by S. aureus infection in the mouse model. This may contribute to the development of treatment to bacterium-infected wounds.
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author_variant	w x wx e d ed a m am k l kl t m tm s h sh r g rg
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publishDate	2020
allfields	10.1007/s00018-020-03545-4 doi (DE-627)SPR04326042X (DE-599)SPRs00018-020-03545-4-e (SPR)s00018-020-03545-4-e DE-627 ger DE-627 rakwb eng 570 610 ASE 42.15 bkl Xu, Wei verfasserin aut Staphylococcus aureus impairs cutaneous wound healing by activating the expression of a gap junction protein, connexin-43 in keratinocytes 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Chronic wounds have been considered as major medical problems that may result in expensive healthcare. One of the common causes of chronic wounds is bacterial contamination that leads to persistent inflammation and unbalanced host cell immune responses. Among the bacterial strains that have been identified from chronic wounds, Staphylococcus aureus is the most common strain. We previously observed that S. aureus impaired mouse cutaneous wound healing by delaying re-epithelialization. Here, we investigated the mechanism of delayed re-epithelialization caused by S. aureus infection. With the presence of S. aureus exudate, the migration of in vitro cultured human keratinocytes was significantly inhibited and connexin-43 (Cx43) was upregulated. Inhibition of keratinocyte migration by S. aureus exudate disappeared in keratinocytes where the expression of Cx43 knocked down. Protein kinase phosphorylation array showed that phosphorylation of Akt-S473 was upregulated by S. aureus exudate. In vivo study of Cx43 in S. aureus-infected murine splinted cutaneous wound model showed upregulation of Cx43 in the migrating epithelial edge by S. aureus infection. Treatment with a PI3K/Akt inhibitor reduced Cx43 expression and overcame the wound closure impairment by S. aureus infection in the mouse model. This may contribute to the development of treatment to bacterium-infected wounds. Skin wound repair (dpeaa)DE-He213 Connexin 43 (dpeaa)DE-He213 Re-epithelialization (dpeaa)DE-He213 Dielubanza, Elodi verfasserin aut Maisel, Amanda verfasserin aut Leung, Kai verfasserin aut Mustoe, Thomas verfasserin aut Hong, Seok verfasserin aut Galiano, Robert verfasserin aut Enthalten in Cellular and molecular life sciences Cham (ZG) : Springer International Publishing AG, 1997 78(2020), 3 vom: 14. Mai, Seite 935-947 (DE-627)253390524 (DE-600)1458497-9 1420-9071 nnns volume:78 year:2020 number:3 day:14 month:05 pages:935-947 https://dx.doi.org/10.1007/s00018-020-03545-4 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 42.15 ASE AR 78 2020 3 14 05 935-947
spelling	10.1007/s00018-020-03545-4 doi (DE-627)SPR04326042X (DE-599)SPRs00018-020-03545-4-e (SPR)s00018-020-03545-4-e DE-627 ger DE-627 rakwb eng 570 610 ASE 42.15 bkl Xu, Wei verfasserin aut Staphylococcus aureus impairs cutaneous wound healing by activating the expression of a gap junction protein, connexin-43 in keratinocytes 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Chronic wounds have been considered as major medical problems that may result in expensive healthcare. One of the common causes of chronic wounds is bacterial contamination that leads to persistent inflammation and unbalanced host cell immune responses. Among the bacterial strains that have been identified from chronic wounds, Staphylococcus aureus is the most common strain. We previously observed that S. aureus impaired mouse cutaneous wound healing by delaying re-epithelialization. Here, we investigated the mechanism of delayed re-epithelialization caused by S. aureus infection. With the presence of S. aureus exudate, the migration of in vitro cultured human keratinocytes was significantly inhibited and connexin-43 (Cx43) was upregulated. Inhibition of keratinocyte migration by S. aureus exudate disappeared in keratinocytes where the expression of Cx43 knocked down. Protein kinase phosphorylation array showed that phosphorylation of Akt-S473 was upregulated by S. aureus exudate. In vivo study of Cx43 in S. aureus-infected murine splinted cutaneous wound model showed upregulation of Cx43 in the migrating epithelial edge by S. aureus infection. Treatment with a PI3K/Akt inhibitor reduced Cx43 expression and overcame the wound closure impairment by S. aureus infection in the mouse model. This may contribute to the development of treatment to bacterium-infected wounds. Skin wound repair (dpeaa)DE-He213 Connexin 43 (dpeaa)DE-He213 Re-epithelialization (dpeaa)DE-He213 Dielubanza, Elodi verfasserin aut Maisel, Amanda verfasserin aut Leung, Kai verfasserin aut Mustoe, Thomas verfasserin aut Hong, Seok verfasserin aut Galiano, Robert verfasserin aut Enthalten in Cellular and molecular life sciences Cham (ZG) : Springer International Publishing AG, 1997 78(2020), 3 vom: 14. Mai, Seite 935-947 (DE-627)253390524 (DE-600)1458497-9 1420-9071 nnns volume:78 year:2020 number:3 day:14 month:05 pages:935-947 https://dx.doi.org/10.1007/s00018-020-03545-4 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 42.15 ASE AR 78 2020 3 14 05 935-947
allfields_unstemmed	10.1007/s00018-020-03545-4 doi (DE-627)SPR04326042X (DE-599)SPRs00018-020-03545-4-e (SPR)s00018-020-03545-4-e DE-627 ger DE-627 rakwb eng 570 610 ASE 42.15 bkl Xu, Wei verfasserin aut Staphylococcus aureus impairs cutaneous wound healing by activating the expression of a gap junction protein, connexin-43 in keratinocytes 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Chronic wounds have been considered as major medical problems that may result in expensive healthcare. One of the common causes of chronic wounds is bacterial contamination that leads to persistent inflammation and unbalanced host cell immune responses. Among the bacterial strains that have been identified from chronic wounds, Staphylococcus aureus is the most common strain. We previously observed that S. aureus impaired mouse cutaneous wound healing by delaying re-epithelialization. Here, we investigated the mechanism of delayed re-epithelialization caused by S. aureus infection. With the presence of S. aureus exudate, the migration of in vitro cultured human keratinocytes was significantly inhibited and connexin-43 (Cx43) was upregulated. Inhibition of keratinocyte migration by S. aureus exudate disappeared in keratinocytes where the expression of Cx43 knocked down. Protein kinase phosphorylation array showed that phosphorylation of Akt-S473 was upregulated by S. aureus exudate. In vivo study of Cx43 in S. aureus-infected murine splinted cutaneous wound model showed upregulation of Cx43 in the migrating epithelial edge by S. aureus infection. Treatment with a PI3K/Akt inhibitor reduced Cx43 expression and overcame the wound closure impairment by S. aureus infection in the mouse model. This may contribute to the development of treatment to bacterium-infected wounds. Skin wound repair (dpeaa)DE-He213 Connexin 43 (dpeaa)DE-He213 Re-epithelialization (dpeaa)DE-He213 Dielubanza, Elodi verfasserin aut Maisel, Amanda verfasserin aut Leung, Kai verfasserin aut Mustoe, Thomas verfasserin aut Hong, Seok verfasserin aut Galiano, Robert verfasserin aut Enthalten in Cellular and molecular life sciences Cham (ZG) : Springer International Publishing AG, 1997 78(2020), 3 vom: 14. Mai, Seite 935-947 (DE-627)253390524 (DE-600)1458497-9 1420-9071 nnns volume:78 year:2020 number:3 day:14 month:05 pages:935-947 https://dx.doi.org/10.1007/s00018-020-03545-4 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 42.15 ASE AR 78 2020 3 14 05 935-947
allfieldsGer	10.1007/s00018-020-03545-4 doi (DE-627)SPR04326042X (DE-599)SPRs00018-020-03545-4-e (SPR)s00018-020-03545-4-e DE-627 ger DE-627 rakwb eng 570 610 ASE 42.15 bkl Xu, Wei verfasserin aut Staphylococcus aureus impairs cutaneous wound healing by activating the expression of a gap junction protein, connexin-43 in keratinocytes 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Chronic wounds have been considered as major medical problems that may result in expensive healthcare. One of the common causes of chronic wounds is bacterial contamination that leads to persistent inflammation and unbalanced host cell immune responses. Among the bacterial strains that have been identified from chronic wounds, Staphylococcus aureus is the most common strain. We previously observed that S. aureus impaired mouse cutaneous wound healing by delaying re-epithelialization. Here, we investigated the mechanism of delayed re-epithelialization caused by S. aureus infection. With the presence of S. aureus exudate, the migration of in vitro cultured human keratinocytes was significantly inhibited and connexin-43 (Cx43) was upregulated. Inhibition of keratinocyte migration by S. aureus exudate disappeared in keratinocytes where the expression of Cx43 knocked down. Protein kinase phosphorylation array showed that phosphorylation of Akt-S473 was upregulated by S. aureus exudate. In vivo study of Cx43 in S. aureus-infected murine splinted cutaneous wound model showed upregulation of Cx43 in the migrating epithelial edge by S. aureus infection. Treatment with a PI3K/Akt inhibitor reduced Cx43 expression and overcame the wound closure impairment by S. aureus infection in the mouse model. This may contribute to the development of treatment to bacterium-infected wounds. Skin wound repair (dpeaa)DE-He213 Connexin 43 (dpeaa)DE-He213 Re-epithelialization (dpeaa)DE-He213 Dielubanza, Elodi verfasserin aut Maisel, Amanda verfasserin aut Leung, Kai verfasserin aut Mustoe, Thomas verfasserin aut Hong, Seok verfasserin aut Galiano, Robert verfasserin aut Enthalten in Cellular and molecular life sciences Cham (ZG) : Springer International Publishing AG, 1997 78(2020), 3 vom: 14. Mai, Seite 935-947 (DE-627)253390524 (DE-600)1458497-9 1420-9071 nnns volume:78 year:2020 number:3 day:14 month:05 pages:935-947 https://dx.doi.org/10.1007/s00018-020-03545-4 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 42.15 ASE AR 78 2020 3 14 05 935-947
allfieldsSound	10.1007/s00018-020-03545-4 doi (DE-627)SPR04326042X (DE-599)SPRs00018-020-03545-4-e (SPR)s00018-020-03545-4-e DE-627 ger DE-627 rakwb eng 570 610 ASE 42.15 bkl Xu, Wei verfasserin aut Staphylococcus aureus impairs cutaneous wound healing by activating the expression of a gap junction protein, connexin-43 in keratinocytes 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Chronic wounds have been considered as major medical problems that may result in expensive healthcare. One of the common causes of chronic wounds is bacterial contamination that leads to persistent inflammation and unbalanced host cell immune responses. Among the bacterial strains that have been identified from chronic wounds, Staphylococcus aureus is the most common strain. We previously observed that S. aureus impaired mouse cutaneous wound healing by delaying re-epithelialization. Here, we investigated the mechanism of delayed re-epithelialization caused by S. aureus infection. With the presence of S. aureus exudate, the migration of in vitro cultured human keratinocytes was significantly inhibited and connexin-43 (Cx43) was upregulated. Inhibition of keratinocyte migration by S. aureus exudate disappeared in keratinocytes where the expression of Cx43 knocked down. Protein kinase phosphorylation array showed that phosphorylation of Akt-S473 was upregulated by S. aureus exudate. In vivo study of Cx43 in S. aureus-infected murine splinted cutaneous wound model showed upregulation of Cx43 in the migrating epithelial edge by S. aureus infection. Treatment with a PI3K/Akt inhibitor reduced Cx43 expression and overcame the wound closure impairment by S. aureus infection in the mouse model. This may contribute to the development of treatment to bacterium-infected wounds. Skin wound repair (dpeaa)DE-He213 Connexin 43 (dpeaa)DE-He213 Re-epithelialization (dpeaa)DE-He213 Dielubanza, Elodi verfasserin aut Maisel, Amanda verfasserin aut Leung, Kai verfasserin aut Mustoe, Thomas verfasserin aut Hong, Seok verfasserin aut Galiano, Robert verfasserin aut Enthalten in Cellular and molecular life sciences Cham (ZG) : Springer International Publishing AG, 1997 78(2020), 3 vom: 14. Mai, Seite 935-947 (DE-627)253390524 (DE-600)1458497-9 1420-9071 nnns volume:78 year:2020 number:3 day:14 month:05 pages:935-947 https://dx.doi.org/10.1007/s00018-020-03545-4 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 42.15 ASE AR 78 2020 3 14 05 935-947
language	English
source	Enthalten in Cellular and molecular life sciences 78(2020), 3 vom: 14. Mai, Seite 935-947 volume:78 year:2020 number:3 day:14 month:05 pages:935-947
sourceStr	Enthalten in Cellular and molecular life sciences 78(2020), 3 vom: 14. Mai, Seite 935-947 volume:78 year:2020 number:3 day:14 month:05 pages:935-947
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Skin wound repair Connexin 43 Re-epithelialization
dewey-raw	570
isfreeaccess_bool	false
container_title	Cellular and molecular life sciences
authorswithroles_txt_mv	Xu, Wei @@aut@@ Dielubanza, Elodi @@aut@@ Maisel, Amanda @@aut@@ Leung, Kai @@aut@@ Mustoe, Thomas @@aut@@ Hong, Seok @@aut@@ Galiano, Robert @@aut@@
publishDateDaySort_date	2020-05-14T00:00:00Z
hierarchy_top_id	253390524
dewey-sort	3570
id	SPR04326042X
language_de	englisch
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author	Xu, Wei
spellingShingle	Xu, Wei ddc 570 bkl 42.15 misc Skin wound repair misc Connexin 43 misc Re-epithelialization Staphylococcus aureus impairs cutaneous wound healing by activating the expression of a gap junction protein, connexin-43 in keratinocytes
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topic_title	570 610 ASE 42.15 bkl Staphylococcus aureus impairs cutaneous wound healing by activating the expression of a gap junction protein, connexin-43 in keratinocytes Skin wound repair (dpeaa)DE-He213 Connexin 43 (dpeaa)DE-He213 Re-epithelialization (dpeaa)DE-He213
topic	ddc 570 bkl 42.15 misc Skin wound repair misc Connexin 43 misc Re-epithelialization
topic_unstemmed	ddc 570 bkl 42.15 misc Skin wound repair misc Connexin 43 misc Re-epithelialization
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title	Staphylococcus aureus impairs cutaneous wound healing by activating the expression of a gap junction protein, connexin-43 in keratinocytes
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title_full	Staphylococcus aureus impairs cutaneous wound healing by activating the expression of a gap junction protein, connexin-43 in keratinocytes
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author_browse	Xu, Wei Dielubanza, Elodi Maisel, Amanda Leung, Kai Mustoe, Thomas Hong, Seok Galiano, Robert
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title_sort	staphylococcus aureus impairs cutaneous wound healing by activating the expression of a gap junction protein, connexin-43 in keratinocytes
title_auth	Staphylococcus aureus impairs cutaneous wound healing by activating the expression of a gap junction protein, connexin-43 in keratinocytes
abstract	Abstract Chronic wounds have been considered as major medical problems that may result in expensive healthcare. One of the common causes of chronic wounds is bacterial contamination that leads to persistent inflammation and unbalanced host cell immune responses. Among the bacterial strains that have been identified from chronic wounds, Staphylococcus aureus is the most common strain. We previously observed that S. aureus impaired mouse cutaneous wound healing by delaying re-epithelialization. Here, we investigated the mechanism of delayed re-epithelialization caused by S. aureus infection. With the presence of S. aureus exudate, the migration of in vitro cultured human keratinocytes was significantly inhibited and connexin-43 (Cx43) was upregulated. Inhibition of keratinocyte migration by S. aureus exudate disappeared in keratinocytes where the expression of Cx43 knocked down. Protein kinase phosphorylation array showed that phosphorylation of Akt-S473 was upregulated by S. aureus exudate. In vivo study of Cx43 in S. aureus-infected murine splinted cutaneous wound model showed upregulation of Cx43 in the migrating epithelial edge by S. aureus infection. Treatment with a PI3K/Akt inhibitor reduced Cx43 expression and overcame the wound closure impairment by S. aureus infection in the mouse model. This may contribute to the development of treatment to bacterium-infected wounds.
abstractGer	Abstract Chronic wounds have been considered as major medical problems that may result in expensive healthcare. One of the common causes of chronic wounds is bacterial contamination that leads to persistent inflammation and unbalanced host cell immune responses. Among the bacterial strains that have been identified from chronic wounds, Staphylococcus aureus is the most common strain. We previously observed that S. aureus impaired mouse cutaneous wound healing by delaying re-epithelialization. Here, we investigated the mechanism of delayed re-epithelialization caused by S. aureus infection. With the presence of S. aureus exudate, the migration of in vitro cultured human keratinocytes was significantly inhibited and connexin-43 (Cx43) was upregulated. Inhibition of keratinocyte migration by S. aureus exudate disappeared in keratinocytes where the expression of Cx43 knocked down. Protein kinase phosphorylation array showed that phosphorylation of Akt-S473 was upregulated by S. aureus exudate. In vivo study of Cx43 in S. aureus-infected murine splinted cutaneous wound model showed upregulation of Cx43 in the migrating epithelial edge by S. aureus infection. Treatment with a PI3K/Akt inhibitor reduced Cx43 expression and overcame the wound closure impairment by S. aureus infection in the mouse model. This may contribute to the development of treatment to bacterium-infected wounds.
abstract_unstemmed	Abstract Chronic wounds have been considered as major medical problems that may result in expensive healthcare. One of the common causes of chronic wounds is bacterial contamination that leads to persistent inflammation and unbalanced host cell immune responses. Among the bacterial strains that have been identified from chronic wounds, Staphylococcus aureus is the most common strain. We previously observed that S. aureus impaired mouse cutaneous wound healing by delaying re-epithelialization. Here, we investigated the mechanism of delayed re-epithelialization caused by S. aureus infection. With the presence of S. aureus exudate, the migration of in vitro cultured human keratinocytes was significantly inhibited and connexin-43 (Cx43) was upregulated. Inhibition of keratinocyte migration by S. aureus exudate disappeared in keratinocytes where the expression of Cx43 knocked down. Protein kinase phosphorylation array showed that phosphorylation of Akt-S473 was upregulated by S. aureus exudate. In vivo study of Cx43 in S. aureus-infected murine splinted cutaneous wound model showed upregulation of Cx43 in the migrating epithelial edge by S. aureus infection. Treatment with a PI3K/Akt inhibitor reduced Cx43 expression and overcame the wound closure impairment by S. aureus infection in the mouse model. This may contribute to the development of treatment to bacterium-infected wounds.
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title_short	Staphylococcus aureus impairs cutaneous wound healing by activating the expression of a gap junction protein, connexin-43 in keratinocytes
url	https://dx.doi.org/10.1007/s00018-020-03545-4
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author2	Dielubanza, Elodi Maisel, Amanda Leung, Kai Mustoe, Thomas Hong, Seok Galiano, Robert
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doi_str	10.1007/s00018-020-03545-4
up_date	2024-07-03T17:34:13.668Z
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One of the common causes of chronic wounds is bacterial contamination that leads to persistent inflammation and unbalanced host cell immune responses. Among the bacterial strains that have been identified from chronic wounds, Staphylococcus aureus is the most common strain. We previously observed that S. aureus impaired mouse cutaneous wound healing by delaying re-epithelialization. Here, we investigated the mechanism of delayed re-epithelialization caused by S. aureus infection. With the presence of S. aureus exudate, the migration of in vitro cultured human keratinocytes was significantly inhibited and connexin-43 (Cx43) was upregulated. Inhibition of keratinocyte migration by S. aureus exudate disappeared in keratinocytes where the expression of Cx43 knocked down. Protein kinase phosphorylation array showed that phosphorylation of Akt-S473 was upregulated by S. aureus exudate. In vivo study of Cx43 in S. aureus-infected murine splinted cutaneous wound model showed upregulation of Cx43 in the migrating epithelial edge by S. aureus infection. Treatment with a PI3K/Akt inhibitor reduced Cx43 expression and overcame the wound closure impairment by S. aureus infection in the mouse model. 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Staphylococcus aureus impairs cutaneous wound healing by activating the expression of a gap junction protein, connexin-43 in keratinocytes

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