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Role for heat shock protein 90α in the proliferation and migration of HaCaT cells and in the deep second-degree burn wound healing in mice.

Zhang Y, Bai X, Wang Y, Li N, Li X, Han F, Su L, Hu D - PLoS ONE (2014)

Bottom Line: The hypoxic wound microenvironment promotes cell migration through a hypoxia--heat shock protein 90 alpha (Hsp90α)--low density lipoprotein receptor-related protein-1 (LRP-1) autocrine loop.Experiments performed with a human keratinocyte cell line--HaCaT also confirmed above results. 17-dimethylaminoethylamino-17demethoxygeldanamycin hydrochloride (17-DMAG), an Hsp90α inhibitor, was used to further evaluate the function of Hsp90α in wound healing.In conclusion, these results provided a rationale for the therapeutic effect of Hsp90α on the burn wound management.

View Article: PubMed Central - PubMed

Affiliation: Department of Burns and Cutaneous Surgery, Xijing Hospital, Fourth Military Medical University, Xi'an, Shannxi, China.

ABSTRACT
Inflammation, proliferation, and tissue remodeling are essential steps for wound healing. The hypoxic wound microenvironment promotes cell migration through a hypoxia--heat shock protein 90 alpha (Hsp90α)--low density lipoprotein receptor-related protein-1 (LRP-1) autocrine loop. To elucidate the role of this autocrine loop on burn wound healing, we investigated the expression profile of Hsp90α at the edge of burn wounds and found a transient increase in both mRNA and protein levels. Experiments performed with a human keratinocyte cell line--HaCaT also confirmed above results. 17-dimethylaminoethylamino-17demethoxygeldanamycin hydrochloride (17-DMAG), an Hsp90α inhibitor, was used to further evaluate the function of Hsp90α in wound healing. Consistently, topical application of Hsp90α in the early stage of deep second-degree burn wounds led to reduced inflammation and increased tissue granulation, with a concomitant reduction in the size of the wound at each time point tested (p<0.05). Consequently, epidermal cells at the wound margin progressed more rapidly causing an expedited healing process. In conclusion, these results provided a rationale for the therapeutic effect of Hsp90α on the burn wound management.

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Related in: MedlinePlus

An in vitro scratch assay showing the effects of Hsp90α on the migration of heat-shocked cells.Images were taken at the indicated time of incubation. Hsp90α-treated group showed more rapid reduction in the gap size at each time point tested than that in the control group, while 17-DMAG group showed slower gap closure even than the control (p<0.05). AG, average gap, normalized to the gap size at 0 h.
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pone-0103723-g004: An in vitro scratch assay showing the effects of Hsp90α on the migration of heat-shocked cells.Images were taken at the indicated time of incubation. Hsp90α-treated group showed more rapid reduction in the gap size at each time point tested than that in the control group, while 17-DMAG group showed slower gap closure even than the control (p<0.05). AG, average gap, normalized to the gap size at 0 h.

Mentions: We used an in vitro assay to determine whether Hsp90α could enhance the skin cell migration in a cell-based heat shock model. A slow reduction in the gap of the scratch was observed in control group, and the gap shrinked to approximately 50% of the initial size 24 h later. Hsp90α-added group showed a more rapid reduction in gap size, and the gap was almost closed 24 h later. While 17-DMAG-treated group showed a slower gap closure even than the control (Fig. 4). These findings suggested that Hsp90α could stimulate skin cell migration in the in vitro heat shock model.


Role for heat shock protein 90α in the proliferation and migration of HaCaT cells and in the deep second-degree burn wound healing in mice.

Zhang Y, Bai X, Wang Y, Li N, Li X, Han F, Su L, Hu D - PLoS ONE (2014)

An in vitro scratch assay showing the effects of Hsp90α on the migration of heat-shocked cells.Images were taken at the indicated time of incubation. Hsp90α-treated group showed more rapid reduction in the gap size at each time point tested than that in the control group, while 17-DMAG group showed slower gap closure even than the control (p<0.05). AG, average gap, normalized to the gap size at 0 h.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4128658&req=5

pone-0103723-g004: An in vitro scratch assay showing the effects of Hsp90α on the migration of heat-shocked cells.Images were taken at the indicated time of incubation. Hsp90α-treated group showed more rapid reduction in the gap size at each time point tested than that in the control group, while 17-DMAG group showed slower gap closure even than the control (p<0.05). AG, average gap, normalized to the gap size at 0 h.
Mentions: We used an in vitro assay to determine whether Hsp90α could enhance the skin cell migration in a cell-based heat shock model. A slow reduction in the gap of the scratch was observed in control group, and the gap shrinked to approximately 50% of the initial size 24 h later. Hsp90α-added group showed a more rapid reduction in gap size, and the gap was almost closed 24 h later. While 17-DMAG-treated group showed a slower gap closure even than the control (Fig. 4). These findings suggested that Hsp90α could stimulate skin cell migration in the in vitro heat shock model.

Bottom Line: The hypoxic wound microenvironment promotes cell migration through a hypoxia--heat shock protein 90 alpha (Hsp90α)--low density lipoprotein receptor-related protein-1 (LRP-1) autocrine loop.Experiments performed with a human keratinocyte cell line--HaCaT also confirmed above results. 17-dimethylaminoethylamino-17demethoxygeldanamycin hydrochloride (17-DMAG), an Hsp90α inhibitor, was used to further evaluate the function of Hsp90α in wound healing.In conclusion, these results provided a rationale for the therapeutic effect of Hsp90α on the burn wound management.

View Article: PubMed Central - PubMed

Affiliation: Department of Burns and Cutaneous Surgery, Xijing Hospital, Fourth Military Medical University, Xi'an, Shannxi, China.

ABSTRACT
Inflammation, proliferation, and tissue remodeling are essential steps for wound healing. The hypoxic wound microenvironment promotes cell migration through a hypoxia--heat shock protein 90 alpha (Hsp90α)--low density lipoprotein receptor-related protein-1 (LRP-1) autocrine loop. To elucidate the role of this autocrine loop on burn wound healing, we investigated the expression profile of Hsp90α at the edge of burn wounds and found a transient increase in both mRNA and protein levels. Experiments performed with a human keratinocyte cell line--HaCaT also confirmed above results. 17-dimethylaminoethylamino-17demethoxygeldanamycin hydrochloride (17-DMAG), an Hsp90α inhibitor, was used to further evaluate the function of Hsp90α in wound healing. Consistently, topical application of Hsp90α in the early stage of deep second-degree burn wounds led to reduced inflammation and increased tissue granulation, with a concomitant reduction in the size of the wound at each time point tested (p<0.05). Consequently, epidermal cells at the wound margin progressed more rapidly causing an expedited healing process. In conclusion, these results provided a rationale for the therapeutic effect of Hsp90α on the burn wound management.

Show MeSH
Related in: MedlinePlus