Increased expression of heat shock protein 72 protects renal proximal tubular cells from gentamicin-induced injury.

Zhipeng Wang; Li Liu; Qibing Mei; Linna Liu; Yuhua Ran; Rong Zhang

Increased expression of heat shock protein 72 protects renal proximal tubular cells from gentamicin-induced injury.

Zhipeng Wang, Li Liu, Qibing Mei, Linna Liu, Yuhua Ran, Rong Zhang

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › peer review

11 Citationer (Scopus)

Abstract

Udgivelsesdato: 2006-Oct

Originalsprog	Engelsk
Tidsskrift	Journal of Korean Medical Science
Vol/bind	21
Udgave nummer	5
Sider (fra-til)	904-10
Antal sider	6
ISSN	1011-8934
Status	Udgivet - 2006
Udgivet eksternt	Ja

Bibliografisk note

Keywords: Cells, Cultured; Cytoprotection; Gentamicins; HSP72 Heat-Shock Proteins; Heat; Humans; Kidney Tubules, Proximal; L-Lactate Dehydrogenase; Oxidation-Reduction; RNA, Messenger; Reactive Oxygen Species

Citationsformater

@article{d86475e05d6711dd8d9f000ea68e967b,

title = "Increased expression of heat shock protein 72 protects renal proximal tubular cells from gentamicin-induced injury.",

abstract = "The nephrotoxicity of gentamicin (GM) has been widely recognized. Heat shock protein 72 (HSP72) has been reported to be a cytoprotectant. However, its cytoprotective effect against GM induced kidney injury has not yet been studied. In this study, we investigated the cytoprotective effect of HSP72 on GM-induced nephrotoxicity in vitro. Human Kidney tubular cell line, HK-2 cells were divided into four groups: control group, GM group (cells incubated with GM only), heat shock (HS) group (cells incubated at 43 degrees C for 30 min), and GM plus HS group, respectively. Lactate dehydrogenase (LDH) release increased time-dependently from 24 hr to 96 hr compared to the data of cells treated with GM only. Results of NAG activities, superoxide dismutase (SOD) activities and malondialdehyde (MDA) content were similar to that of the LDH release. The amount of HSP72 positive cells increased significantly at 72 hr after cells were treated with GM only. Both HSP72 protein and gene expression increased significantly at 72 hr when cells were treated with GM. On the other hand, HS induced HSP72 expression markedly. Pretreatment of HS inhibited HK-2 cells from GM-induced injury. It could reduce LDH release and NAG activity. HS also increased SOD activity, and decreased MDA content when cells were damaged by GM. These findings suggested that HS may protect kidney cells from GM-induced injury. Pre-induction of HSP72 may provide therapeutic strategies for nephrotoxicity induced by GM.",

author = "Zhipeng Wang and Li Liu and Qibing Mei and Linna Liu and Yuhua Ran and Rong Zhang",

note = "Keywords: Cells, Cultured; Cytoprotection; Gentamicins; HSP72 Heat-Shock Proteins; Heat; Humans; Kidney Tubules, Proximal; L-Lactate Dehydrogenase; Oxidation-Reduction; RNA, Messenger; Reactive Oxygen Species",

year = "2006",

language = "English",

volume = "21",

pages = "904--10",

journal = "Journal of Korean Medical Science",

issn = "1011-8934",

publisher = "Korean Academy of Medical Sciences",

number = "5",

}

TY - JOUR

T1 - Increased expression of heat shock protein 72 protects renal proximal tubular cells from gentamicin-induced injury.

AU - Wang, Zhipeng

AU - Liu, Li

AU - Mei, Qibing

AU - Liu, Linna

AU - Ran, Yuhua

AU - Zhang, Rong

N1 - Keywords: Cells, Cultured; Cytoprotection; Gentamicins; HSP72 Heat-Shock Proteins; Heat; Humans; Kidney Tubules, Proximal; L-Lactate Dehydrogenase; Oxidation-Reduction; RNA, Messenger; Reactive Oxygen Species

PY - 2006

Y1 - 2006

N2 - The nephrotoxicity of gentamicin (GM) has been widely recognized. Heat shock protein 72 (HSP72) has been reported to be a cytoprotectant. However, its cytoprotective effect against GM induced kidney injury has not yet been studied. In this study, we investigated the cytoprotective effect of HSP72 on GM-induced nephrotoxicity in vitro. Human Kidney tubular cell line, HK-2 cells were divided into four groups: control group, GM group (cells incubated with GM only), heat shock (HS) group (cells incubated at 43 degrees C for 30 min), and GM plus HS group, respectively. Lactate dehydrogenase (LDH) release increased time-dependently from 24 hr to 96 hr compared to the data of cells treated with GM only. Results of NAG activities, superoxide dismutase (SOD) activities and malondialdehyde (MDA) content were similar to that of the LDH release. The amount of HSP72 positive cells increased significantly at 72 hr after cells were treated with GM only. Both HSP72 protein and gene expression increased significantly at 72 hr when cells were treated with GM. On the other hand, HS induced HSP72 expression markedly. Pretreatment of HS inhibited HK-2 cells from GM-induced injury. It could reduce LDH release and NAG activity. HS also increased SOD activity, and decreased MDA content when cells were damaged by GM. These findings suggested that HS may protect kidney cells from GM-induced injury. Pre-induction of HSP72 may provide therapeutic strategies for nephrotoxicity induced by GM.

AB - The nephrotoxicity of gentamicin (GM) has been widely recognized. Heat shock protein 72 (HSP72) has been reported to be a cytoprotectant. However, its cytoprotective effect against GM induced kidney injury has not yet been studied. In this study, we investigated the cytoprotective effect of HSP72 on GM-induced nephrotoxicity in vitro. Human Kidney tubular cell line, HK-2 cells were divided into four groups: control group, GM group (cells incubated with GM only), heat shock (HS) group (cells incubated at 43 degrees C for 30 min), and GM plus HS group, respectively. Lactate dehydrogenase (LDH) release increased time-dependently from 24 hr to 96 hr compared to the data of cells treated with GM only. Results of NAG activities, superoxide dismutase (SOD) activities and malondialdehyde (MDA) content were similar to that of the LDH release. The amount of HSP72 positive cells increased significantly at 72 hr after cells were treated with GM only. Both HSP72 protein and gene expression increased significantly at 72 hr when cells were treated with GM. On the other hand, HS induced HSP72 expression markedly. Pretreatment of HS inhibited HK-2 cells from GM-induced injury. It could reduce LDH release and NAG activity. HS also increased SOD activity, and decreased MDA content when cells were damaged by GM. These findings suggested that HS may protect kidney cells from GM-induced injury. Pre-induction of HSP72 may provide therapeutic strategies for nephrotoxicity induced by GM.

M3 - Journal article

C2 - 17043427

SN - 1011-8934

VL - 21

SP - 904

EP - 910

JO - Journal of Korean Medical Science

JF - Journal of Korean Medical Science

IS - 5

ER -