TGF-β1 mediates 70-kDa heat shock protein induction due to ultraviolet irradiation in human skin fibroblasts

Cao, Yu; Ohwatari, Nobu; Matsumoto, Takaaki; Kosaka, Mitsuo; Ohtsuru, Akira; Yamashita, Shunichi

doi:10.1007/s004240050905

Cited by 73 publications

(42 citation statements)

References 26 publications

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“…TGF-β1 is an attractive candidate as an anti-inflammatory and cytoprotective signaling molecule in response to volatile anesthetic treatment as: (1) it has been shown to be released in response to cell surface PS membrane externalization [9,10,11,12,13]; (2) it has potent anti-inflammatory effects and inhibits leukocyte adhesiveness, and (3) exogenous TGF-β1 reduces IR injury in many organ systems [14,15,16]. Moreover, TGF-β1 is a well-known activator of ERK and Akt signaling and TGF-β1 causes upregulation of HSP70 in several cell lines [23,24,25]. We previously demonstrated that sevoflurane caused phosphorylation of ERK and Akt and upregulated HSP70 in human proximal tubule (HK-2) cells [17].…”

Section: Discussionmentioning

confidence: 99%

TGF-Beta1 Release by Volatile Anesthetics Mediates Protection against Renal Proximal Tubule Cell Necrosis

Lee

Kim

et al. 2007

Am J Nephrol

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Background/Aims:We have previously demonstrated that clinically utilized volatile anesthetics protect against renal ischemia reperfusion injury in rats in vivo and reduce necrosis in vitro via activation of ERK and Akt and by upregulating HSP70. In this study, we further deciphered the upstream cellular signaling mechanism(s) of volatile anesthetic-mediated antinecrotic effects in vitro. We hypothesized that volatile anesthetics perturb the structure of the plasma membrane lipid bilayer, causing externalization of phosphatidylserine (PS) to the outer surface on renal tubule cells leading to the increased generation of transforming growth factor-β1 (TGF-β1), a cytokine with antinecrotic properties. Methods and Results: In human proximal tubule (HK-2) cell culture, 16-hour exposure to volatile anesthetics (isoflurane, halothane, sevoflurane) caused membrane externalization of PS detected by positive annexin-V staining and increased the release of TGF-β1 into the cell culture media. Exogenous TGF-β1 induced protection and neutralizing TGF-β1 antibody prevented the cytoprotection by volatile anesthetics against hydrogen peroxide-induced HK-2 cell necrosis. Conclusions: Volatile anesthetics induce a cytoprotective signaling cascade in proximal tubule cells via membrane externalization of PS initiating TGF-β1-mediated cytoprotection.

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Section: Discussionmentioning

confidence: 99%

TGF-Beta1 Release by Volatile Anesthetics Mediates Protection against Renal Proximal Tubule Cell Necrosis

Lee

Kim

et al. 2007

Am J Nephrol

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“…Heat shock proteins (HSPs) are produced by cells and tissues in response to various stressful conditions, including cold [17], UV light [18], wound healing or tissue remodeling [19]. Recently, accumulated evidences indicated that HSPs are aberrantly overexpressed in many types of human cancers and play critical roles in tumor progression.…”

Section: Discussionmentioning

confidence: 99%

Distinct prognostic roles of HSPB1 expression in non-small cell lung cancer

Huang¹,

Li²,

Sun³

et al. 2018

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Lung cancer is the leading cause of cancer morbidity and mortality around world. Heat shock protein beta-1 (HSPB1) expression is aberrantly increased in non-small cell lung cancer (NSCLC) patients. However, the roles of HSPB1 expression in the prognosis of NSCLC are still elusive. In this study, we investigated the prognostic roles of HSPB1 in NSCLC by using "The Kaplan-Meier plotter" (KM plotter) database. Our data indicated that HSPB1 mRNA low expression was correlated to better overall survival (OS) for all NSCLC patients, hazard ratio (HR) 1.41 (1.24-1.61), p=1.1e-7, and better OS in lung adenocarcinoma (LUAD) patients, HR 1.81 (1.42-2.32), p=1.5e-06, but not in lung squamous cell carcinoma (LUSC) patients, HR 1.21 (0.94-1.55), p=0.14. In addition, mRNA low expression of HSPB1 is also significantly associated with better OS of NSCLC patients in different smoking status, in different chemotherapy status, in clinical stage I & II, as well as patients with successful surgery treatment. Our results indicated that HSPB1 expression may have distinct prognostic values in NSCLC patients, and may provide an effective clinical strategy to accurately predict the prognosis of NSCLC patients.

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“…Their amount increases rapidly when cells are subjected or exposed to a wide variety of stresses such as heat, xenobiotics or drugs; pathological stimuli such as viral, bacterial and parasitic infections, inflammation and autoimmunity (Wu & Tanguay, 2006). In skin biopsy we can explore the expression of HSPs by WB and qRT-PCR (Cao et al, 1999;Rossner et al, 2003).…”

Section: Heat-shock Proteins (Hsps)mentioning

confidence: 99%