Association of Stat3 with HSF1 plays a critical role in G-CSF-induced cardio-protection against ischemia/reperfusion injury

Ma, Hong; Gong, Hui; Chen, Zhidan; Liang, Yanyan; Yuan, Jie; Zhang, Guoping; Wu, Jian; Ye, Yong; Yang, Chunjie; Nakai, Asami; Komuro, Issei; Ge, Junbo; Zou, Yunzeng

doi:10.1016/j.yjmcc.2012.02.011

Cited by 48 publications

(42 citation statements)

References 38 publications

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“…HSF1 represents a central hub in cancer cells that, besides HSP expression, regulates several other prosurvival pathways [10,14]. We show for the first time an interplay between STAT3 and HSF1 in PEL cells, even if a cross-talk between STAT family members and HSF1 has been reported in other cell types [12,13]. More importantly, in this study, we found that, due to the reduction of HSF1 and HSP response, AG490 triggered a complete autophagy, aimed at the elimination of the accumulating unfolded proteins [30] which is a rapidly occurring event in cancer cells characterized by an elevated level of protein synthesis, such as PEL cells [18].…”

Section: Discussionmentioning

confidence: 77%

“…STAT family members can interact with HSF1 regulating HSP expression [12]. In particular, phospho-STAT3 interacts with HSF1 promoting its transcriptional activity [13]. Besides inducing the expression of HSPs, HSF1 positively regulates other prosurvival pathways in cancer cells, that is the reason why it is itself emerging as a promising target in anticancer therapy [14,15].…”

Section: Introductionmentioning

confidence: 99%

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Tyrosine kinase inhibitor tyrphostin AG490 triggers both apoptosis and autophagy by reducing HSF1 and Mcl-1 in PEL cells

Granato¹,

Chiozzi²,

Filardi³

et al. 2015

Cancer Letters

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Section: Discussionmentioning

confidence: 77%

Section: Introductionmentioning

confidence: 99%

Tyrosine kinase inhibitor tyrphostin AG490 triggers both apoptosis and autophagy by reducing HSF1 and Mcl-1 in PEL cells

Granato¹,

Chiozzi²,

Filardi³

et al. 2015

Cancer Letters

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“…A comprehensive echocardiographic study was performed, including 2-dimensional imaging and M-mode imaging using the Vevo 2100 system (VisualSonics, Toronto, Canada). 21 For hemodynamic measurement, a 1.4 F pressure catheter (SPR 671, Millar Instruments) was inserted into the LV through the right common carotid artery after anesthesia. Left ventricular systolic pressure, left ventricular end diastolic pressure, left ventricular developed pressure, dP/dt max and dP/dt min were measured as described previously.…”

Section: Echocardiography and Hemodynamic Measurementmentioning

confidence: 99%

“…Left ventricular systolic pressure, left ventricular end diastolic pressure, left ventricular developed pressure, dP/dt max and dP/dt min were measured as described previously. 21 Subsequent data calculations were performed by operators blinded to the treatment assignment. Mice were then euthanized for further analysis.…”

Section: Echocardiography and Hemodynamic Measurementmentioning

confidence: 99%

Involvement of Endoplasmic Reticulum Stress–Mediated C/EBP Homologous Protein Activation in Coxsackievirus B3–Induced Acute Viral Myocarditis

Cai

Shen

et al. 2015

Circ: Heart Failure

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Background— This study tested the hypothesis whether endoplasmic reticulum (ER) stress/C/EBP homologous protein (CHOP) signaling is linked with coxsackievirus B3 (CVB3)–induced acute viral myocarditis (AVMC) in vivo. Methods and Results— AVMC was induced by intraperitoneal injection of 1000 tissue culture infectious dose (TCID 50 ) of CVB3 virus in mice. In AVMC mouse hearts (n=11), ER stress and CHOP were significantly activated, and were linked to the induction of proapoptotic signaling including reduction of Bcl-2, activation of Bax and caspase 3, compared with the controls (n=10), whereas these could be markedly blocked by ER stress inhibitor tauroursodeoxycholic acid administration (n=11). Moreover, chemical inhibition of ER stress significantly attenuated cardiomyocytes apoptosis, and prevented cardiac troponin I elevation, ameliorated cardiac dysfunction assessed by both hemodynamic and echocardiographic analysis, reduced viral replication, and increased survival rate after CVB3 inoculation. We further discovered that genetic ablation of CHOP (n=10) suppressed cardiac Bcl-2/Bax ratio reduction and caspase 3 activation, and prevented cardiomyotes apoptosis in vivo, compared with wild-type receiving CVB3 inoculation (n=10). Strikingly, CHOP deficiency exhibited dramatic protective effects on cardiac damage, cardiac dysfunction, viral replication, and promoted survival in CVB3-caused AVMC. Conclusions— Our data imply the involvement of ER stress/CHOP signaling in CVB3-induced AVMC via proapoptotic pathways, and provide a novel strategy for AVMC treatment.

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“…141 In contrast, interaction of Stat3 with Hsf1 also has been shown to result in increased Stat3 activity: G-CSF-stimulated Stat3 signaling mediated cardio-protection by decreasing cardiomyocyte apoptosis in a mouse heart ischemia/reperfusion model; decrease in cardiomyocyte apoptosis was shown to be critically dependent on the association of Stat3 and Hsf1. 142 …”

mentioning

confidence: 99%

Contribution of chaperones to STAT pathway signaling

et al. 2014

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Aberrant STAT signaling is associated with the development and progression of many cancers and immune related diseases. Recent findings demonstrate that proteostasis modulators under clinical investigation for cancer therapy have a significant impact on STAT signaling, which may be critical for mediating their anti-cancer effects. Chaperones are critical for protein folding, stability and function and, thus, play an essential role in the maintenance of proteostasis. In this review we discuss the role of chaperones in STAT and tyrosine kinase (TK) protein folding, modulation of STAT and TK activity, and degradation of TKs. We highlight the important role of chaperones in STAT signaling, and how this knowledge has provided a framework for the development of new therapeutic avenues of targeting STAT signaling related pathologies.

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Association of Stat3 with HSF1 plays a critical role in G-CSF-induced cardio-protection against ischemia/reperfusion injury

Cited by 48 publications

References 38 publications

Tyrosine kinase inhibitor tyrphostin AG490 triggers both apoptosis and autophagy by reducing HSF1 and Mcl-1 in PEL cells

Tyrosine kinase inhibitor tyrphostin AG490 triggers both apoptosis and autophagy by reducing HSF1 and Mcl-1 in PEL cells

Involvement of Endoplasmic Reticulum Stress–Mediated C/EBP Homologous Protein Activation in Coxsackievirus B3–Induced Acute Viral Myocarditis

Contribution of chaperones to STAT pathway signaling

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