HSF1 Attenuates the Release of Inflammatory Cytokines Induced by Lipopolysaccharide through Transcriptional Regulation of
            <i>Atg10</i>

Tan, Hong; Huang, F.; Huang, Minghui; Wu, Xia; Tong, Zhongyi

doi:10.1128/spectrum.03059-22

Cited by 5 publications

(2 citation statements)

References 37 publications

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“…In addition to the role of HSPs, the response to HS also involves autophagy that degrades and recycles damaged organelles in lysosomes [26]. The heat shock factor-1 enhances the expression of autophagy genes, which participate in generating a protective response and extend cellular lifespan [27]. In stressful situations, mitochondria and endoplasmic reticulum can trigger the unfolded protein response (UPR), which promotes the functional recovery of these organelles [28].…”

Section: Introductionmentioning

confidence: 99%

The effects of heat stress on intrauterine development, reproductive function, and ovarian gene expression of F1 female mice as well as gene expression of F2 embryos

Silva,

Souza-Fabjan,

Bento

et al. 2023

Biology of Reproduction

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Exposure to heat stress (HS) in utero was postulated to trigger an adaptive molecular response that can be transmitted to the next generation. Hence, this study assessed the impact of HS exposure at different stages of the gestational period of mice on the female F1 population and their offspring. Heat stress exposure (41°C and 65% relative humidity-RH) occurred during the first half (FP), the second half (SP), or the entire pregnancy (TP). A control group (C) was maintained in normothermic conditions (25°C, 45% RH) throughout the experiment. Heat stress had a significant negative effect on intrauterine development, mainly when HS exposure occurred in the first half of pregnancy (FP and TP groups). Post-natal growth of FP and TP mice was hindered until four weeks of age. The total number of follicles per ovary did not vary (P > 0.05) between the control and HS-exposed groups. Mean numbers of primordial follicles were lower (P < 0.05) in the sexually mature FP than those in SP and TP F1 females. However, the mean number of viable embryos after superovulation was lower (P < 0.05) in TP compared with C group. The expression of genes associated with physiological and cellular response to HS, autophagy, and apoptosis was significantly affected in the ovarian tissue of F1 females and F2 in vivo-derived blastocysts in all HS-exposed groups. In conclusion, exposure to HS during pregnancy compromised somatic development and reproductive parameters as well as altered gene expression profile that was then transmitted to the next generation of mice.

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Section: Introductionmentioning

confidence: 99%

The effects of heat stress on intrauterine development, reproductive function, and ovarian gene expression of F1 female mice as well as gene expression of F2 embryos

Silva,

Souza-Fabjan,

Bento

et al. 2023

Biology of Reproduction

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“…The disparity in results for the function of CCL5 in cancer is puzzling but is possibly related to expression of the CCL5 receptor, CCR5, on cancer cells. There is also precedent for an increase in cytokine-related signaling with HSF1 inhibition in other contexts, such as LPS exposure (43,44). Because these results saw a partial loss of CD8+ T cell attraction by silencing CCL5, it is likely that attraction of T cells after HSF1 depletion is regulated by additional mechanisms, including antigen presentation (45).…”

Section: Discussionmentioning

confidence: 99%

HSF1 excludes CD8+ T cells from breast tumors via suppression of CCL5

Carpenter

Ray

Wang

et al. 2022

Preprint

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Cells have evolved mechanisms for response to external stressors in order to maintain cell viability in the face of changes in the environment. The response to heat stress is driven by the transcription factor heat shock factor 1 (HSF1), which is considered the master regulator of the heat shock response. Here we report a new HSF1 gene signatured termed “HSF1 Activity Signature,” or HAS, which is a 23-gene signature that more specifically assesses HSF1 transcriptional activity. We first identified genes that are direct transcriptional targets of HSF1 utilizing more than 40 ChIP-Seq samples in the public domain. Genes identified from ChIP-Seq were then reduced by removing genes whose expression was not altered or showed increased expression with the knockdown of HSF1. These genes were then assessed for their correlation with every other gene across 11 cancer expression datasets to develop an adjacency matrix to identify subgroups of genes that have high inter-gene correlation. The resulting 23-gene set (HAS) was then tested for its performance of assessing HSF1 activity wherein it was found to decreased when HSF1 was knocked down and increase in response to heat shock. The HAS was also able to predict outcomes of breast cancer patients that are previously observed such as high HAS was associated with worse overall survival and metastasis-free survival. This association with cancer patient outcomes extended to many other tumor types. In total, the 23-gene set we termed HAS, is an accurate tool to assess HSF1 activity from transcript expression data that is not limited to cancer-related functions of HSF1.

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Inhibiting autophagy enhances idarubicin chemosensitivity and induces immune escape in FAT1-low-expressing AML cells

Zhang,

Wang,

Dai

et al. 2025

International Immunopharmacology

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HSF1 Attenuates the Release of Inflammatory Cytokines Induced by Lipopolysaccharide through Transcriptional Regulation of Atg10

Abstract: HSF1 plays an important protective role in endotoxemic mice. However, the protective mechanisms of HSF1 are poorly understood.

Cited by 5 publications

References 37 publications

The effects of heat stress on intrauterine development, reproductive function, and ovarian gene expression of F1 female mice as well as gene expression of F2 embryos

The effects of heat stress on intrauterine development, reproductive function, and ovarian gene expression of F1 female mice as well as gene expression of F2 embryos

HSF1 excludes CD8+ T cells from breast tumors via suppression of CCL5

Inhibiting autophagy enhances idarubicin chemosensitivity and induces immune escape in FAT1-low-expressing AML cells

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