scholarly journals The Cross-Talk Between the TNF-α and RASSF-Hippo Signalling Pathways

2019 ◽  
Vol 20 (9) ◽  
pp. 2346 ◽  
Author(s):  
Delvac Oceandy ◽  
Bella Amanda ◽  
Faisal Ashari ◽  
Zakiyatul Faizah ◽  
M Aziz ◽  
...  
Keyword(s):  
Cross Talk ◽  
Hippo Pathway ◽  
Signalling Pathways ◽  
Physiological Processes ◽  
Tnf Α ◽  
The Cross ◽  
Factor Α ◽  
Apoptosis Regulation ◽  
The Hippo Pathway ◽  
Hippo Signalling

The regulation of cell death through apoptosis is essential to a number of physiological processes. Defective apoptosis regulation is associated with many abnormalities including anomalies in organ development, altered immune response and the development of cancer. Several signalling pathways are known to regulate apoptosis including the Tumour Necrosis Factor-α (TNF-α) and Hippo signalling pathways. In this paper we review the cross-talk between the TNF-α pathway and the Hippo signalling pathway. Several molecules that tightly regulate the Hippo pathway, such as members of the Ras-association domain family member (RASSF) family proteins, interact and modulate some key proteins within the TNF-α pathway. Meanwhile, TNF-α stimulation also affects the expression and activation of core components of the Hippo pathway. This implies the crucial role of signal integration between these two major pathways in regulating apoptosis.

Role of the HIPPO pathway as potential key player in the cross talk between oncology and cardiology

2021 ◽  
Vol 159 ◽  
pp. 103246
Author(s):  
Girolamo Manno ◽  
Clarissa Filorizzo ◽  
Daniele Fanale ◽  
Chiara Brando ◽  
Daniela Di Lisi ◽  
...  
Keyword(s):  
Cross Talk ◽  
Hippo Pathway ◽  
The Cross ◽  
The Hippo Pathway

Ionizing radiation promotes CCL27 secretion from keratinocytes through the cross talk between TNF-α and ROS

2016 ◽  
Vol 31 (3) ◽  
pp. e21868 ◽  
Author(s):  
Qian Zhang ◽  
Linlin Zhu ◽  
Gang Wang ◽  
Ye Zhao ◽  
Na Xiong ◽  
...  
Keyword(s):  
Ionizing Radiation ◽  
Cross Talk ◽  
Tnf Α ◽  
The Cross

1183Beta-Adrenoceptor activation increases cardiac galectin-3 levels via the hippo signaling pathway

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
X.-J Du ◽  
W B Zhao ◽  
Q Lu ◽  
M N Nguyen ◽  
M Ziemann ◽  
...  
Keyword(s):  
Hippo Pathway ◽  
Fold Increase ◽  
Signalling Pathway ◽  
Mutant Form ◽  
Wild Type ◽  
Galectin 3 ◽  
Β Blockers ◽  
The Hippo Pathway ◽  
Hippo Signalling

Abstract Background Galectin-3 (Gal-3) is a clinical biomarker for risk of cardiovascular disease and a disease mediator forming a therapeutic target. However, the mechanism(s) that regulate cardiac expression of Gal-3 remains unknown. Activation of the sympatho-β-adrenergic system is a hallmark of heart disease, but the relationship of βAR activation and cardiac content of Gal-3 remains unknown. Purpose To determine the role of βAR activation in regulating cardiac Gal-3 level and the responsible mechanism focusing on the Hippo signalling pathway. Methods Wild-type and Gal-3 gene deleted (Gal3-KO) mice were used. To test the role of the Hippo pathway, we used transgenic (TG) mouse strains with cardiac overexpression of mammalian-20-like sterile kinase 1 (Mst1, mammalian orthology of Drosophila Hippo kinase) either in wild-type form (TG-Mst1) or dominative-negative kinase dead mutant form (TG-dnMst1). Effects of β-antagonist (isoprenaline, ISO) and antagonists were determined. We measured phosphorylation (Ser127) of YAP as a transcription co-regulator acting as the main signal output of the Hippo pathway. Results In wild-type mice, treatment with ISO led to a time- and dose-dependent increase in cardiac expression of Gal-3 (Fig. A) accompanied by elevated circulating Gal-3 levels (Fig. B). ISO treatment stimulated cardiac expression of Mst1 and YAP hyper-phosphorylation (i.e. inactivation, Fig. C), indicating activation of the Hippo signalling. These effects of ISO were inhibited by β-blockers (propranolol, Prop; carvedilol, Carv; Fig. D,E). Relative to non-TG controls, ISO-induced expression of Gal-3 was inhibited by 75% in TG-dnMst1 mice (inactivated Mst1), but exaggerated by 7-fold in TG-Mst1 mice (activated Mst1). Mst1-TG mice had a 45-fold increase in Gal-3 content, YAP hyper-phosphorylation and enhanced pro-fibrotic signaling. In Mst1-TG mice, whilst blood Gal-3 level was unchanged, treatment with ISO (6 mg, 2 days) evoked a marked increase in cardiac and blood Gal-3 levels. Using rat cardiomyoblasts, we showed that ISO-mediated Mst1 expression and YAP phosphorylation were PKA-dependent and that siRNA-mediated YAP knockdown led to Gal-3 upregulation. The role of Gal-3 in mediating ISO-induced cardiomyopathy was examined by treating wild-type and Gal3-KO mice with ISO (30 mg/kg, 7 days). ISO-treated wild-type mice had 8-fold increase in cardiac Gal-3, ventricular dysfunction, fibrosis, hypertrophy and activated inflammatory or fibrotic signalling. All these changes, except hypertrophy, were abolished by Gal3-KO. beta-AR regulates galectin-3 Conclusion βAR stimulation increases cardiac expression of Gal-3 through activation of the Hippo signalling pathway. This is accompanied by elevated circulating Gal-3 level. βAR antagonists inhibited βAR-Mst1 (Hippo) signalling and cardiac Gal-3 expression, actions likely contributing to the overall efficacy of β-blockers. Acknowledgement/Funding NHMRC of Australia; Nature Science Fund of China

scholarly journals Monocytes Upregulate Endothelial Cell Expression of Tissue Factor: A Role for Cell-Cell Contact and Cross-Talk

Blood ◽  
1997 ◽  
Vol 89 (2) ◽  
pp. 541-549 ◽  
Author(s):  
Emanuela Napoleone ◽  
Angelomaria Di Santo ◽  
Roberto Lorenzet
Keyword(s):  
Endothelial Cell ◽  
Tissue Factor ◽  
Cross Talk ◽  
Umbilical Vein ◽  
Cell Types ◽  
Cell Contact ◽  
Tnf Α ◽  
Factor Α ◽  
Cell Expression ◽  
Cell Cell

Abstract Monocytes and endothelial cells interact at sites of vascular injury during inflammatory response, thrombosis, and development of atherosclerotic lesions. Such interactions result in modulation of several biological functions of the two cell types. Because both cells, on appropriate stimulation, synthesize tissue factor (TF), we examined the effect of human umbilical vein endothelial cell (HUVEC)/monocyte coculture on the expression of TF. We found that the coincubation resulted in TF generation, which was maximal at 4 hours, increased with increasing numbers of monocytes, and required mRNA and protein synthesis. Supernatant from HUVEC/monocyte coculture induced TF activity in HUVECs, but not in monocytes, indicating that HUVEC were the cells responsible for the activity, and that soluble mediators were involved. Interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α), well-known inducers of TF in HUVECs, were found in the supernatant from the coculture, and specific antibodies directed against either cytokine inhibited TF generation. The need of IL-1β and TNF-α synthesis in order to elicit TF expression was also suggested by the delay observed in TF mRNA formation and TF activity generation when monocytes were incubated with HUVECs. IL-1β and TNF-α antigen levels in the coculture supernatant, and, consequently, HUVEC TF expression, were inhibited in the presence of anti-CD18 monoclonal antibody. These findings emphasize the role of cell-cell contact and cross-talk in the procoagulant activity, which could be responsible for the thromboembolic complications observed in those vascular disorders in which monocyte infiltration is a common feature.

scholarly journals Carvacrol and Thymol Modulate the Cross-Talk between TNF-α and IGF-1 Signaling in Radiotherapy-Induced Ovarian Failure

2019 ◽  
Vol 2019 ◽  
pp. 1-10
Author(s):  
Yasmen F. Mahran ◽  
Amira M. Badr ◽  
Alhanouf Aldosari ◽  
Raghad Bin-Zaid ◽  
Hind N. Alotaibi
Keyword(s):  
Oxidative Stress ◽  
Cross Talk ◽  
Ovarian Failure ◽  
Radioprotective Effect ◽  
Whole Body ◽  
Nuclear Antigen ◽  
Hormonal Changes ◽  
Tnf Α ◽  
Ovarian Damage ◽  
The Cross

Premature ovarian failure (POF) is a common cause of infertility in premenopausal women who are unavoidably exposed to cytotoxic therapy. Radiotherapy is one of the most effective cytotoxic treatments. However, the radiosensitivity of ovarian tissues limits its therapeutic outcome and results in the depletion of the primordial follicle and loss of fertility. Therefore, the need for an effective radioprotective therapy is evident especially when none of the current clinically used modalities for radioprotection succeeds efficiently. The present study investigated the potential radioprotective effect of carvacrol (CAR) (80 mg) or thymol (80 mg) on gamma- (γ-) irradiation-induced ovarian damage as well as their role in the cross-talk between IGF-1 and TNF-α signaling and antioxidative activity. In immature female Wister rats, a single dose of whole-body irradiation (3.2 Gy, L D 20 ) produced considerable ovarian damage, which was evident by histopathological findings and hormonal changes. Interestingly, pretreatment with CAR or thymol significantly enhanced the follicular development and restored the anti-Mullerian hormone (AMH), E2, and FSH levels. Both essential oils improved the irradiation-mediated oxidative stress and reduction in proliferating cell nuclear antigen (PCNA) expression. Moreover, irradiated rats exhibited an inverse relationship between IGF-1 and TNF-α levels two days post irradiation, which was further inverted by the pretreatment with CAR and thymol and ought to contribute in their radioprotective mechanisms. In conclusion, CAR and thymol showed a radioprotective effect and rescued the ovarian reserve mainly through counteracting oxidative stress and the dysregulated cross-talk between IGF-1 and TNF-α.

scholarly journals Cross-Talk Between Mitochondrial Fusion and the Hippo Pathway in Controlling Cell Proliferation During Drosophila Development

Genetics ◽  
2016 ◽  
Vol 203 (4) ◽  
pp. 1777-1788 ◽  
Author(s):  
Qiannan Deng ◽  
Ting Guo ◽  
Xiu Zhou ◽  
Yongmei Xi ◽  
Xiaohang Yang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cross Talk ◽  
Hippo Pathway ◽  
Mitochondrial Fusion ◽  
Drosophila Development ◽  
The Hippo Pathway

A novel role for reciprocal CD30-CD30L signaling in the cross-talk between natural killer and dendritic cells

2012 ◽  
Vol 393 (1-2) ◽  
pp. 101-106 ◽  
Author(s):  
Vijaya Lakshmi Simhadri ◽  
Hinrich P. Hansen ◽  
Venkateswara R. Simhadri ◽  
Katrin S. Reiners ◽  
Martina Bessler ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Immune Responses ◽  
Nk Cells ◽  
Natural Killer ◽  
Cross Talk ◽  
Mitogen Activated Protein Kinase ◽  
Tnf Α ◽  
Mitogen Activated Protein ◽  
Ifn Γ ◽  
The Cross

Abstract The interplay between dendritic cells (DCs) and natural killer (NK) cells directs adaptive immune responses. The molecular basis of the cross-talk is largely undefined. Here, we provide evidence for a contribution of CD30 (TNFRSF8) and its ligand CD30L (TNFSF8) expressed on NK cells and DCs, respectively. We demonstrate that CD30-mediated engagement of CD30L induced cytokine secretion from immature DCs via the mitogen-activated protein kinase pathway. Moreover, CD30L engagement promoted differentiation to mature DCs. On the contrary, the engagement of CD30 on NK cells resulted in an NF-κB-dependent release of TNF-α/IFN-γ. These data uncover a novel and unexpected role for CD30/CD30L that contributes to proinflammatory immune responses.

scholarly journals Disease implication of hyper-Hippo signalling

Open Biology ◽  
2016 ◽  
Vol 6 (10) ◽  
pp. 160119 ◽  
Author(s):  
Shu-Ping Wang ◽  
Lan-Hsin Wang
Keyword(s):  
Cellular Proliferation ◽  
Current Knowledge ◽  
Hippo Pathway ◽  
Living Cells ◽  
Regulatory Mechanisms ◽  
Arrhythmogenic Cardiomyopathy ◽  
Tumour Suppressor Function ◽  
The Hippo Pathway ◽  
Lateral Sclerosis ◽  
Hippo Signalling

The Hippo signalling pathway regulates cellular proliferation, apoptosis and differentiation, thus exerting profound effects on cellular homeostasis. Inhibition of Hippo signalling has been frequently implicated in human cancers, indicating a well-known tumour suppressor function of the Hippo pathway. However, it is less certain whether and how hyperactivation of the Hippo pathway affects biological outcome in living cells. This review describes current knowledge of the regulatory mechanisms of the Hippo pathway, mainly focusing on hyperactivation of the Hippo signalling nexus. The disease implications of hyperactivated Hippo signalling have also been discussed, including arrhythmogenic cardiomyopathy, Sveinsson's chorioretinal atrophy, Alzheimer's disease, amyotrophic lateral sclerosis and diabetes. By highlighting the significance of disease-relevant Hippo signalling activation, this review can offer exciting prospects to address the onset and potential reversal of Hippo-related disorders.

scholarly journals Crumbs and the apical spectrin cytoskeleton regulate r8 cell fate in the Drosophila eye

PLoS Genetics ◽  
2021 ◽  
Vol 17 (6) ◽  
pp. e1009146
Author(s):  
Jonathan M. Pojer ◽  
Abdul Jabbar Saiful Hilmi ◽  
Shu Kondo ◽  
Kieran F. Harvey
Keyword(s):  
Cell Fate ◽  
Hippo Pathway ◽  
Green Light ◽  
Photoreceptor Cells ◽  
Organ Growth ◽  
Important Regulator ◽  
Spectrin Cytoskeleton ◽  
Fate Decision ◽  
The Hippo Pathway ◽  
Hippo Signalling

The Hippo pathway is an important regulator of organ growth and cell fate. In the R8 photoreceptor cells of the Drosophila melanogaster eye, the Hippo pathway controls the fate choice between one of two subtypes that express either the blue light-sensitive Rhodopsin 5 (Hippo inactive R8 subtype) or the green light-sensitive Rhodopsin 6 (Hippo active R8 subtype). The degree to which the mechanism of Hippo signal transduction and the proteins that mediate it are conserved in organ growth and R8 cell fate choice is currently unclear. Here, we identify Crumbs and the apical spectrin cytoskeleton as regulators of R8 cell fate. By contrast, other proteins that influence Hippo-dependent organ growth, such as the basolateral spectrin cytoskeleton and Ajuba, are dispensable for the R8 cell fate choice. Surprisingly, Crumbs promotes the Rhodopsin 5 cell fate, which is driven by Yorkie, rather than the Rhodopsin 6 cell fate, which is driven by Warts and the Hippo pathway, which contrasts with its impact on Hippo activity in organ growth. Furthermore, neither the apical spectrin cytoskeleton nor Crumbs appear to regulate the Hippo pathway through mechanisms that have been observed in growing organs. Together, these results show that only a subset of Hippo pathway proteins regulate the R8 binary cell fate decision and that aspects of Hippo signalling differ between growing organs and post-mitotic R8 cells.

Sign in / Sign up

Export Citation Format

Share Document