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2. PAR2 activation on human tubular epithelial cells engages converging signaling pathways to induce an inflammatory and fibrotic milieu.

Author

Vesey, David A., Iyer, Abishek, Owen, Evan, Kamato, Danielle, Johnson, David W., Gobe, Glenda C., Fairlie, David P., and Nikolic-Paterson, David J.

Subjects
EPITHELIAL cells, PRIMARY cell culture, G protein coupled receptors, CELLULAR signal transduction, HUMAN cell culture
Abstract

Key features of chronic kidney disease (CKD) include tubulointerstitial inflammation and fibrosis. Protease activated receptor-2 (PAR2), a G-protein coupled receptor (GPCR) expressed by the kidney proximal tubular cells, induces potent proinflammatory responses in these cells. The hypothesis tested here was that PAR2 signalling can contribute to both inflammation and fibrosis in the kidney by transactivating known disease associated pathways. Using a primary cell culture model of human kidney tubular epithelial cells (HTEC), PAR2 activation induced a concentration dependent, PAR2 antagonist sensitive, secretion of TNF, CSF2, MMP-9, PAI-1 and CTGF. Transcription factors activated by the PAR2 agonist 2F, including NFκB, AP1 and Smad2, were critical for production of these cytokines. A TGF-β receptor-1 (TGF-βRI) kinase inhibitor, SB431542, and an EGFR kinase inhibitor, AG1478, ameliorated 2F induced secretion of TNF, CSF2, MMP-9, and PAI-1. Whilst an EGFR blocking antibody, cetuximab, blocked PAR2 induced EGFR and ERK phosphorylation, a TGF-βRII blocking antibody failed to influence PAR2 induced secretion of PAI-1. Notably simultaneous activation of TGF-βRII (TGF-β1) and PAR2 (2F) synergistically enhanced secretion of TNF (2.2-fold), CSF2 (4.4-fold), MMP-9 (15-fold), and PAI-1 (2.5-fold). In summary PAR2 activates critical inflammatory and fibrotic signalling pathways in human kidney tubular epithelial cells. Biased antagonists of PAR2 should be explored as a potential therapy for CKD. [ABSTRACT FROM AUTHOR]

Published
2024
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15. Endothelial Dysfunction in Atherosclerotic Cardiovascular Diseases and Beyond: From Mechanism to Pharmacotherapies

Author

Xu, Suowen, primary, Ilyas, Iqra, additional, Little, Peter J., additional, Li, Hong, additional, Kamato, Danielle, additional, Zheng, Xueying, additional, Luo, Sihui, additional, Li, Zhuoming, additional, Liu, Peiqing, additional, Han, Jihong, additional, Harding, Ian C., additional, Ebong, Eno E., additional, Cameron, Scott J., additional, Stewart, Alastair G., additional, and Weng, Jianping, additional

Published
2021
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17. Akt acts as a switch for GPCR transactivation of the TGF‐β receptor type 1.

Author

Mohamed, Raafat, Shajimoon, Aravindra, Afroz, Rizwana, Gabr, Mai, Thomas, Walter G., Little, Peter J., and Kamato, Danielle

Subjects
CELL receptors, PROTEIN kinase B, G protein coupled receptors, TRANSFORMING growth factors, VASCULAR smooth muscle, ANGIOTENSIN II
Abstract

Transforming growth factor (TGF)‐β signalling commences with the engagement of TGF‐β ligand to cell surface TGF‐β receptors (TGFBR) stimulating Smad2 carboxyl‐terminal phosphorylation (phospho‐Smad2C) and downstream biological responses. In several cell models, G protein‐coupled receptors (GPCRs) transactivate the TGF‐β receptors type‐1 (TGFBR1) leading to phospho‐Smad2C, however, we have recently published that in keratinocytes thrombin did not transactivate the TGFBR1. The bulk of TGFBRs reside in the cytosol and in response to protein kinase B (Akt phosphorylation) can translocate to the cell surface increasing the cell's responsiveness to TGF‐β. In this study, we investigate the role of Akt in GPCR transactivation of the TGFBR1. We demonstrate that angiotensin II and thrombin do not phosphorylate Smad2C in human vascular smooth muscle cells and in keratinocytes respectively. We used Akt agonist, SC79 to sensitise the cells to Akt and observed that Ang II and thrombin phosphorylate Smad2C via Akt/AS160‐dependent pathways. We show that SC79 rapidly translocates TGFBRs to the cell surface thus increasing the cell's response to the GPCR agonist. These findings highlight novel mechanistic insight for the role of Akt in GPCR transactivation of the TGFBR1. [ABSTRACT FROM AUTHOR]

Published
2022
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31. Gaq proteins: molecular pharmacology and therapeutic potential

Author

Kamato, Danielle, primary, Mitra, Partha, additional, Davis, Felicity, additional, Osman, Narin, additional, Chaplin, Rebecca, additional, Cabot, Peter J., additional, Afroz, Rizwana, additional, Thomas, Walter, additional, Zheng, Wenhua, additional, Kaur, Harveen, additional, Brimble, Margaret, additional, and Little, Peter J., additional

Published
2016
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34. 25 Years of endothelin research: the next generation

Author

Emoto, Noriaki, Vignon-Zellweger, Nicolas, Moreira Lopes, Rheure Alves, Cacioppo, Joseph, Desbiens, Louisane, Kamato, Danielle, Leurgans, Thomas, Moorhouse, Rebecca, Straube, Julia, Wurm, Raphael, Heiden, Susi, Ergul, Adviye, Yanagisawa, Masashi, Barton, Matthias, Emoto, Noriaki, Vignon-Zellweger, Nicolas, Moreira Lopes, Rheure Alves, Cacioppo, Joseph, Desbiens, Louisane, Kamato, Danielle, Leurgans, Thomas, Moorhouse, Rebecca, Straube, Julia, Wurm, Raphael, Heiden, Susi, Ergul, Adviye, Yanagisawa, Masashi, and Barton, Matthias

Abstract

In the past three decades, endothelin and endothelin receptor antagonists have received great scientific and clinical interest, leading to the publication of more than 27,000 scientific articles since its discovery. The Thirteenth International Conference on Endothelin (ET-13) was held on September 8-11, 2013, at Tokyo Campus of the University of Tsukuba in Japan. Close to 300 scientists from 25 countries from around the world came to Tokyo to celebrate the anniversary of the discovery of the endothelin peptide discovered 25 years ago at the University of Tsukuba. This article summarizes some of the highlights of the conference, the anniversary celebration ceremony, and particularly the participation of next generation of endothelin researchers in endothelin science and the anniversary celebration. As a particular highlight, next generation endothelin researchers wrote a haiku (a traditional form of Japanese poetry originating from consisting of no more than three short verses and 27 on, or Japanese phonetic units) to describe the magic of endothelin science which they presented to the conference audience at the anniversary ceremony. The text of each haiku - both in its original language together with the English translation - is part of this article providing in an exemplary fashion how poetry can be bridged with science. Finally, we give an outlook towards the next 25 years of endothelin research. (C) 2014 Elsevier Inc. All rights reserved.

Published
2014

37. The expansion of GPCR transactivation-dependent signalling to include serine/threonine kinase receptors represents a new cell signalling frontier.

Author

Kamato, Danielle, Rostam, Muhamad, Bernard, Rebekah, Piva, Terrence, Mantri, Nitin, Guidone, Daniel, Zheng, Wenhua, Osman, Narin, and Little, Peter

Subjects
*G protein coupled receptors, *CELLULAR signal transduction, *SERINE/THREONINE kinases, *TRANSFORMING growth factors-beta, *MOLECULAR recognition
Abstract

G protein-coupled receptor (GPCR) signalling is mediated through transactivation-independent signalling pathways or the transactivation of protein tyrosine kinase receptors and the recently reported activation of the serine/threonine kinase receptors, most notably the transforming growth factor-β receptor family. Since the original observation of GPCR transactivation of protein tyrosine kinase receptors, there has been considerable work on the mechanism of transactivation and several pathways are prominent. These pathways include the 'triple membrane bypass' pathway and the generation of reactive oxygen species. The recent recognition of GPCR transactivation of serine/threonine kinase receptors enormously broadens the GPCR signalling paradigm. It may be predicted that the transactivation of serine/threonine kinase receptors would have mechanistic similarities with transactivation of tyrosine kinase pathways; however, initial studies suggest that these two transactivation pathways are mechanistically distinct. Important questions are the relative importance of tyrosine and serine/threonine transactivation pathways, the contribution of transactivation to overall GPCR signalling, mechanisms of transactivation and the range of cell types in which this phenomenon occurs. The ultimate significance of transactivation-dependent signalling remains to be defined but it appears to be prominent and if so will represent a new cell signalling frontier. [ABSTRACT FROM AUTHOR]

Published
2015
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