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MKP2 suppresses TGF-β1-induced epithelial-to-mesenchymal transition through JNK inhibition.
Clin Sci (Lond). 2019 02 14; 133(3):545-550.CS

Abstract

Interstitial fibrosis is a typical feature of end-stage renal diseases, regardless of the initial cause of kidney injury. Epithelial-to-mesenchymal transition (EMT) is a mechanism that is thought to play a role in generating the interstitial matrix-producing myofibroblasts and is prominently induced by the transforming growth factor-β 1 (TGF-β1). TGF-β1 signals through a variety of Smad and non-Smad signaling pathways, including the mitogen-activated protein kinase (MAPK) pathways. In a study published in a recent issue of Clinical Science (Clin. Sci. (2018) 132(21),2339-2355), Li et al. investigated the potential role of the Mitogen-activated protein kinase phosphatase 2 (MKP2), also known as Dusp4, in the control of EMT and renal fibrosis. Based on results obtained with an animal model of kidney fibrosis and a proximal tubular epithelial cell line system, the authors put forward a role for MKP2 as a negative feedback regulator of TGF-β1-induced EMT and fibrosis in the kidney. Intriguingly, MKP2 is found to down-regulate activity of c-Jun, but not that of other MAPKs, extracellular signal-regulated kinases or p38, implying a role for c-Jun N-terminal kinase-dependent signaling in renal fibrosis. In this commentary, I discuss the findings of Li and co-workers in the context of the recent literature placing a focus on potential clinical/therapeutic implications.

Authors+Show Affiliations

Department of Internal Medicine III, Jena University Hospital, Am Klinikum 1, 07747 Jena, Germany Ivonne.loeffler@med.uni-jena.de.

Pub Type(s)

Journal Article
Comment

Language

eng

PubMed ID

30760641

Citation

Loeffler, Ivonne. "MKP2 Suppresses TGF-β1-induced Epithelial-to-mesenchymal Transition Through JNK Inhibition." Clinical Science (London, England : 1979), vol. 133, no. 3, 2019, pp. 545-550.
Loeffler I. MKP2 suppresses TGF-β1-induced epithelial-to-mesenchymal transition through JNK inhibition. Clin Sci (Lond). 2019;133(3):545-550.
Loeffler, I. (2019). MKP2 suppresses TGF-β1-induced epithelial-to-mesenchymal transition through JNK inhibition. Clinical Science (London, England : 1979), 133(3), 545-550. https://doi.org/10.1042/CS20180881
Loeffler I. MKP2 Suppresses TGF-β1-induced Epithelial-to-mesenchymal Transition Through JNK Inhibition. Clin Sci (Lond). 2019 02 14;133(3):545-550. PubMed PMID: 30760641.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - MKP2 suppresses TGF-β1-induced epithelial-to-mesenchymal transition through JNK inhibition. A1 - Loeffler,Ivonne, Y1 - 2019/02/13/ PY - 2018/12/06/received PY - 2019/01/24/revised PY - 2019/01/30/accepted PY - 2019/2/15/entrez PY - 2019/2/15/pubmed PY - 2019/11/12/medline KW - EMT KW - MKP2 KW - transforming growth factors SP - 545 EP - 550 JF - Clinical science (London, England : 1979) JO - Clin Sci (Lond) VL - 133 IS - 3 N2 - Interstitial fibrosis is a typical feature of end-stage renal diseases, regardless of the initial cause of kidney injury. Epithelial-to-mesenchymal transition (EMT) is a mechanism that is thought to play a role in generating the interstitial matrix-producing myofibroblasts and is prominently induced by the transforming growth factor-β 1 (TGF-β1). TGF-β1 signals through a variety of Smad and non-Smad signaling pathways, including the mitogen-activated protein kinase (MAPK) pathways. In a study published in a recent issue of Clinical Science (Clin. Sci. (2018) 132(21),2339-2355), Li et al. investigated the potential role of the Mitogen-activated protein kinase phosphatase 2 (MKP2), also known as Dusp4, in the control of EMT and renal fibrosis. Based on results obtained with an animal model of kidney fibrosis and a proximal tubular epithelial cell line system, the authors put forward a role for MKP2 as a negative feedback regulator of TGF-β1-induced EMT and fibrosis in the kidney. Intriguingly, MKP2 is found to down-regulate activity of c-Jun, but not that of other MAPKs, extracellular signal-regulated kinases or p38, implying a role for c-Jun N-terminal kinase-dependent signaling in renal fibrosis. In this commentary, I discuss the findings of Li and co-workers in the context of the recent literature placing a focus on potential clinical/therapeutic implications. SN - 1470-8736 UR - https://www.unboundmedicine.com/medline/citation/30760641/MKP2_suppresses_TGF_β1_induced_epithelial_to_mesenchymal_transition_through_JNK_inhibition_ L2 - https://portlandpress.com/clinsci/article-lookup/doi/10.1042/CS20180881 DB - PRIME DP - Unbound Medicine ER -