TGFβ1-Smad canonical and -Erk noncanonical pathways participate in interleukin-17-induced epithelial–mesenchymal transition in Sjögren’s syndrome

Interleukin-17 (IL-17) is a pleiotropic cytokine that plays a primary role in triggering epithelial–mesenchymal transition (EMT) in many chronic inflammatory diseases. EMT plays a critical role in the progression of salivary gland (SG) fibrosis in primary Sjögren’s syndrome (pSS). This study focused...

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Vydáno v:	Laboratory investigation Ročník 100; číslo 6; s. 824 - 836
Hlavní autoři:	Sisto, Margherita, Lorusso, Loredana, Ingravallo, Giuseppe, Ribatti, Domenico, Lisi, Sabrina
Médium:	Journal Article
Jazyk:	angličtina
Vydáno:	New York Nature Publishing Group US 01.06.2020 Nature Publishing Group
Témata:	13/21 13/31 14/63 38/77 692/308/575 692/420/256/2515 82/80 Activation Activation analysis Aged Cells, Cultured Cytokines Enzyme inhibitors Epithelial cells Epithelial-Mesenchymal Transition - physiology Extracellular signal-regulated kinase Fibrosis Humans Inflammatory diseases Interleukin 17 Interleukin-17 - metabolism Interleukins Kinases Laboratory Medicine Lip - cytology MAP Kinase Signaling System - physiology Medicine Medicine & Public Health Mesenchyme Middle Aged Pathology Salivary gland Salivary glands Signal transduction Sjogren's syndrome Sjogren's Syndrome - metabolism Sjogren's Syndrome - pathology Smad protein Smad Proteins - metabolism Smad2 protein Transforming Growth Factor beta1 - metabolism Transforming growth factor-b1
ISSN:	0023-6837, 1530-0307, 1530-0307
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Abstract	Interleukin-17 (IL-17) is a pleiotropic cytokine that plays a primary role in triggering epithelial–mesenchymal transition (EMT) in many chronic inflammatory diseases. EMT plays a critical role in the progression of salivary gland (SG) fibrosis in primary Sjögren’s syndrome (pSS). This study focused on the activation of the canonical TGF-β1/Smad2/3 and noncanonical TGF-β1/Erk1/2 pathways in IL-17-dependent TGFβ1-induced EMT in human SG epithelial cells (SGEC) derived from healthy subjects. The expression of phosphorylated Smad2/3 and Erk1/2 during IL-17 treatment-stimulated EMT was evaluated in healthy SGEC. Cotreatment with IL-17 and specific TGFβ receptor type I kinase inhibitor SB431542, or Erk 1/2 inhibitor U0126, abrogates the corresponding morphological changes and EMT phenotypic markers expression in healthy SGEC. Interestingly, inhibition of canonical TGFβ1/Smad2/3 signal transduction had no effect on activation of the noncanonical TGFβ1/Erk1/2/EMT pathway, suggesting that the two pathways act independently in activating IL-17-dependent EMT in SGEC. Epithelial–mesenchymal transition (EMT) plays a critical role in the progression of salivary gland (SG) fibrosis in primary Sjögren’s syndrome. This study demonstrates the IL-17-dependent activation of EMT in human SG epithelial cells that occurs through both the canonical TGF-β1/Smad2/3 and noncanonical TGF-β1/Erk1/2 pathways.
AbstractList	Interleukin-17 (IL-17) is a pleiotropic cytokine that plays a primary role in triggering epithelial–mesenchymal transition (EMT) in many chronic inflammatory diseases. EMT plays a critical role in the progression of salivary gland (SG) fibrosis in primary Sjögren’s syndrome (pSS). This study focused on the activation of the canonical TGF-β1/Smad2/3 and noncanonical TGF-β1/Erk1/2 pathways in IL-17-dependent TGFβ1-induced EMT in human SG epithelial cells (SGEC) derived from healthy subjects. The expression of phosphorylated Smad2/3 and Erk1/2 during IL-17 treatment-stimulated EMT was evaluated in healthy SGEC. Cotreatment with IL-17 and specific TGFβ receptor type I kinase inhibitor SB431542, or Erk 1/2 inhibitor U0126, abrogates the corresponding morphological changes and EMT phenotypic markers expression in healthy SGEC. Interestingly, inhibition of canonical TGFβ1/Smad2/3 signal transduction had no effect on activation of the noncanonical TGFβ1/Erk1/2/EMT pathway, suggesting that the two pathways act independently in activating IL-17-dependent EMT in SGEC.Epithelial–mesenchymal transition (EMT) plays a critical role in the progression of salivary gland (SG) fibrosis in primary Sjögren’s syndrome. This study demonstrates the IL-17-dependent activation of EMT in human SG epithelial cells that occurs through both the canonical TGF-β1/Smad2/3 and noncanonical TGF-β1/Erk1/2 pathways. Interleukin-17 (IL-17) is a pleiotropic cytokine that plays a primary role in triggering epithelial-mesenchymal transition (EMT) in many chronic inflammatory diseases. EMT plays a critical role in the progression of salivary gland (SG) fibrosis in primary Sjögren's syndrome (pSS). This study focused on the activation of the canonical TGF-β1/Smad2/3 and noncanonical TGF-β1/Erk1/2 pathways in IL-17-dependent TGFβ1-induced EMT in human SG epithelial cells (SGEC) derived from healthy subjects. The expression of phosphorylated Smad2/3 and Erk1/2 during IL-17 treatment-stimulated EMT was evaluated in healthy SGEC. Cotreatment with IL-17 and specific TGFβ receptor type I kinase inhibitor SB431542, or Erk 1/2 inhibitor U0126, abrogates the corresponding morphological changes and EMT phenotypic markers expression in healthy SGEC. Interestingly, inhibition of canonical TGFβ1/Smad2/3 signal transduction had no effect on activation of the noncanonical TGFβ1/Erk1/2/EMT pathway, suggesting that the two pathways act independently in activating IL-17-dependent EMT in SGEC.Interleukin-17 (IL-17) is a pleiotropic cytokine that plays a primary role in triggering epithelial-mesenchymal transition (EMT) in many chronic inflammatory diseases. EMT plays a critical role in the progression of salivary gland (SG) fibrosis in primary Sjögren's syndrome (pSS). This study focused on the activation of the canonical TGF-β1/Smad2/3 and noncanonical TGF-β1/Erk1/2 pathways in IL-17-dependent TGFβ1-induced EMT in human SG epithelial cells (SGEC) derived from healthy subjects. The expression of phosphorylated Smad2/3 and Erk1/2 during IL-17 treatment-stimulated EMT was evaluated in healthy SGEC. Cotreatment with IL-17 and specific TGFβ receptor type I kinase inhibitor SB431542, or Erk 1/2 inhibitor U0126, abrogates the corresponding morphological changes and EMT phenotypic markers expression in healthy SGEC. Interestingly, inhibition of canonical TGFβ1/Smad2/3 signal transduction had no effect on activation of the noncanonical TGFβ1/Erk1/2/EMT pathway, suggesting that the two pathways act independently in activating IL-17-dependent EMT in SGEC. Interleukin-17 (IL-17) is a pleiotropic cytokine that plays a primary role in triggering epithelial-mesenchymal transition (EMT) in many chronic inflammatory diseases. EMT plays a critical role in the progression of salivary gland (SG) fibrosis in primary Sjögren's syndrome (pSS). This study focused on the activation of the canonical TGF-β1/Smad2/3 and noncanonical TGF-β1/Erk1/2 pathways in IL-17-dependent TGFβ1-induced EMT in human SG epithelial cells (SGEC) derived from healthy subjects. The expression of phosphorylated Smad2/3 and Erk1/2 during IL-17 treatment-stimulated EMT was evaluated in healthy SGEC. Cotreatment with IL-17 and specific TGFβ receptor type I kinase inhibitor SB431542, or Erk 1/2 inhibitor U0126, abrogates the corresponding morphological changes and EMT phenotypic markers expression in healthy SGEC. Interestingly, inhibition of canonical TGFβ1/Smad2/3 signal transduction had no effect on activation of the noncanonical TGFβ1/Erk1/2/EMT pathway, suggesting that the two pathways act independently in activating IL-17-dependent EMT in SGEC. Interleukin-17 (IL-17) is a pleiotropic cytokine that plays a primary role in triggering epithelial–mesenchymal transition (EMT) in many chronic inflammatory diseases. EMT plays a critical role in the progression of salivary gland (SG) fibrosis in primary Sjögren’s syndrome (pSS). This study focused on the activation of the canonical TGF-β1/Smad2/3 and noncanonical TGF-β1/Erk1/2 pathways in IL-17-dependent TGFβ1-induced EMT in human SG epithelial cells (SGEC) derived from healthy subjects. The expression of phosphorylated Smad2/3 and Erk1/2 during IL-17 treatment-stimulated EMT was evaluated in healthy SGEC. Cotreatment with IL-17 and specific TGFβ receptor type I kinase inhibitor SB431542, or Erk 1/2 inhibitor U0126, abrogates the corresponding morphological changes and EMT phenotypic markers expression in healthy SGEC. Interestingly, inhibition of canonical TGFβ1/Smad2/3 signal transduction had no effect on activation of the noncanonical TGFβ1/Erk1/2/EMT pathway, suggesting that the two pathways act independently in activating IL-17-dependent EMT in SGEC. Epithelial–mesenchymal transition (EMT) plays a critical role in the progression of salivary gland (SG) fibrosis in primary Sjögren’s syndrome. This study demonstrates the IL-17-dependent activation of EMT in human SG epithelial cells that occurs through both the canonical TGF-β1/Smad2/3 and noncanonical TGF-β1/Erk1/2 pathways.
Author	Lorusso, Loredana Sisto, Margherita Lisi, Sabrina Ribatti, Domenico Ingravallo, Giuseppe
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Snippet	Interleukin-17 (IL-17) is a pleiotropic cytokine that plays a primary role in triggering epithelial–mesenchymal transition (EMT) in many chronic inflammatory... Interleukin-17 (IL-17) is a pleiotropic cytokine that plays a primary role in triggering epithelial-mesenchymal transition (EMT) in many chronic inflammatory...
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SubjectTerms	13/21 13/31 14/63 38/77 692/308/575 692/420/256/2515 82/80 Activation Activation analysis Aged Cells, Cultured Cytokines Enzyme inhibitors Epithelial cells Epithelial-Mesenchymal Transition - physiology Extracellular signal-regulated kinase Fibrosis Humans Inflammatory diseases Interleukin 17 Interleukin-17 - metabolism Interleukins Kinases Laboratory Medicine Lip - cytology MAP Kinase Signaling System - physiology Medicine Medicine & Public Health Mesenchyme Middle Aged Pathology Salivary gland Salivary glands Signal transduction Sjogren's syndrome Sjogren's Syndrome - metabolism Sjogren's Syndrome - pathology Smad protein Smad Proteins - metabolism Smad2 protein Transforming Growth Factor beta1 - metabolism Transforming growth factor-b1
Title	TGFβ1-Smad canonical and -Erk noncanonical pathways participate in interleukin-17-induced epithelial–mesenchymal transition in Sjögren’s syndrome
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