scholarly journals Human Peripheral Blood-derived Mast Cells Contribute to Epithelial to Mesenchymal Transition in Bronchial Epithelial Cells in the Presence of IL-1β

2020 ◽  
Author(s):  
Xian-Song Wang ◽  
Li Xie ◽  
Kaiyu Zheng
Keyword(s):  
Mast Cells ◽  
Peripheral Blood ◽  
Epithelial To Mesenchymal Transition ◽  
Human Peripheral Blood ◽  
Cell Junctions ◽  
Vimentin Expression ◽  
Bronchial Epithelial ◽  
Mesenchymal Transition ◽  
Tgf Β1 ◽  
E Cadherin

Abstract Background: Bronchial epithelial to mesenchymal transition （EMT）is an important mechanism for the airway remodeling in asthmatics. Mast cell is one of the critical effector cells in pathogenesis of asthma. Although mast cells have been shown to release a plethora of pro-fibrotic factors with the potential to induce EMT, it is not clear whether mast cells also directly have an impact on the bronchial EMT. In this study, we investigated the contribution of human mast cells to EMT in human bronchial epithelial cell line 16-HBE. Methods: Human peripheral blood-derived mast cells were co-cultured with 16-HBE cells. The protein and mRNA expression of E-cadherin and vimentin in 16-HBE cells were analyzed by Western blot and quantitative real-time PCR. A scratch wound assay was performed to evaluate the migratory properties of the 16-HBE cells.Results: Mast cells alone failed to produce significant effects on the epithelial morphology, mobility, and expression of E-cadherin and vimentin. However, mast cells in combination of interleukin (IL)-1β significantly decreased E-cadherin expression but increased vimentin expression in the co-cultured 16-HBE cells, which exhibited a spindle-like appearance with reduced cell junctions and enhanced migration. The down-regulation of E-cadherin expression and up-regulation of vimentin expression were not abrogated by the transforming growth factor (TGF)-β1 neutralizing antibody.Conclusion: Mast cells combined with IL-1β, not mast cells alone, were able to induce EMT in 16-HBE cells through a TGF-β1-independent mechanism. The results of in vitro culture suggest the possibility that mast cells contribute to human bronchial epithelial EMT in the asthmatic airway tissues with high level of IL-1β.

scholarly journals The unjamming transition is distinct from the epithelial-to-mesenchymal transition

2019 ◽  
Author(s):  
Jennifer A. Mitchel ◽  
Amit Das ◽  
Michael J. O’Sullivan ◽  
Ian T. Stancil ◽  
Stephen J. DeCamp ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Epithelial To Mesenchymal Transition ◽  
Body Cavity ◽  
Cellular Migration ◽  
Cell Junctions ◽  
Bronchial Epithelial ◽  
Mesenchymal Transition ◽  
Well Differentiated ◽  
Epithelial Sheets ◽  
Tgf Β1

AbstractEvery organ surface and body cavity is lined by a confluent collective of epithelial cells. In homeostatic circumstances the epithelial collective remains effectively solid-like and sedentary. But during morphogenesis, remodeling or repair, as well as during malignant invasion or metastasis, the epithelial collective becomes fluid-like and migratory1–4. This conversion from sedentary to migratory behavior has traditionally been understood as a manifestation of the epithelial-to-mesenchymal transition (EMT) or the partial EMT (pEMT)5–8. However, in certain contexts this conversion has been attributed to the recently discovered unjamming transition (UJT), in which epithelial cells move collectively and cooperatively9–11. UJT and pEMT share certain aspects of collective cellular migration, but the extent to which these processes are distinct, overlapping or perhaps even identical has remained undefined. Using the confluent layer of well-differentiated primary human bronchial epithelial (HBE) cells, here we triggered UJT by exposing the sedentary layer to mechanical compression9–12. Cells thereafter migrated cooperatively, aligned into packs locally, and elongated systematically. Nevertheless, cell-cell junctions, apico-basal polarity, and barrier function remained intact in response, and mesenchymal markers remained unapparent. As such, pEMT was not evident. When we triggered pEMT and associated cellular migration by exposing the sedentary layer to TGF-β1, metrics of UJT versus pEMT diverged. To account for these striking physical observations a new mathematical model attributes the effects of pEMT mainly to diminished junctional tension but attributes those of UJT mainly to augmented cellular propulsion. Together, these findings establish that UJT is sufficient to account for vigorous epithelial layer migration even in the absence of pEMT. Distinct gateways to cellular migration therefore become apparent – UJT as it might apply to migration of epithelial sheets, and EMT/pEMT as it might apply to migration of mesenchymal cells on a solitary or collective basis, activated during development, remodeling, repair or tumor invasion. Through the actions of UJT and pEMT working independently, sequentially, or interactively, living tissue is therefore seen to comprise an active engineering material whose modules for plasticity, self-repair and regeneration, are far richer than had been previously appreciated.

scholarly journals A-Kinase Anchoring Proteins Diminish TGF-β1/Cigarette Smoke-Induced Epithelial-To-Mesenchymal Transition

Cells ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 356 ◽  
Author(s):  
Haoxiao Zuo ◽  
Marina Trombetta-Lima ◽  
Irene H. Heijink ◽  
Christina H. T. J. van der Veen ◽  
Laura Hesse ◽  
...  
Keyword(s):  
Cell Migration ◽  
Cigarette Smoke ◽  
Epithelial To Mesenchymal Transition ◽  
Transforming Growth Factor ◽  
Epithelial Cell Line ◽  
Intracellular Camp ◽  
Mesenchymal Transition ◽  
Anchoring Proteins ◽  
Tgf Β1 ◽  
E Cadherin

Epithelial-to-mesenchymal transition (EMT) plays a role in chronic obstructive pulmonary diseases (COPD). Cyclic adenosine monophosphate (cAMP) can inhibit transforming growth factor-β1 (TGF-β1) mediated EMT. Although compartmentalization via A-kinase anchoring proteins (AKAPs) is central to cAMP signaling, functional studies regarding their therapeutic value in the lung EMT process are lacking. The human bronchial epithelial cell line (BEAS-2B) and primary human airway epithelial (pHAE) cells were exposed to TGF-β1. Epithelial (E-cadherin, ZO-1) and mesenchymal markers (collagen Ӏ, α-SMA, fibronectin) were analyzed (mRNA, protein). ELISA measured TGF-β1 release. TGF-β1-sensitive AKAPs Ezrin, AKAP95 and Yotiao were silenced while using siRNA. Cell migration was analyzed by wound healing assay, xCELLigence, Incucyte. Prior to TGF-β1, dibutyryl-cAMP (dbcAMP), fenoterol, rolipram, cilostamide, and forskolin were used to elevate intracellular cAMP. TGF-β1 induced morphological changes, decreased E-cadherin, but increased collagen Ӏ and cell migration, a process that was reversed by the inhibitor of δ/epsilon casein kinase I, PF-670462. TGF-β1 altered (mRNA, protein) expression of Ezrin, AKAP95, and Yotiao. St-Ht31, the AKAP antagonist, decreased E-cadherin (mRNA, protein), but counteracted TGF-β1-induced collagen Ӏ upregulation. Cigarette smoke (CS) increased TGF-β1 release, activated TGF signaling, augmented cell migration, and reduced E-cadherin expression, a process that was blocked by TGF-β1 neutralizing antibody. The silencing of Ezrin, AKAP95, and Yotiao diminished TGF-β1-induced collagen Ӏ expression, as well as TGF-β1-induced cell migration. Fenoterol, rolipram, and cilostamide, in AKAP silenced cells, pointed to distinct cAMP compartments. We conclude that Ezrin, AKAP95, and Yotiao promote TGF-β1-mediated EMT, linked to a TGF-β1 release by CS. AKAP members might define the ability of fenoterol, rolipram, and cilostamide to modulate the EMT process, and they might represent potential relevant targets in the treatment of COPD.

scholarly journals Microparticles derived from human erythropoietin mRNA-transfected mesenchymal stem cells inhibit epithelial-to-mesenchymal transition and ameliorate renal interstitial fibrosis

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Mirae Lee ◽  
Seok-hyung Kim ◽  
Jong Hyun Jhee ◽  
Tae Yeon Kim ◽  
Hoon Young Choi ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Epithelial To Mesenchymal Transition ◽  
Transforming Growth Factor ◽  
Mdck Cells ◽  
Mesenchymal Transition ◽  
Human Erythropoietin ◽  
Renal Tubulointerstitial Fibrosis ◽  
Tgf Β1 ◽  
E Cadherin

Abstract Background Renal tubulointerstitial fibrosis (TIF) plays an important role in the progression of chronic kidney disease (CKD) and its pathogenesis involves epithelial-to-mesenchymal transition (EMT) upon renal injury. Recombinant human erythropoietin (rhEPO) has been shown to display novel cytoprotective effects, in part by inhibiting transforming growth factor (TGF)-β1-induced EMT. Here, we evaluated the inhibitory effects of microparticles (MPs) derived from human EPO gene-transfected kidney mesenchymal stem cells (hEPO-KMSCs) against TGF-β1-induced EMT in Madin-Darby canine kidney (MDCK) cells and against TIF in mouse kidneys with unilateral ureteral obstruction (UUO). Methods EMT was induced in MDCK cells by treatment with TGF-β1 (5 ng/mL) for 48 h and then inhibited by co-treatment with rhEPO (100 IU/mL), mock gene-transfected KMSC-derived MPs (MOCK-MPs), or hEPO-KMSC-derived MPs (hEPO-MPs) for a further 48 h. UUO was induced in FVB/N mice, which were then treated with rhEPO (1000 IU/kg, intraperitoneally, every other day for 1 week), MOCK-MPs, or hEPO-MPs (80 μg, intravenously). Alpha-smooth muscle actin (α-SMA), fibronectin, and E-cadherin expression were evaluated in MDCK cells and kidney tissues, and the extent of TIF in UUO kidneys was assessed by immunohistochemical staining. Results TGF-β1 treatment significantly increased α-SMA and fibronectin expression in MDCK cells and decreased that of E-cadherin, while co-treatment with rhEPO, MOCK-MPs, or hEPO-MPs markedly attenuated these changes. In addition, rhEPO and hEPO-MP treatment effectively decreased phosphorylated Smad2 and Smad3, as well as phosphorylated p38 mitogen-activated protein kinase (MAPK) expression, suggesting that rhEPO and rhEPO-MPs can inhibit TGF-β1-induced EMT via both Smad and non-Smad pathways. rhEPO and hEPO-MP treatment also significantly attenuated the extent of renal TIF after 1 week of UUO compared to MOCK-MPs, with hEPO-MPs significantly reducing myofibroblast and F4/80+ macrophage infiltration as well as EMT marker expression in UUO renal tissues in a similar manner to rhEPO. Conclusions Our results demonstrate that hEPO-MPs modulate TGF-β1-induced EMT in MDCK cells via the Smad2, Smad3, and p38 MAPK pathways and significantly attenuated renal TIF in UUO kidneys.

scholarly journals β-catenin activation down-regulates cell-cell junction-related genes and induces epithelial-to-mesenchymal transition in colorectal cancers

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Won Kyu Kim ◽  
Yujin Kwon ◽  
Mi Jang ◽  
Minhee Park ◽  
Jiyoon Kim ◽  
...  
Keyword(s):  
Nuclear Localization ◽  
Epithelial To Mesenchymal Transition ◽  
Cell Junctions ◽  
Nuclear Accumulation ◽  
Colorectal Cancers ◽  
Wild Type ◽  
Mesenchymal Transition ◽  
Nuclear Expression ◽  
E Cadherin ◽  
Cell Cell

AbstractWNT signaling activation in colorectal cancers (CRCs) occurs through APC inactivation or β-catenin mutations. Both processes promote β-catenin nuclear accumulation, which up-regulates epithelial-to-mesenchymal transition (EMT). We investigated β-catenin localization, transcriptome, and phenotypic differences of HCT116 cells containing a wild-type (HCT116-WT) or mutant β-catenin allele (HCT116-MT), or parental cells with both WT and mutant alleles (HCT116-P). We then analyzed β-catenin expression and associated phenotypes in CRC tissues. Wild-type β-catenin showed membranous localization, whereas mutant showed nuclear localization; both nuclear and non-nuclear localization were observed in HCT116-P. Microarray analysis revealed down-regulation of Claudin-7 and E-cadherin in HCT116-MT vs. HCT116-WT. Claudin-7 was also down-regulated in HCT116-P vs. HCT116-WT without E-cadherin dysregulation. We found that ZEB1 is a critical EMT factor for mutant β-catenin-mediated loss of E-cadherin and Claudin-7 in HCT116-P and HCT116-MT cells. We also demonstrated that E-cadherin binds to both WT and mutant β-catenin, and loss of E-cadherin releases β-catenin from the cell membrane and leads to its degradation. Alteration of Claudin-7, as well as both Claudin-7 and E-cadherin respectively caused tight junction (TJ) impairment in HCT116-P, and dual loss of TJs and adherens junctions (AJs) in HCT116-MT. TJ loss increased cell motility, and subsequent AJ loss further up-regulated that. Immunohistochemistry analysis of 101 CRCs revealed high (14.9%), low (52.5%), and undetectable (32.6%) β-catenin nuclear expression, and high β-catenin nuclear expression was significantly correlated with overall survival of CRC patients (P = 0.009). Our findings suggest that β-catenin activation induces EMT progression by modifying cell-cell junctions, and thereby contributes to CRC aggressiveness.

scholarly journals In primary airway epithelial cells, the unjamming transition is distinct from the epithelial-to-mesenchymal transition

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Jennifer A. Mitchel ◽  
Amit Das ◽  
Michael J. O’Sullivan ◽  
Ian T. Stancil ◽  
Stephen J. DeCamp ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Epithelial To Mesenchymal Transition ◽  
Airway Epithelial Cells ◽  
Cellular Migration ◽  
Cell Junctions ◽  
Airway Epithelial ◽  
Human Bronchial Epithelial Cells ◽  
Intact Cells ◽  
Bronchial Epithelial ◽  
Mesenchymal Transition

Abstract The epithelial-to-mesenchymal transition (EMT) and the unjamming transition (UJT) each comprises a gateway to cellular migration, plasticity and remodeling, but the extent to which these core programs are distinct, overlapping, or identical has remained undefined. Here, we triggered partial EMT (pEMT) or UJT in differentiated primary human bronchial epithelial cells. After triggering UJT, cell-cell junctions, apico-basal polarity, and barrier function remain intact, cells elongate and align into cooperative migratory packs, and mesenchymal markers of EMT remain unapparent. After triggering pEMT these and other metrics of UJT versus pEMT diverge. A computational model attributes effects of pEMT mainly to diminished junctional tension but attributes those of UJT mainly to augmented cellular propulsion. Through the actions of UJT and pEMT working independently, sequentially, or interactively, those tissues that are subject to development, injury, or disease become endowed with rich mechanisms for cellular migration, plasticity, self-repair, and regeneration.

scholarly journals Integrin α3β1–dependent β-catenin phosphorylation links epithelial Smad signaling to cell contacts

2009 ◽  
Vol 184 (2) ◽  
pp. 309-322 ◽  
Author(s):  
Young Kim ◽  
Matthias C. Kugler ◽  
Ying Wei ◽  
Kevin K. Kim ◽  
Xiaopeng Li ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Epithelial To Mesenchymal Transition ◽  
Target Genes ◽  
Laminin Receptor ◽  
Laminin 5 ◽  
Mesenchymal Transition ◽  
Smad Signaling ◽  
Smad2 Phosphorylation ◽  
Tgf Β1 ◽  
E Cadherin

Injury-initiated epithelial to mesenchymal transition (EMT) depends on contextual signals from the extracellular matrix, suggesting a role for integrin signaling. Primary epithelial cells deficient in their prominent laminin receptor, α3β1, were found to have a markedly blunted EMT response to TGF-β1. A mechanism for this defect was explored in α3-null cells reconstituted with wild-type (wt) α3 or point mutants unable to engage laminin 5 (G163A) or epithelial cadherin (E-cadherin; H245A). After TGF-β1 stimulation, wt epithelial cells but not cells expressing the H245A mutant internalize complexes of E-cadherin and TGF-β1 receptors, generate phospho-Smad2 (p-Smad2)–pY654–β-catenin complexes, and up-regulate mesenchymal target genes. Although Smad2 phosphorylation is normal, p-Smad2–pY654–β-catenin complexes do not form in the absence of α3 or when α3β1 is mainly engaged on laminin 5 or E-cadherin in adherens junctions, leading to attenuated EMT. These findings demonstrate that α3β1 coordinates cross talk between β-catenin and Smad signaling pathways as a function of extracellular contact cues and thereby regulates responses to TGF-β1 activation.

Prostaglandin D2 inhibits TGF-β1-induced epithelial-to-mesenchymal transition in MDCK cells

2006 ◽  
Vol 291 (6) ◽  
pp. F1332-F1342 ◽  
Author(s):  
Aihua Zhang ◽  
Zheng Dong ◽  
Tianxin Yang
Keyword(s):  
Epithelial To Mesenchymal Transition ◽  
Epithelial Mesenchymal Transition ◽  
Mdck Cells ◽  
Smooth Muscle Actin ◽  
Antioxidant Property ◽  
Prostaglandin D2 ◽  
Mesenchymal Transition ◽  
Species Production ◽  
Tgf Β1 ◽  
E Cadherin

In a separate study, we identified PGE2 as a potent inhibitor of TGF-β1-induced epithelial-mesenchymal transition (EMT) in cultured Madin-Darby canine kidney (MDCK) cells (Zhang A, Wang M-H, Dong Z, and Yang T. Am J Physiol Renal Physiol 291: F1323–F1331, 2006). This finding prompted us to examine the roles of other prostanoids: PGD2, PGF2α, PGI2, and thromboxane A2 (TXA2). Treatment with 10 ng/ml TGF-β1 for 3 days induced EMT as reflected by conversion to the spindle-like morphology, loss of E-cadherin, and activation of α-smooth muscle actin (α-SMA). Treatment with PGD2 remarkably preserved the epithelial-like morphology, restored the expression of E-cadherin, and abolished the activation of α-SMA. In contrast, PGF2α, carbocyclic thromboxane A2, PGI2 and its stable analog beraprost were without an effect. MDCK cells expressed DP1 and DP2 receptors; however, the effect of PGD2 was neither prevented by DP1 antagonist BW-A868C or DP2 antagonist BAY-u3405 nor was mimicked by DP1 agonist BW-245C. cAMP-elevating agents forskolin and 8-Br-cAMP blocked EMT. However, cAMP blockers H89 and Rp-cAMP failed to block the effect of PGD2. PGD2 did not seem to act via its metabolites as 15-deoxy-Delta( 12 , 14 )-prostaglandin J2 (15d-PGJ2) levels in the medium following incubation with 3 μM PGD2 were well below the values predicted from the cross activity of the assay. Exposure to TGF-β1 induced a threefold increase in reactive oxygen species production that was completely abolished by PGD2. We conclude that 1) PGD2, but not PGI2, PGF2α, and TXA2 inhibit EMT, 2) PGD2 inhibits EMT independently of DP1 and DP2 receptors, and 3) PGD2 exhibits antioxidant property which may, in part, account for the antifibrotic action of this PG.

Chimaphilin inhibits human osteosarcoma cell invasion and metastasis through suppressing the TGF-β1-induced epithelial-to-mesenchymal transition markers via PI-3K/Akt, ERK1/2, and Smad signaling pathways

2018 ◽  
Vol 96 (1) ◽  
pp. 1-7 ◽  
Author(s):  
Feng Dong ◽  
Tingting Liu ◽  
Hao Jin ◽  
Wenbo Wang
Keyword(s):  
Cell Invasion ◽  
Epithelial To Mesenchymal Transition ◽  
Metastatic Potential ◽  
U2os Cell ◽  
Osteosarcoma Cell ◽  
Invasion And Metastasis ◽  
Mesenchymal Transition ◽  
U2os Cells ◽  
Tgf Β1 ◽  
E Cadherin

Epithelial-to-mesenchymal transition is a cellular process associated with cancer invasion and metastasis. However, the antimetastatic effects of chimaphilin remain elusive. In this study, we attempted to investigate the potential use of chimaphilin as an inhibitor of TGF-β1-induced epithelial-to-mesenchymal transition in U2OS cells. We found that TGF-β1 induced epithelial-to-mesenchymal transition to promote U2OS cell invasion and metastasis. Western blotting demonstrated that chimaphilin inhibited U2OS cell invasion and migration, increased the expression of the epithelial phenotype marker E-cadherin, repressed the expression of the mesenchymal phenotype marker vimentin, as well as decreased the level of epithelial-to-mesenchymal-inducing transcription factors Snail1 and Slug during the initiation of TGF-β1-induced epithelial-to-mesenchymal transition. In this study, we revealed that chimaphilin up-regulated the E-cadherin expression level and inhibited the production of vimentin, Snail1, and Slug in TGF-β1-induced U2OS cells by blocking PI-3K/Akt and ERK 1/2 signaling pathway. Additionally, the TGF-β1-mediated phosphorylated levels of Smad2/3 were inhibited by chimaphilin pretreatment. Above all, we conclude that chimaphilin represents an effective inhibitor of the metastatic potential of U2OS cells through suppression of TGF-β1-induced epithelial-to-mesenchymal transition.

scholarly journals Microparticles derived from human erythropoietin mRNA-transfected mesenchymal stem cells inhibit epithelial-to-mesenchymal transition and ameliorate renal interstitial fibrosis

2020 ◽  
Author(s):  
Mirae Lee ◽  
Seok-hyung Kim ◽  
Jong Hyun Jhee ◽  
Tae Yeon Kim ◽  
Hoon Young Choi ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Epithelial To Mesenchymal Transition ◽  
Transforming Growth Factor ◽  
Mdck Cells ◽  
Mesenchymal Transition ◽  
Human Erythropoietin ◽  
Renal Tubulointerstitial Fibrosis ◽  
Tgf Β1 ◽  
E Cadherin

Abstract Background: Renal tubulointerstitial fibrosis (TIF) plays an important role in the progression of chronic kidney disease (CKD) and its pathogenesis involves epithelial-to-mesenchymal transition (EMT) upon renal injury. Recombinant human erythropoietin (rhEPO) has been shown to display novel cytoprotective effects, in part by inhibiting transforming growth factor (TGF)-β1-induced EMT. Here, we evaluated the inhibitory effects of microparticles (MPs) derived from human EPO gene-transfected kidney mesenchymal stem cells (hEPO-KMSCs) against TGF-β1-induced EMT in Madin-Darby canine kidney (MDCK) cells and against TIF in mouse kidneys with unilateral ureteral obstruction (UUO).Methods: EMT was induced in MDCK cells by treatment with TGF-β1 (5 ng/mL) for 48 h and then inhibited by co-treatment with rhEPO (100 IU/mL), mock gene-transfected KMSC-derived MPs (MOCK-MPs), or hEPO-KMSC-derived MPs (hEPO-MPs) for a further 48 h. UUO was induced in FVB/N mice, which were then treated with rhEPO (1000 IU/kg, intraperitoneally, every other day for 1 week), MOCK-MPs, or hEPO-MPs (80 mg, intravenously). Alpha-smooth muscle actin (α-SMA), fibronectin, and E-cadherin expression were evaluated in MDCK cells and kidney tissues, and the extent of TIF in UUO kidneys was assessed by immunohistochemical staining.Results: TGF-β1 treatment significantly increased α-SMA and fibronectin expression in MDCK cells and decreased that of E-cadherin, while co-treatment with rhEPO, MOCK-MPs, or hEPO-MPs markedly attenuated these changes. In addition, rhEPO and hEPO-MP treatment effectively decreased phosphorylated Smad2 and Smad3, as well as phosphorylated p38 mitogen-activated protein kinase (MAPK) expression, suggesting that rhEPO and rhEPO-MPs can inhibit TGF-β1-induced EMT via both Smad and non-Smad pathways. rhEPO and hEPO-MP treatment also significantly attenuated the extent of renal TIF after one week of UUO compared to MOCK-MPs, with hEPO-MPs significantly reducing myofibroblast and F4/80+ macrophage infiltration as well as EMT marker expression in UUO renal tissues in a similar manner to rhEPO. Conclusions: Our results demonstrate that hEPO-MPs modulate TGF-β1-induced EMT in MDCK cells via the Smad2, Smad3, and p38 MAPK pathways and significantly attenuated renal TIF in UUO kidneys.

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