SDF-1 in Mammary Fibroblasts of Bovine with Mastitis Induces EMT and Inflammatory Response of Epithelial Cells

He, Guiliang; Ma, Mingchao; Yang, Wei; Wang, Hao; Zhang, Yong; Gao, Ming-Qing

doi:10.7150/ijbs.19591

Cited by 26 publications

(16 citation statements)

References 33 publications

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“…Epithelial mesenchymal transition (EMT) is the process by which epithelial cells gradually acquire certain characteristics of mesenchymal cells to produce fibroblasts and myofibroblasts ( He et al, 2017 ). It is characterized by morphological changes in epithelial cells from a cobblestone-shape to a spindle-shape and expression changes in some EMT markers, such as decreased E-cadherin and increased vimentin and α-smooth muscle actin (α-SMA) ( Thiery, 2002 ).…”

Section: Introductionmentioning

confidence: 99%

lncRNA H19 is involved in TGF-β1-induced epithelial to mesenchymal transition in bovine epithelial cells through PI3K/AKT Signaling Pathway

Yang

et al. 2017

PeerJ

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Increased levels of long noncoding RNA H19 (H19) have been observed in many inflammatory and organ fibrosis diseases including ulcerative colitis, osteoarthritis, liver fibrosis, renal fibrosis and pulmonary fibrosis. However, the role of H19 in bovine mastitis and mastitis-caused fibrosis is still unclear. In our study, H19 was characterized as a novel regulator of EMT induced by transforming growth factor-β1 (TGF-β1) in bovine mammary alveolar cell-T (MAC-T) cell line. We found that H19 was highly expressed in bovine mastitis tissues and inflammatory MAC-T cells induced by virulence factors of pathogens. TGF-β1 was also highly expressed in inflammatory MAC-T cells, and exogenous TGF-β1 could induce EMT, enhance extracellular matrix protein expression, and upregulate H19 expression in epithelial cells. Stable expression of H19 significantly promotes EMT progression and expression of ECM protein induced by TGF-β1 in MAC-T cells. Furthermore, by using a specific inhibitor of the PI3K/AKT pathway, we demonstrated that TGF-β1 upregulated H19 expression through PI3K/AKT pathway. All these observations imply that the lncRNA H19 modulated TGF-β1-induced epithelial to mesenchymal transition in bovine epithelial cells through PI3K/AKT signaling pathway, which suggests that mammary epithelial cells might be one source for myofibroblasts in vivo in the mammary glands under an inflammatory condition, thereby contributing to mammary gland fibrosis.

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Section: Introductionmentioning

confidence: 99%

lncRNA H19 is involved in TGF-β1-induced epithelial to mesenchymal transition in bovine epithelial cells through PI3K/AKT Signaling Pathway

Yang

et al. 2017

PeerJ

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“…Numerous studies have discovered that EMT is associated specially with the early progression of tumor invasion and distance metastasis in diverse solid tumors, including lung cancer, liver cancer, gastric carcinoma, and colon carcinoma . EMT is theoretically considered to increase the production of fibroblasts and myofibroblasts secreted by extracellular matrix (ECM) . These cells perpetuate the fibrotic conditions and lead to the increase of tissue stiffness.…”

Section: Introductionmentioning

confidence: 99%

“…3 EMT is theoretically considered to increase the production of fibroblasts and myofibroblasts secreted by extracellular matrix (ECM). 4 These cells perpetuate the fibrotic conditions and lead to the increase of tissue stiffness. However, some recent studies have shown that tissue stiffness increased maybe precedes fibrotic responses.…”

Section: Introductionmentioning

confidence: 99%

Micropillar‐based culture platform induces epithelial–mesenchymal transition in the alveolar epithelial cell line

et al. 2018

J Biomedical Materials Res

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Topography and rigidity are two typical biophysical cues in extracellular matrix mechanical microenvironment. Extracellular matrix can regulate cells biological behaviors, including epithelial-to-mesenchymal transition (EMT). A growing body of evidence suggests that EMT plays an important role in the development of tumor and fibrosis. Moreover, EMT also contributes to drug resistance in cancer cells. Currently, the majority of studies about EMT are based on the induction of growth factors or cytokines in vitro. Here, we adopt polydimethylsiloxane (PDMS)-micropillars-based matrix platform to culture human alveolar epithelial cells for studying the influence of topography and rigidity on EMT. This study reports a previously undefined role of mechanical microenvironment in EMT induction. Different topography and rigidity can induce EMT directly without the use of exogenous cytokines. Notably, rigidity-induced EMT activation is associated with the topography. Furthermore, we investigate preliminarily the role of PI3K/Akt signaling pathway in mechanical microenvironment regulation of EMT. These findings provide a fresh perspective to the researches of tumor and pulmonary fibrosis, and the potential platform for cell-based drug screening. © 2018 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 106A: 3165-3174, 2018.

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“…Studies demonstrated that SDF-1 and its receptor, CXCR4, are involved in embryogenesis, migration, progenitor cell homing, survival, proliferation, differentiation and fibrosis [12,13] . Reports showed that SDF-1 binding to the specific receptor CXCR4 participates in the immune and inflammation reaction [14] . Angiotensin II receptor blockers has been shown to reduce the progression of DN [15] .…”

mentioning

confidence: 99%

SDF-1 Improves Renal Fibrosis in Type 2 Diabetes Mellitus Involving TGF-beta-mediated ECM via PI3K/AKT Signaling

Xie¹,

Ji²,

Shuai³

2020

ijps

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Xie et al.: SDF-1 improves renal fibrosis in DNThe present study investigated the role of stromal cell-derived factor-1 in the progression of renal injury in type 2 diabetic nephropathy. The 8-week old male db/db mice were used as the model of diabetic nephropathy and aged-matched male C57BL/6 mice constituted the control group. Fasting blood glucose, 24 hour urinary albumin and the creatinine clearance rate were measured. The expressions of stromal cell-derived factor-1, CXC chemokine receptor 4 and F4/80 were detected. Normal rat kidney epithelial cells were exposed to stromal cell-derived factor-1α, high glucose, tumour growth factor-β1, valsartan and LY294002, respectively. The extracellular matrix expression was evaluated. It was found that creatinine clearance rate was significantly decreased in 28-week db/db mice compared to the age-matched C57BL/6 mice and valsartan could significantly increase creatinine clearance rate. The expression of stromal cell-derived factor-1, CXC chemokine receptor 4 and F4/80 was significantly increased in the kidney of db/db mice but not in C57BL/6 mice, which was improved with valsartan treatment. In vitro, the expression of CXC chemokine receptor 4 was detected in the rat kidney epithelial cells. Tumour growth factor-β1 increased the expressions of type IV collagen and fibronectin in rat kidney epithelial cells under low glucose and high glucose condition. Stromal cell-derived factor-1α inhibited the harmful effect of tumour growth factor-β1 on extracellular matrix expression, and valsartan exerted synergistic effect on stromal cell-derived factor-1α. Stromal cell-derived factor-1α decreased tumour growth factor-β1expression and increased p-AKT expression, which were inhibited by LY294002 treatment. Stromal cell-derived factor-1 improved renal fibrosis which might partly involve TGF-β-mediated extracellular matrix via PI3K/AKT pathway.

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SDF-1 in Mammary Fibroblasts of Bovine with Mastitis Induces EMT and Inflammatory Response of Epithelial Cells

Cited by 26 publications

References 33 publications

lncRNA H19 is involved in TGF-β1-induced epithelial to mesenchymal transition in bovine epithelial cells through PI3K/AKT Signaling Pathway

lncRNA H19 is involved in TGF-β1-induced epithelial to mesenchymal transition in bovine epithelial cells through PI3K/AKT Signaling Pathway

Micropillar‐based culture platform induces epithelial–mesenchymal transition in the alveolar epithelial cell line

SDF-1 Improves Renal Fibrosis in Type 2 Diabetes Mellitus Involving TGF-beta-mediated ECM via PI3K/AKT Signaling

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