Epithelial–mesenchymal transition (EMT) of renal tubular cells in canine glomerulonephritis

Aresu, Luca; Rastaldi, Maria Pia; Scanziani, Eugenio; Baily, James; Radælli, Enrico; Pregel, Paola; Valenza, F.

doi:10.1007/s00428-007-0482-8

Cited by 30 publications

(26 citation statements)

References 27 publications

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“…We found that the TIMP-1 directly regulated transformation of fibroblasts into myofibroblasts, evident from the examination on α-SMA and TGFβ1 levels. α-SMA is specific marker for myofibroblasts, and is not express by normal fibroblast [24][25][26][27]. The EMT is a process by which epithelial cells acquire a migratory, mesenchymal phenotype, as a result of its repression of E-cadherin [28][29][30].…”

Section: Discussionmentioning

confidence: 99%

TIMP-1 Induces α-Smooth Muscle Actin in Fibroblasts to Promote Urethral Scar Formation

et al. 2015

Cell Physiol Biochem

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Background/Aims: Tissue inhibitor of metalloproteinases-1 (TIMP-1) has been reported to upregulate in urethral scar. However, the underlying molecular mechanisms remain undefined. Methods: Here, we studied levels of TIMP-1 and α-smooth muscle actin (α-SMA) in the fibroblasts isolated from urethral scar tissues, compared to the fibroblasts isolated from normal urethra. Then we either overexpressed TIMP-1, or inhibited TIMP-1 by lentiviruses carrying a transgene or a short hairpin small interfering RNA for TIMP-1 in human fibroblasts. We examined the effects of modulation of TIMP-1 on α-SMA, and on epithelial-mesenchymal transition (EMT)-related genes. We also studied the underlying mechanisms. Results: We detected significantly higher levels of TIMP-1 and α-smooth muscle actin (α-SMA) in the fibroblasts isolated from urethral scar tissues, compared to the fibroblasts isolated from normal urethra. Moreover, the levels of TIMP-1 and α-SMA strongly correlated. Moreover, we found that TIMP-1 significantly increased levels of α-SMA, transforming growth factor β 1 (TGFβ1), Collagen I and some other key factors related to an enhanced EMT, suggesting that TIMP-1 may induce transformation of fibroblasts into myofibroblasts to promote tissue EMT to enhance the formation of urethral scar. Moreover, increases in TIMP-1 also induced an increase in fibroblast cell growth and cell invasion, in an ERK/MAPK-signaling-dependent manner. Conclusion: Our study thus highlights a pivotal role of TIMP-1 in urethral scar formation.

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Section: Discussionmentioning

confidence: 99%

TIMP-1 Induces α-Smooth Muscle Actin in Fibroblasts to Promote Urethral Scar Formation

et al. 2015

Cell Physiol Biochem

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“…Although the origin of myofibroblasts has not yet been clearly elucidated, results from numerous studies indicate that a large number of myofibroblasts arise through a mechanism of epithelial-mesenchymal transition [1,2,3,4]. …”

Section: Discussionmentioning

confidence: 99%

“…Emerging evidence indicates that tubular epithelial cells are capable of transforming into myofibroblasts under pathological conditions; this process is called tubular epithelial cell-myofibroblast transdifferentiation (TEMT). A number of studies have demonstrated evidence of TEMT [1,2,3,4]. …”

Section: Introductionmentioning

confidence: 99%

Suppressors of Cytokine Signaling Inhibit Tubular Epithelial Cell-Myofibroblast Transdifferentiation

Liu

Shi

et al. 2011

Am J Nephrol

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Background/Aims: Tubular epithelial cell-myofibroblast transdifferentiation (TEMT) can be induced by diverse cytokines. The suppressors of cytokine signaling (SOCS) proteins negatively regulate cytokine signaling. This study is aimed at examining the role of SOCS-1 and SOCS-3 in TEMT induced by cytokines. Methods: The cell ultrastructure was observed using transmission electron microscopy. The protein and mRNA levels of cytokeratin 18 (CK18) and α-smooth muscle actin (α-SMA) were detected by immunocytochemistry, Western blot and real-time PCR. The levels of phosphorylated-signal transducer and activator of transcription (p-STAT) 1 and 3 were detected by Western blot. The protein and mRNA levels of SOCS-1 and SOCS-3 were detected by Western blot and real-time PCR. The levels of collagen type I and fibronectin (FN) were determined by ELISA. Results: Interleukin-1β (IL-1β) and oncostatin M (OSM) were able to downregulate CK18 expression and upregulate α-SMA, p-STAT1, p-STAT3, collagen type I and FN expression in cultured human renal proximal tubular epithelial cells (HKCs), whereas pretreatment with AG490 prevented these expression changes from occurring. All of the changes induced by IL-1β or OSM could be decreased by SOCS-1 and SOCS-3 overexpression, and were increased by SOCS-1 and SOCS-3 knockdown. Conclusions: SOCS-1 and SOCS-3 can prevent tubulointerstitial fibrosis by inhibiting TEMT, which may be connected with the activation of STAT1 and STAT3.

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“…In normal canine kidneys, the visceral glomerular epithelial cells (podocytes) expressed only vimentin, and cytokeratin was found exclusively in parietal glomerular epithelial cells. Aresu et al [27] showed that in dogs' kidneys, epithelial tubular cells lose their cytokeratin staining characteristics and transdifferentiate into cells exhibiting a key mesenchymal feature of vimentin-positive staining in glomerulonephritis.…”

Section: Discussionmentioning

confidence: 99%

Morphological, histochemical and immunohistochemical studies of polar fox kidney

Ożgo

Szymeczko

Wylot

et al. 2012

Folia Histochem Cytobiol.

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Abstract:The aim of the present study was to evaluate the morphology and intermediate filaments cytokeratin, desmin and vimentin expression in the kidneys of the polar fox (Alopex lagopus). Routine morphological, histochemical and immunohistochemical techniques of examinations of the kidneys of adult male and female polar foxes were used. We found different localizations and different levels of immunoexpression of cytokeratin in epithelia of calyxes, distal tubules and Henle's loops, and also in endothelial cells. We also noted immunolocalization and immunoexpression of vimentin in mesangial cells, interstitial tissue and distal tubules. Desmin reactivity was revealed for muscle cells of arteries and mesangial cells. Our study is the first attempt to localize cytoskeletal intermediate filaments performed on polar fox kidneys. It is worth noting that our observations concerning the distribution of vimentin in the polar fox kidney may suggest that protein as being useful as a marker of distal tubules in the polar fox kidney.

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Epithelial–mesenchymal transition (EMT) of renal tubular cells in canine glomerulonephritis

Cited by 30 publications

References 27 publications

TIMP-1 Induces α-Smooth Muscle Actin in Fibroblasts to Promote Urethral Scar Formation

TIMP-1 Induces α-Smooth Muscle Actin in Fibroblasts to Promote Urethral Scar Formation

Suppressors of Cytokine Signaling Inhibit Tubular Epithelial Cell-Myofibroblast Transdifferentiation

Morphological, histochemical and immunohistochemical studies of polar fox kidney

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