scholarly journals Murine Precision-Cut Kidney Slices as an ex vivo Model to Evaluate the Role of Transforming Growth Factor-β1 Signaling in the Onset of Renal Fibrosis

2017 ◽  
Vol 8 ◽  
Author(s):  
Elisabeth G. D. Stribos ◽  
Marc A. Seelen ◽  
Harry van Goor ◽  
Peter Olinga ◽  
Henricus A. M. Mutsaers
Keyword(s):  
Growth Factor ◽  
Renal Fibrosis ◽  
Transforming Growth Factor ◽  
Ex Vivo ◽  
Transforming Growth Factor Β1 ◽  
Ex Vivo Model ◽  
Kidney Slices

Carvacrol Ameliorates Transforming Growth Factor-β1-Induced Extracellular Matrix Deposition and Reduces Epithelial-Mesenchymal Transition by Regulating The Phosphatidylinositol 3-Kinase/Protein Kinase B Pathway In Hk-2 Cells

2021 ◽  
Vol 19 (4) ◽  
pp. 501-507
Author(s):  
Yunhe Gu ◽  
Peiyao Guo ◽  
Guangbiao Xu
Keyword(s):  
Extracellular Matrix ◽  
Growth Factor ◽  
Renal Fibrosis ◽  
Transforming Growth Factor ◽  
Epithelial Mesenchymal Transition ◽  
Transforming Growth Factor Β1 ◽  
Mesenchymal Transition ◽  
Matrix Deposition ◽  
Extracellular Matrix Deposition ◽  
Dose Dependent

Transforming growth factor-β1 promotes excessive extracellular matrix deposition and epithelial-mesenchymal transition of tubular epithelial cells, thus stimulating the progression of renal fibrosis. Carvacrol has been shown to alleviate cardiac and liver fibrosis and attenuate renal injury. However, the role of carvacrol on renal fibrosis has not been examined. First, measurements using Cell Counting Kit-8 showed that carvacrol reduced cell viability of tubular epithelial cell line HK-2 in a dose-dependent fashion. Second, transforming growth factor-β1 induced excessive extracellular matrix deposition in HK-2 cells with enhanced collagen I, collagen IV, and fibronectin expression. However, carvacrol decreased the expression of collagen I, collagen IV in a dose-dependent manner and fibronectin to attenuate the extracellular matrix deposition in HK-2. Third, carvacrol attenuated TGF-β1-induced decrease of E-cadherin and increase of snail, vimentin, and alpha-smooth muscle actin in HK-2 cells. Transforming growth factor-β1-induced increase in PI3K and AKT phosphorylation in HK-2 were also reversed by carvacrol. Collectively, carvacrol ameliorates renal fibrosis through inhibition of transforming growth factor-β1-induced extracellular matrix deposition and epithelial-mesenchymal transition of HK-2 cells, providing potential therapy for the treatment of renal fibrosis.

Role of tissue transforming growth factor-β1 in pancreatic fibrosis

1998 ◽  
Vol 114 ◽  
pp. A498 ◽  
Author(s):  
M. Shiozaki ◽  
Y. Takeda ◽  
H. Morikawa ◽  
Y. Nakagawa ◽  
K. Katsu
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Pancreatic Fibrosis

scholarly journals The Role of Transforming Growth Factor-β1 in Airway Inflammation of Childhood Asthma

2013 ◽  
Vol 26 (3) ◽  
pp. 725-738 ◽  
Author(s):  
R. Gagliardo ◽  
P. Chanez ◽  
M. Gjomarkaj ◽  
S. La Grutta ◽  
A. Bonanno ◽  
...  
Keyword(s):  
Growth Factor ◽  
Airway Inflammation ◽  
Childhood Asthma ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1

Potential role of multiple members of the kallikrein-related peptidase family of serine proteases in activating latent TGFβ1 in semen

2010 ◽  
Vol 391 (1) ◽  
Author(s):  
Nashmil Emami ◽  
Eleftherios P. Diamandis
Keyword(s):  
Conformational Changes ◽  
Seminal Plasma ◽  
Serine Proteases ◽  
Transforming Growth Factor ◽  
Ex Vivo ◽  
Transforming Growth Factor Β1 ◽  
Peptide Fragments ◽  
Biochemical Mechanisms

Abstract Transforming growth factor β1 (TGFβ1) has been implicated as a key contributor of immunosuppression in seminal plasma. The biochemical mechanisms that lead to production of active seminal TGFβ1 are not fully understood. It is plausible that TGFβ1 activation is partly induced simultaneously with the release of motile spermatozoa following liquefaction of the semen coagulum. Several members of the kallikrein-related peptidase (KLK) family are involved in the regulation of semen liquefaction. This study examines the involvement of these KLKs in TGFβ1 activation in vitro and ex vivo, in seminal plasma. Latent TGFβ1 was rapidly activated by KLK14. The latency-associated propeptide (LAP) was shown to be cleaved by KLK14 into small peptide fragments, providing a possible mechanism for TGFβ1 activation. KLK14 also cleaved the latent TGFβ binding protein 1 (LTBP1). KLK1, 2, and 5 might also contribute to TGFβ1 activation by nicking the LAP motif and inducing conformational changes that aid in subsequent processing of LAP or through LTBP1 cleavage. Our study provides strong evidence for the involvement of multiple members of the seminal KLK cascade in activation of latent TGFβ1 in seminal plasma. These findings might have clinical implications in infertility treatment of cases with concurrent delayed liquefaction and TGFβ1-related semen antigenicity.

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