Immunohistochemical analysis of hepatocyte growth factor in human coronary atherectomy specimens: comparison with transforming growth factor beta isoforms

1997 ◽  
Vol 430 (5) ◽  
pp. 407-415 ◽  
Author(s):  
H. Ueda ◽  
Michinori Imazu ◽  
Yasuhiko Hayashi ◽  
Koichi Ono ◽  
Wataru Yasui ◽  
...  
Keyword(s):  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Immunohistochemical Analysis ◽  
Growth Factor Beta ◽  
Hepatocyte Growth

scholarly journals Clinical Significance of Hepatocyte Growth Factor and Transforming Growth Factor-Beta-1 Levels in Assessing Disease Activity in Inflammatory Bowel Disease

2020 ◽  
Vol 2020 ◽  
pp. 1-5
Author(s):  
Rania Naguib ◽  
Wafaa Mohamed El-Shikh
Keyword(s):  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Disease Activity ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Inflammatory Responses ◽  
Control Group ◽  
Inflammatory Bowel ◽  
Growth Factor Beta ◽  
Hepatocyte Growth

Background. Transforming growth factor-beta (TGF-β) and hepatocyte growth factor (HGF) are inflammatory cytokines which function as key regulators of immunological homeostasis and inflammatory responses. They have been linked to inflammatory bowel diseases (IBD). In this study, we aim to assess the levels of TGF-β and HGF and other inflammatory markers in patients with IBD and correlate them with the disease activity. Study Design. A cross-sectional study involving 100 patients with ulcerative colitis (UC) and 100 patients with Crohn’s disease (CD) and 50 control subjects. TGF-β and HGF levels were measured and correlated with disease activity. Results and Conclusion. Serum levels of TGF-β and HGF were significantly higher in IBD patients compared with the control group. In the UC group, the levels of HGF and TGF-β were significantly higher than in the CD group. Levels of TGF-β and HGF correlate with the activity of IBD.

scholarly journals Mesenchymal Stem Cells Attenuates TGF-β1-Induced EMT by Increasing HGF Expression in HK-2 Cells

2021 ◽  
Author(s):  
Jun-Jun Wei ◽  
Li Tang ◽  
Liang-Liang Chen ◽  
Zhen-Hua Xie ◽  
Yu Ren ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Hepatocyte Growth ◽  
Tgf Β1

Background: Mesenchymal stem cells (MSCs) have recently shown promise for the treatment of various types of chronic kidney disease models. However, the mechanism of this effect is still not well understood. Our study is aimed to investigate the effect of MSCs on transforming growth factor beta 1 (TGF-β1)-induced epithelial mesenchymal transition (EMT) in renal tubular epithelial cells (HK-2 cells) and the underlying mechanism related to the reciprocal balance between hepatocyte growth factor (HGF) and TGF-β1. Methods: Our study was performed at Ningbo University, Ningbo, Zhejiang, China between Mar 2017 and Jun 2018. HK-2 cells were initially treated with TGF-β1，then co-cultured with MSCs. The induced EMT was assessed by cellular morphology and the expressions of alpha-smooth muscle actin (α-SMA) and EMT-related proteins. MTS assay and flow cytometry were employed to detect the effect of TGF-β1 and MSCs on HK-2 cell proliferation and apoptosis. SiRNA against hepatocyte growth factor (siHGF) was transfected to decrease the expression of HGF to identify the role of HGF in MSCs inhibiting HK-2 cells EMT. Results: Overexpressing TGF-β1 decreased HGF expression, induced EMT, suppressed proliferation and promoted apoptosis in HK-2 cells; but when co-cultured with MSCs all the outcomes were reversed. However, after treated with siHGF, all the benefits taken from MSCs vanished. Conclusion: TGF-β1 was a motivating factor of kidney cell EMT and it suppressed the HGF expression. However, MSCs provided protection against EMT by increasing HGF level and decreasing TGF-β1 level. Our results also demonstrated HGF is one of the critical factor in MSCs anti- fibrosis.  

Matrix Metalloproteinases 2 and 9 are Concentrated in the Luminal Aspect of the Cricoid Cartilage, Diminish with Loss of Perichondrium, and are Reinstated by Transforming Growth Factor Beta 3

2008 ◽  
Vol 117 (12) ◽  
pp. 925-930 ◽  
Author(s):  
Efrain A. Martinez-Alvernia ◽  
Leila A. Mankarious
Keyword(s):  
Growth Factor ◽  
Matrix Metalloproteinases ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Cricoid Cartilage ◽  
Immunohistochemical Analysis ◽  
Basic Medium ◽  
Group A ◽  
Growth Factor Beta ◽  
Group B

Objectives: We determined the location of matrix metalloproteinases (MMP) 2 and 9, and whether the luminal perichondrium or transforming growth factor (TGF) β3 influences the presence of MMP-2 and/or −9 within the chondrocytes of the cricoid cartilage. Methods: Subglottises from 15 neonatal mice were divided into group A (N = 5; luminal epithelium intact, grown in basic medium), group B (N = 5; epithelium-free, with sections of luminal perichondrium removed, grown in basic medium), and group C (N = 5; epithelium-free, with sections of luminal perichondrium removed, grown in basic medium with supplemental TGF-β3). Immunohistochemical analysis was done to identify MMP-2 and −9 distributions. Results: Group A demonstrated concentrations of MMP-2 and −9 in the luminal perichondrial and adjacent chondrocytes with a gradual decrease in signal intensity toward the outer perichondrium. Group B showed findings similar to those in group A, but in the region of removed perichondrium, the adjacent chondrocytes lost MMP-2 and −9 signal. The group C rings demonstrated reestablishment of MMP-2 and −9 signal in regions of luminal perichondrial loss. Conclusions: Localization of MMP-2 and −9 is predominantly in the luminal perichondrium and gradually decreases toward the outer perichondrium. The luminal perichondrium maintains expression of MMP-2 and −9 within the adjacent chondrocytes. Exogenous TGF-β3 reestablishes production of at least MMP-9, and probably MMP-2, in cricoid cartilages missing luminal perichondrium.

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