Hepatocyte growth factor regulates HIF-1α-induced nucleus pulposus cell proliferation through MAPK-, PI3K/Akt-, and STAT3-mediated signaling

2020 ◽  
Author(s):  
Tomonori Itsuji ◽  
Hitoshi Tonomura ◽  
Hidenobu Ishibashi ◽  
Yasuo Mikami ◽  
Masateru Nagae ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Nucleus Pulposus ◽  
Nucleus Pulposus Cell ◽  
Hepatocyte Growth

scholarly journals Hepatocyte Growth Factor Overexpression in the Islet of Transgenic Mice Increases Beta Cell Proliferation, Enhances Islet Mass, and Induces Mild Hypoglycemia

2000 ◽  
Vol 275 (2) ◽  
pp. 1226-1232 ◽  
Author(s):  
Adolfo Garcia-Ocaña ◽  
Karen K. Takane ◽  
Mushtaq A. Syed ◽  
William M. Philbrick ◽  
Rupangi C. Vasavada ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Growth Factor ◽  
Transgenic Mice ◽  
Hepatocyte Growth Factor ◽  
Beta Cell ◽  
Beta Cell Proliferation ◽  
Islet Mass ◽  
Hepatocyte Growth

scholarly journals Monocyte activation state regulates monocyte-induced endothelial proliferation through Met signaling

Blood ◽  
2010 ◽  
Vol 115 (16) ◽  
pp. 3407-3412 ◽  
Author(s):  
Shai Y. Schubert ◽  
Alejandro Benarroch ◽  
Juan Monter-Solans ◽  
Elazer R. Edelman
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cells ◽  
Endothelial Cell ◽  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Direct Interaction ◽  
Endothelial Cell Proliferation ◽  
Specific Cell ◽  
Mrna Levels ◽  
Hepatocyte Growth

Abstract Direct interaction of unactivated primary monocytes with endothelial cells induces a mitogenic effect in subconfluent, injured endothelial monolayers through activation of endothelial Met. We now report that monocytes' contact-dependent mitogenicity is controlled by activation-mediated regulation of hepatocyte growth factor. Direct interaction of unactivated monocytes with subconfluent endothelial cells for 12 hours resulted in 9- and 120-fold increase in monocyte tumor necrosis factor-α (TNFα) and interleukin-1β (IL-1β) mRNA levels and bitemporal spike in hepatocyte growth factor that closely correlates with endothelial Met and extracellular signal-related kinase (ERK) phosphorylation. Once activated, monocytes cannot induce a second wave of endothelial cell proliferation and endothelial Met phosphorylation and soluble hepatocyte growth factor levels fall off. Monocyte-induced proliferation is dose dependent and limited to the induction of a single cell cycle. Monocytes retain their ability to activate other endothelial cells for up to 8 hours after initial interaction, after which they are committed to the specific cell. There is therefore a profoundly sophisticated mode of vascular repair. Confluent endothelial cells ensure vascular quiescence, whereas subconfluence promotes vessel activation. Simultaneously, circulating monocytes stimulate endothelial cell proliferation, but lose this potential once activated. Such a system provides for the fine balance that can restore vascular and endothelial homeostasis with minimal overcompensation.

Hepatocyte growth factor plays a dual role in tendon‐derived stem cell proliferation, migration, and differentiation

2019 ◽  
Vol 234 (10) ◽  
pp. 17382-17391 ◽  
Author(s):  
Peilin Han ◽  
Qingbo Cui ◽  
Wenjun Lu ◽  
Shulong Yang ◽  
Manyu Shi ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Stem Cell ◽  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Dual Role ◽  
Stem Cell Proliferation ◽  
Hepatocyte Growth

Hepatocyte growth factor/scatter factor, angiogenesis and tumour cell proliferation in primary breast cancer

The Breast ◽  
1996 ◽  
Vol 5 (2) ◽  
pp. 105-109 ◽  
Author(s):  
J. Nagy ◽  
G.W. Curry ◽  
K.J. Hillan ◽  
E. Mallont ◽  
A.D. Purushotham ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Tumour Cell ◽  
Primary Breast Cancer ◽  
Scatter Factor ◽  
Tumour Cell Proliferation ◽  
Hepatocyte Growth
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