scholarly journals T Cell Deficits and Overexpression of Hepatocyte Growth Factor in Anti-inflammatory Circulating Monocytes of Middle-Aged Patients with Bipolar Disorder Characterized by a High Prevalence of the Metabolic Syndrome

2017 ◽  
Vol 8 ◽  
Author(s):  
Rogier J. Vogels ◽  
Manja A. Koenders ◽  
Elisabeth F. C. van Rossum ◽  
Annet T. Spijker ◽  
Hemmo A. Drexhage
1997 ◽  
Vol 185 (12) ◽  
pp. 2121-2131 ◽  
Author(s):  
Robbert van der Voort ◽  
Taher E.I. Taher ◽  
Robert M.J. Keehnen ◽  
Lia Smit ◽  
Martijn Groenink ◽  
...  

T cell–dependent humoral immune responses are initiated by the activation of naive B cells in the T cell areas of the secondary lymphoid tissues. This primary B cell activation leads to migration of germinal center (GC) cell precursors into B cell follicles where they engage follicular dendritic cells (FDC) and T cells, and differentiate into memory B cells or plasma cells. Both B cell migration and interaction with FDC critically depend on integrin-mediated adhesion. To date, the physiological regulators of this adhesion were unkown. In the present report, we have identified the c-met–encoded receptor tyrosine kinase and its ligand, the growth and motility factor hepatocyte growth factor/scatter factor (HGF/SF), as a novel paracrine signaling pathway regulating B cell adhesion. We observed that c-Met is predominantly expressed on CD38+CD77+ tonsillar B cells localized in the dark zone of the GC (centroblasts). On tonsil B cells, ligation of CD40 by CD40-ligand, induces a transient strong upregulation of expression of the c-Met tyrosine kinase. Stimulation of c-Met with HGF/SF leads to receptor phosphorylation and, in addition, to enhanced integrin-mediated adhesion of B cells to both VCAM-1 and fibronectin. Importantly, the c-Met ligand HGF/SF is produced at high levels by tonsillar stromal cells thus providing signals for the regulation of adhesion and migration within the lymphoid microenvironment.


2006 ◽  
Vol 5 (2) ◽  
pp. 109-114 ◽  
Author(s):  
Yasemin H. Balaban ◽  
Hale Sumer ◽  
Halis Simsek ◽  
Durdal Us ◽  
Gonca Tatar

2005 ◽  
Vol 90 (5) ◽  
pp. 2927-2931 ◽  
Author(s):  
Akiko Hiratsuka ◽  
Hisashi Adachi ◽  
Yoshihisa Fujiura ◽  
Sho-Ichi Yamagishi ◽  
Yuji Hirai ◽  
...  

2021 ◽  
Author(s):  
Akiko Sakaue ◽  
Hisashi Adachi ◽  
Mika Enomoto ◽  
Ako Fukami ◽  
Yume Nohara ◽  
...  

Abstract Background: We have previously reported that hepatocyte growth factor (HGF) levels were significantly associated with insulin resistance or components of the metabolic syndrome. However, it has been unknown how physical activity (PA) affects HGF levels after a long-term follow-up.Aims: Our aim was to clarify the association between PA changes and HGF levels /cerebro-cardiovascular disease (CVD) development during 10 years follow-up period in a community-dwelling Japanese general population.Methods: Of 1,320 subjects who received a health check-up examination in Tanushimaru town in 1999, 903 subjects (341 males and 562 females) were enrolled, who received the examination both in 1999 and 2009. We evaluated their PA levels by Baecke questionnaire in 1999 and evaluated their PA levels by a simple questionnaire in 2009. We measured the serum HGF levels by ELISA method in 1999 and 2009. We divided into four physical activity groups such as stable low PA, increased PA, decreased PA, and stable high PA. Using these questionnaires, we compared their PA and HGF levels in 10 years.Results: A significant inverse association was found between PA changes and serum HGF levels in 10 years after adjustment for age and sex. The serum HGF levels of increased PA group were significantly lower than stable low PA (p=0.038), and the former group showed the reduced CVD development compared to the latter group after adjustment for age and sex (p=0.012).Conclusions: Our data demonstrated that improvement of PA levels was associated with reduced HGF levels and CVD development.


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