scholarly journals Fluid Shear Stress Synergizes with Insulin-like Growth Factor-I (IGF-I) on Osteoblast Proliferation through Integrin-dependent Activation of IGF-I Mitogenic Signaling Pathway

2005 ◽  
Vol 280 (20) ◽  
pp. 20163-20170 ◽  
Author(s):  
Sonia Kapur ◽  
Subburaman Mohan ◽  
David J. Baylink ◽  
K.-H. William Lau
Keyword(s):  
Shear Stress ◽  
Growth Factor ◽  
Signaling Pathway ◽  
Fluid Shear Stress ◽  
Insulin Like Growth Factor ◽  
Osteoblast Proliferation ◽  
Mitogenic Signaling ◽  
Fluid Shear ◽  
Factor I ◽  
Igf I

scholarly journals Insulin-like Growth Factor-I (IGF-I) Receptor Activation Rescues UV-damaged Cells through a p38 Signaling Pathway

2001 ◽  
Vol 276 (21) ◽  
pp. 18185-18192 ◽  
Author(s):  
Lisa Héron-Milhavet ◽  
Michael Karas ◽  
Corinne M. Goldsmith ◽  
Bruce J. Baum ◽  
Derek LeRoith
Keyword(s):  
Growth Factor ◽  
Signaling Pathway ◽  
Receptor Activation ◽  
Insulin Like Growth Factor ◽  
Factor I ◽  
Igf I ◽  
Growth Factor I

P 7 Fluid shear stress promotes placental growth factor upregulation in human syncytiotrophoblast through the camp-pka signaling pathway

2017 ◽  
Vol 9 ◽  
pp. 39-40
Author(s):  
Edouard Lecarpentier ◽  
Anthony Atallah ◽  
Jean Guibourdenche ◽  
Marylise Hebert-Schuster ◽  
Bassam Haddad ◽  
...  
Keyword(s):  
Shear Stress ◽  
Growth Factor ◽  
Signaling Pathway ◽  
Fluid Shear Stress ◽  
Placental Growth Factor ◽  
Fluid Shear

scholarly journals Fluid Shear Stress Promotes Placental Growth Factor Upregulation in Human Syncytiotrophoblast Through the cAMP–PKA Signaling Pathway

Hypertension ◽  
2016 ◽  
Vol 68 (6) ◽  
pp. 1438-1446 ◽  
Author(s):  
Edouard Lecarpentier ◽  
Anthony Atallah ◽  
Jean Guibourdenche ◽  
Marylise Hebert-Schuster ◽  
Sarah Vieillefosse ◽  
...  
Keyword(s):  
Shear Stress ◽  
Growth Factor ◽  
Signaling Pathway ◽  
Fluid Shear Stress ◽  
Placental Growth Factor ◽  
Fluid Shear

Fluid shear stress promotes osteoblast proliferation via the Gαq–ERK5 signaling pathway

2016 ◽  
Vol 57 (4) ◽  
pp. 299-306 ◽  
Author(s):  
Zhang Bo ◽  
Geng Bin ◽  
Wang Jing ◽  
Wang Cuifang ◽  
An Liping ◽  
...  
Keyword(s):  
Shear Stress ◽  
Signaling Pathway ◽  
Fluid Shear Stress ◽  
Osteoblast Proliferation ◽  
Fluid Shear

scholarly journals Aspects of Growth Hormone and Insulin-Like Growth Factor-I Related to Neuroprotection, Regeneration, and Functional Plasticity in the Adult Brain

2006 ◽  
Vol 6 ◽  
pp. 53-80 ◽  
Author(s):  
N. David Åberg ◽  
Katarina Gustafson Brywe ◽  
Jörgen Isgaard
Keyword(s):  
Growth Hormone ◽  
Growth Factor ◽  
Signaling Pathway ◽  
Cell Types ◽  
Adult Brain ◽  
Insulin Like Growth Factor ◽  
Gh Treatment ◽  
Factor I ◽  
Igf I ◽  
Growth Factor I

Apart from regulating somatic growth and metabolic processes, accumulating evidence suggests that the growth hormone (GH)/insulin-like growth factor-I (IGF-I) axis is involved in the regulation of brain growth, development, and myelination. In addition, both GH and IGF-I affect cognition and biochemistry in the adult brain. Some of the effects of GH are attributable to circulating IGF-I, while others may be due to IGF-I produced locally within the brain. Some of the shared effects in common to GH and IGF-I may also be explained by cross-talk between the GH and IGF-I transduction pathways, as indicated by recent data from other cell systems. Otherwise, it also seems that GH may act directly without involving IGF-I (either circulating or locally). Plasticity in the central nervous system (CNS) may be viewed as changes in the functional interplay between the major cell types, neurons, astrocytes, and oligodendrocytes. GH and IGF-I affect all three of these cell types in several ways. Apart from the neuroprotective effects of GH and IGF-I posited in different experimental models of CNS injury, IGF-I has been found to increase progenitor cell proliferation and new neurons, oligodendrocytes, and blood vessels in the dentate gyrus of the hippocampus. It appears that the MAPK signaling pathway is required for IGF-I–stimulated proliferationin vitro, whereas the PI3K/Akt or MAPK/Erk signaling pathway appears to mediate antiapoptotic effects. The increase of IGF-I on endothelial cell phenotype may explain the increase in cerebral arteriole density observed after GH treatment. The functional role of GH and IGF-I in the adult brain will be reviewed with reference to neurotransmitters, glucose metabolism, cerebral blood flow, gap junctional communication, dendritic arborization, exercise, enriched environment, depression, learning, memory, and aging.Briefly, these findings suggest that IGF-I functions as a putative regenerative agent in the adult CNS. Hitherto less studied regarding in these aspects, GH may have similar effects, especially as it is the main regulator of IGF-Iin vivo. Some of the positive cognitive features of GH treatment are likely attributable to the mechanisms reviewed here.

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