scholarly journals Fibroblast Growth Factor Type 2 Signaling Is Critical for DNA Repair in Human Keratinocyte Stem Cells

Stem Cells ◽  
2010 ◽  
Vol 28 (9) ◽  
pp. 1639-1648 ◽  
Author(s):  
Ghida Harfouche ◽  
Pierre Vaigot ◽  
Walid Rachidi ◽  
Odile Rigaud ◽  
Sandra Moratille ◽  
...  
Keyword(s):  
Stem Cells ◽  
Dna Repair ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth ◽  
Human Keratinocyte ◽  
Factor Type ◽  
Keratinocyte Stem Cells

scholarly journals Fibroblast Growth Factor Type 2 (FGF2) Administration Attenuated the Clinical Manifestations of Preeclampsia in a Murine Model Induced by L-NAME

2021 ◽  
Vol 12 ◽  
Author(s):  
Margarita L Martinez-Fierro ◽  
Gloria Patricia Hernadez-Delgadillo ◽  
Jose Feliciano Flores-Mendoza ◽  
Claudia Daniela Alvarez-Zuñiga ◽  
Martha Lizeth Diaz-Lozano ◽  
...  
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Murine Model ◽  
Clinical Manifestations ◽  
Histological Evaluation ◽  
Growth Delay ◽  
Hypertensive Disorder ◽  
Fibroblast Growth ◽  
Factor Type

Background: In preeclampsia, a hypertensive disorder of pregnancy, the poor remodeling of spiral arteries leads to placental hypoperfusion and ischemia, provoking generalized maternal endothelial dysfunction and, in severe cases, death. Endothelial and placental remodeling is important for correct pregnancy evolution and is mediated by cytokines and growth factors such as fibroblast growth factor type 2 (FGF2). In this study, we evaluated the effect of human recombinant FGF2 (rhFGF2) administration in a murine model of PE induced by NG-nitro-L-arginine methyl ester (L-NAME) to test if rhFGF2 administration can lessen the clinical manifestations of PE.Methods: Pregnant rats were administrated with 0.9% of NaCl (vehicle), L-NAME (60 mg/kg), FGF2 (666.6 ng/kg), L-NAME+FGF2 or L-NAME + hydralazine (10 mg/kg) from the 10th to 19th days of gestation. Blood pressure (BP), urine protein concentrations and anthropometric values both rat and fetuses were assessed. Histological evaluation of organs from rats delivered by cesarean section was carried out using hematoxylin and eosin staining.Results: A PE-like model was established, and it included phenotypes such as maternal hypertension, proteinuria, and fetal growth delay. Compared to the groups treated with L-NAME, the L-NAME + FGF2 group was similar to vehicle: the BP remained stable and the rats did not develop enhanced proteinuria. Both the fetuses and placentas from rats treated with L-NAME + FGF2 had similar values of weight and size compared with the vehicle.Conclusion: The intravenous administration of rhFGF2 showed beneficial and hypotensive effects, reducing the clinical manifestations of PE in the evaluated model.

Fgfr2 and osteopontin domains in the developing skull vault are mutually exclusive and can be altered by locally applied FGF2

Development ◽  
1997 ◽  
Vol 124 (17) ◽  
pp. 3375-3384 ◽  
Author(s):  
S. Iseki ◽  
A.O. Wilkie ◽  
J.K. Heath ◽  
T. Ishimaru ◽  
K. Eto ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Growth Factor Receptor ◽  
Coronal Suture ◽  
Fibroblast Growth ◽  
Skull Vault ◽  
Fgfr2 Gene ◽  
Factor Type

Mutations in the human fibroblast growth factor receptor type 2 (FGFR2) gene cause craniosynostosis, particularly affecting the coronal suture. We show here that, in the fetal mouse skull vault, Fgfr2 transcripts are most abundant at the periphery of the membrane bones; they are mutually exclusive with those of osteopontin (an early marker of osteogenic differentiation) but coincide with sites of rapid cell proliferation. Fibroblast growth factor type 2 (FGF2) protein, which has a high affinity for the FGFR2 splice variant associated with craniosynostosis, is locally abundant; immunohistochemical detection showed it to be present at low levels in Fgfr2 expression domains and at high levels in differentiated areas. Implantation of FGF2-soaked beads onto the fetal coronal suture by ex utero surgery resulted in ectopic osteopontin expression, encircled by Fgfr2 expression, after 48 hours. We suggest that increased FGF/FGFR signalling in the developing skull, whether due to FGFR2 mutation or to ectopic FGF2, shifts the cell proliferation/differentiation balance towards differentiation by enhancing the normal paracrine down-regulation of Fgfr2.

Fibroblast Growth Factor Type 1 (FGF1)-Overexpressed Adipose-Derived Mesenchaymal Stem Cells (AD-MSCFGF1) Induce Neuroprotection and Functional Recovery in a Rat Stroke Model

2017 ◽  
Vol 13 (5) ◽  
pp. 670-685 ◽  
Author(s):  
Hamed Ghazavi ◽  
Seyed Javad Hoseini ◽  
Alireza Ebrahimzadeh-Bideskan ◽  
Baratali Mashkani ◽  
Soghra Mehri ◽  
...  
Keyword(s):  
Stem Cells ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Functional Recovery ◽  
Fibroblast Growth ◽  
Stroke Model ◽  
Factor Type
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