Cardiac microvascular endothelial cells express and release nerve growth factor but not fibroblast growth factor-2

2010 ◽  
Vol 46 (5) ◽  
pp. 469-476 ◽  
Author(s):  
Shimon Lecht ◽  
Carola Foerster ◽  
Hadar Arien-Zakay ◽  
Cezary Marcinkiewicz ◽  
Philip Lazarovici ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor 2 ◽  
Microvascular Endothelial Cells ◽  
Fibroblast Growth ◽  
Nerve Growth ◽  
Microvascular Endothelial ◽  
Cardiac Microvascular Endothelial Cells

Human Dermal Microvascular Endothelial Cells Produce Nerve Growth Factor: Implications for Wound Repair

Shock ◽  
2003 ◽  
Vol 19 (2) ◽  
pp. 127-130 ◽  
Author(s):  
Nicole S. Gibran ◽  
Richard Tamura ◽  
Ray Tsou ◽  
F. Frank Isik
Keyword(s):  
Endothelial Cells ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Wound Repair ◽  
Microvascular Endothelial Cells ◽  
Nerve Growth ◽  
Microvascular Endothelial

scholarly journals MicroRNA-Regulated Rickettsial Invasion into Host Endothelium via Fibroblast Growth Factor 2 and Its Receptor FGFR1

Cells ◽  
2018 ◽  
Vol 7 (12) ◽  
pp. 240 ◽  
Author(s):  
Abha Sahni ◽  
Hema Narra ◽  
Jignesh Patel ◽  
Sanjeev Sahni
Keyword(s):  
Gene Expression ◽  
Endothelial Cells ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Host Cells ◽  
Microvascular Endothelial Cells ◽  
Target Cells ◽  
Fibroblast Growth ◽  
Wide Range ◽  
Microvascular Endothelial

Microvascular endothelial cells (ECs) represent the primary target cells during human rickettsioses and respond to infection via the activation of immediate–early signaling cascades and the resultant induction of gene expression. As small noncoding RNAs dispersed throughout the genome, microRNAs (miRNAs) regulate gene expression post-transcriptionally to govern a wide range of biological processes. Based on our recent findings demonstrating the involvement of fibroblast growth factor receptor 1 (FGFR1) in facilitating rickettsial invasion into host cells and published reports suggesting miR-424 and miR-503 as regulators of FGF2/FGFR1, we measured the expression of miR-424 and miR-503 during R. conorii infection of human dermal microvascular endothelial cells (HMECs). Our results revealed a significant decrease in miR-424 and miR-503 expression in apparent correlation with increased expression of FGF2 and FGFR1. Considering the established phenomenon of endothelial heterogeneity and pulmonary and cerebral edema as the prominent pathogenic features of rickettsial infections, and significant pathogen burden in the lungs and brain in established mouse models of disease, we next quantified miR-424 and miR-503 expression in pulmonary and cerebral microvascular ECs. Again, R. conorii infection dramatically downregulated both miRNAs in these tissue-specific ECs as early as 30 min post-infection in correlation with higher FGF2/FGFR1 expression. Changes in the expression of both miRNAs and FGF2/FGFR1 were next confirmed in a mouse model of R. conorii infection. Furthermore, miR-424 overexpression via transfection of a mimic into host ECs reduced the expression of FGF2/FGFR1 and gave a corresponding decrease in R. conorii invasion, while an inhibitor of miR-424 had the expected opposite effect. Together, these findings implicate the rickettsial manipulation of host gene expression via regulatory miRNAs to ensure efficient cellular entry as the critical requirement to establish intracellular infection.

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