Tufted‐angioma‐like lesion associated with vascular endothelial growth factor and interleukin‐6 in TAFRO syndrome: Is it a common histological feature of multicentric Castleman disease/POEMS syndrome?

2019 ◽  
Vol 46 (4) ◽  
pp. 280-284 ◽  
Author(s):  
Kumi Fujita ◽  
Kazuhiro Hatta
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Interleukin 6 ◽  
Castleman Disease ◽  
Vascular Endothelial ◽  
Histological Feature ◽  
Tafro Syndrome ◽  
Multicentric Castleman Disease ◽  
Tufted Angioma ◽  
Endothelial Growth Factor

scholarly journals HSP22 (HSPB8) positively regulates PGF2α-induced synthesis of interleukin-6 and vascular endothelial growth factor in osteoblasts

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Gen Kuroyanagi ◽  
Go Sakai ◽  
Takanobu Otsuka ◽  
Naohiro Yamamoto ◽  
Kazuhiko Fujita ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Map Kinase ◽  
Interleukin 6 ◽  
Prostaglandin F2α ◽  
P38 Map Kinase ◽  
Vascular Endothelial ◽  
Mitogen Activated Protein ◽  
Endothelial Growth Factor ◽  
Vegf Release

Abstract Background Heat shock protein 22 (HSP22) belongs to class I of the small HSP family that displays ubiquitous expression in osteoblasts. We previously demonstrated that prostaglandin F2α (PGF2α), a potent bone remodeling factor, induces the synthesis of interleukin-6 (IL-6) and vascular endothelial growth factor (VEGF) via p44/p42 mitogen-activated protein (MAP) kinase and p38 MAP kinase in osteoblast-like MC3T3-E1 cells. In the present study, we investigated whether HSP22 is implicated in the PGF2α-induced synthesis of IL-6 and VEGF and the mechanism of MC3T3-E1 cells. Methods MC3T3-E1 cells were transfected with HSP22-siRNA. IL-6 and VEGF release was assessed by ELISA. Phosphorylation of p44/p42 MAP kinase and p38 MAP kinase was detected by Western blotting. Results The PGF2α-induced release of IL-6 in HSP22 knockdown cells was significantly suppressed compared with that in the control cells. HSP22 knockdown also reduced the VEGF release by PGF2α. Phosphorylation of p44/p42 MAP kinase and p38 MAP kinase was attenuated by HSP22 downregulation. Conclusions Our results strongly suggest that HSP22 acts as a positive regulator in the PGF2α-induced synthesis of IL-6 and VEGF in osteoblasts.

scholarly journals Modulation of Oxidative and Nitrosative Stress Attenuates Microvascular Hyperpermeability in Ovine Model of Pseudomonas Aeruginosa Sepsis

2021 ◽  
Author(s):  
Satoshi Fukuda ◽  
Yosuke Niimi ◽  
Yasutaka Hirasawa ◽  
Ennert R. Manyeza ◽  
C. Edwin Garner ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Pseudomonas Aeruginosa ◽  
Growth Factor ◽  
Lung Tissue ◽  
Interleukin 6 ◽  
Nitrosative Stress ◽  
Vascular Endothelial ◽  
Ovine Model ◽  
Organ Function ◽  
Endothelial Growth Factor

Abstract Background: Sepsis is one of the most frequent causes of death in the ICU, and microvascular hyperpermeability caused by oxidative/nitrosative stress plays an important role in tissue edema leading to multi-organ dysfunctions and increased mortality. This study tested the efficacy of a novel compound R-107, a modulator of oxidative/nitrosative stress, in an ovine model of sepsis. We hypothesized that R-107 effectively ameliorates the severity of microvascular hyperpermeability and preserves multi-organ function.Methods: Sepsis was induced in twenty-two adult female Merino sheep by intravenous infusion of Pseudomonas aeruginosa (1x1010 CFUs) for 60 minutes. After injury, animals were allocated into the following groups: 1) Control: intramuscular injection (IM) of saline, n=13; and 2) Treatment: IM of 50 mg/kg R-107, n=9. The IM treatment was given after the completion of the Pseudomonas aeruginosa injection. Animals were placed on a mechanical ventilator, fluid resuscitated, and monitored for 24 hours in a conscious state. Results: R-107 treatment attenuated 24-hour mortality (11 vs. 30%). R-107 significantly reduced fluid requirement (15 – 24 hours, p<0.05), net fluid balance (9 – 24 hours, p<0.05), and water content in lung, heart, and kidney (p=0.02, 0.04, and 0.01, respectively) compared to control. R-107 treatment significantly delayed the onset of positive qSOFA (3.3 vs. 6.8 hours, p=0.04), and significantly decreased lung injury score and modified sheep SOFA score at 24 hours (p=0.01 and 0.04). The R-107 treatment group had significantly lower arterial lactate (21 – 24 hours, p<0.05), shed syndecan-1 (3 – 6 hours, p<0.05), and interleukin-6 (6 – 12 hours, p<0.05) levels in plasma, and significantly attenuated lung tissue 3-nitrotyrosine and vascular endothelial growth factor-A expression (p=0.03 and 0.002) compared to control. There was no adverse effect observed during R-107 treatment.Conclusions: Modulation of oxidative/nitrosative stress by R-107 reduced lung tissue vascular endothelial growth factor-A, plasma shed syndecan-1, and interleukin-6 and attenuated severe microvascular hyperpermeability resulting in improved multi-organ function and survival in Pseudomonas aeruginosa sepsis.

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