Pulmonary Expression of Vascular Endothelial Growth Factor in Sepsis

2003 ◽  
Vol 127 (3) ◽  
pp. 331-335 ◽  
Author(s):  
Michael Tsokos ◽  
Thomas Pufe ◽  
Friedrich Paulsen ◽  
Sven Anders ◽  
Rolf Mentlein
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Alveolar Macrophages ◽  
Sepsis Group ◽  
Normal Lung ◽  
Vascular Endothelial ◽  
Rt Pcr ◽  
Vegf Expression ◽  
Endothelial Growth Factor

Abstract Context.—Vascular endothelial growth factor (VEGF), an angiogenic and chemotactic peptide, is abundantly expressed in normal lung tissue, especially in alveolar and bronchial epithelium, glandular cells of the bronchi, and activated alveolar macrophages. Objective.—To investigate the role of VEGF in progressively impaired lung function as the major complication and cause of death in septic patients. Materials and Methods.—We evaluated pulmonary VEGF expression in lung autopsy material from septic patients who had been cared for by intensive care medicine using enzyme-linked immunosorbent assay (ELISA), reverse transcriptase–polymerase chain reaction (RT-PCR), and immunohistochemical methods. Results.—Compared with expression in nonseptic control individuals (n = 10), pulmonary VEGF expression as determined by ELISA was significantly (P < .001) decreased in septic patients (n = 8). As monitored by RT-PCR, mRNA for the 2 splice variants, VEGF121 and VEGF165, and for VEGFR-2/KDR were expressed in both groups, the yields being lower in the sepsis group. Samples from septic patients lacked or showed only sparse immunoreaction on bronchial and alveolar epithelium, whereas this reaction was strong in all control samples. However, alveolar macrophages were similarly immunopositive in both groups. Conclusions.—The precise underlying mechanisms for the distinctly different expression of pulmonary VEGF in septic patients and nonseptic control individuals are not clear at present. Particularly the role of VEGF in the development of sepsis-induced lung injury and acute respiratory distress syndrome in mechanically ventilated patients suffering from severe sepsis remains to be clarified.

Chronic Subdural Hematoma: Role of Vascular Endothelial Growth Factor and Craniotomy in Pathophysiology and Prevention of Recurrence

2017 ◽  
Vol 14 (01) ◽  
pp. 001-005
Author(s):  
Prabal Deb ◽  
Shashivadhanan Sundaravadhanan
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Subdural Hematoma ◽  
Chronic Subdural Hematoma ◽  
Vascular Endothelial ◽  
Vegf Expression ◽  
Immunohistochemical Examination ◽  
Endothelial Growth Factor ◽  
Prevention Of Recurrence

AbstractCurrent body of evidence suggests that the maintenance or enlargement of chronic subdural hematoma (cSDH) is caused by multiple factors. Inflammatory and vascular endothelial growth factor (VEGF)–induced accumulation of hematoma plays an important role in pathophysiology of cSDH. If neomembrane is implicated in the propagation of inflammatory mediators, excision of the culprit membrane becomes essential to treat and prevent recurrence of cSDH. This retrospective study was conducted in a service hospital where 48 cases of cSDH were operated in 2 years. Patients were evaluated clinically and radiologically. Surgical procedure offered included burr hole craniotomy (BHC), twist drill craniotomy (TDC), or craniotomy (Cr) with excision of neomembrane. Cr was offered whenever there was suspicion or evidence of reaccumulation, solid or calcified hematoma formation, nonobliteration of the subdural space, or numerous thick membranes as were demonstrated in imaging. In Cr maximum part of outer neomembrane was excised and margins were coagulated. The excised outer neomembrane was sent for immunohistochemical examination to assess the VEGF expression. Depending on the VEGF expression as seen on the microscope, these expressions were grouped into weak, moderate, or strong VEGF expression. The study showed that cSDH patients with neomembrane formation benefit from Cr. The strong VEGF expression from the excised neomembrane further strengthens the proinflammatory VEGF theory propagation of cSDH. It further proves that excision of the culprit membrane is essential to prevent recurrences.

scholarly journals Impaired Angiogenesis in the Remnant Kidney Model: I. Potential Role of Vascular Endothelial Growth Factor and Thrombospondin-1

2001 ◽  
Vol 12 (7) ◽  
pp. 1434-1447 ◽  
Author(s):  
DUK-HEE KANG ◽  
ALISON H. JOLY ◽  
SE-WOONG OH ◽  
CHRISTIAN HUGO ◽  
DONTSCHO KERJASCHKI ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Renal Disease ◽  
Vascular Endothelial ◽  
Vegf Expression ◽  
Endothelial Growth Factor ◽  
Progressive Renal Disease ◽  
Remnant Kidney ◽  
Impaired Angiogenesis

Abstract. Few studies have examined the role of the microvasculature in progressive renal disease. It was hypothesized that impaired angiogenesis might occur in the diseased kidney and could contribute to renal scarring. Progressive renal disease was induced in rats by 5/6 renal ablation and those rats were compared with sham-operated control animals at multiple time points, for examination of changes in the microvasculature and the expression of angiogenic factors. An early angiogenic response was documented in remnant kidneys, with increases in the proliferation of peritubular (1 wk) and glomerular (2 wk) endothelial cells. Subsequently, however, there was a decrease in endothelial cell proliferation, which was reduced to levels below those of sham-treated animals, in conjunction with interstitial expression of the antiangiogenic factor thrombospondin-1 (TSP-1) and decreased tubular expression of the proangiogenic factor vascular endothelial growth factor (VEGF). Both the increase in TSP-1 expression and the loss of VEGF expression were correlated with capillary loss and the development of glomerulosclerosis and interstitial fibrosis. Progressive macrophage infiltration was correlated both spatially and quantitatively with the sites of absent or diminished VEGF expression. In addition, macrophage-associated cytokines (interleukin-1β, interleukin-6, and tumor necrosis factor-α) inhibited VEGF mRNA expression and protein secretion by cultured tubular epithelial cells of the medullary thick ascending limb, under both normoxic and hypoxic conditions. Impaired angiogenesis characterizes the remnant kidney model and is correlated with progression. The impaired angiogenesis may be mediated by alterations in the renal expression of TSP-1 and VEGF, with the latter being regulated by macrophage-associated cytokines.

scholarly journals Neutralization of vascular endothelial growth factor antiangiogenic isoforms or administration of proangiogenic isoforms stimulates vascular development in the rat testis

Reproduction ◽  
2010 ◽  
Vol 140 (2) ◽  
pp. 319-329 ◽  
Author(s):  
Michelle M Baltes-Breitwisch ◽  
Robin A Artac ◽  
Rebecca C Bott ◽  
Renee M McFee ◽  
Jill G Kerl ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Gonadal Development ◽  
Vascular Density ◽  
Mrna Levels ◽  
Vascular Endothelial ◽  
Rt Pcr ◽  
Protein Levels ◽  
Endothelial Growth Factor

Vascular endothelial growth factor A (VEGFA) plays a role in both angiogenesis and seminiferous cord formation, and alternative splicing of theVegfagene produces both proangiogenic isoforms and antiangiogenic isoforms (B-isoforms). The objectives of this study were to evaluate the expression of pro- and antiangiogenic isoforms during testis development and to determine the role of VEGFA isoforms in testis morphogenesis. Quantitative RT-PCR determined thatVegfa_165bmRNA was most abundant between embryonic days 13.5 and 16 (E13.5 and 16;P<0.05). Compared with ovarian mRNA levels,Vegfa_120was more abundant at E13–14 (P<0.05),Vegfa_164was less abundant at E13 (P<0.05), andVegfa_165btended to be less abundant at E13 (P<0.09) in testes. Immunohistochemical staining localized antiangiogenic isoforms to subsets of germ cells at E14–16, and western blot analysis revealed similar protein levels for VEGFA_165B, VEGFA_189B, and VEGFA_206B at this time point. Treatment of E13 organ culture testes with VEGFA_120, VEGFA_164, and an antibody to antiangiogenic isoforms (anti-VEGFAxxxB) resulted in less organized and defined seminiferous cords compared with paired controls. In addition, 50 ng/ml VEGFA_120 and VEGFA_164 treatments increased vascular density in cultured testes by 60 and 48% respectively, and treatment with VEGFAxxxB antibody increased vascular density by 76% in testes (0.5 ng/ml) and 81% in ovaries (5 ng/ml) compared with controls (P<0.05). In conclusion, both pro- and antiangiogenic VEGFA isoforms are involved in the development of vasculature and seminiferous cords in rat testes, and differential expression of these isoforms may be important for normal gonadal development.

Cigarette Smoke Extract Increases Vascular Endothelial Growth Factor Production via TLR4/ROS/MAPKs/NF-kappaB Pathway in Nasal Fibroblast

2017 ◽  
Vol 31 (2) ◽  
pp. 78-84 ◽  
Author(s):  
Jae-Min Shin ◽  
Joo-Hoo Park ◽  
Hwee-Jin Kim ◽  
Il-Ho Park ◽  
Heung-Man Lee
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Cigarette Smoke ◽  
Cigarette Smoke Extract ◽  
Expression Level ◽  
Vascular Endothelial ◽  
Rt Pcr ◽  
Vegf Expression ◽  
Nf Kappab ◽  
Endothelial Growth Factor

Purpose Cigarette smoke is a complex mixture of various chemical compounds, including free radicals and highly toxic compounds. Cigarette smoke exposure has been shown to be associated with chronic rhinosinusitis and tissue remodeling in upper airway. Vascular endothelial growth factor (VEGF) is one of the cytokines with a crucial role in tissue remodeling of airway. The aims of this study were to determine the effects of cigarette smoke extract (CSE) on VEGF expression and to investigate the underlying molecular mechanisms of CSE in nasal fibroblasts. Methods Nasal fibroblasts were stimulated with CSE. Cytotoxicity was evaluated by 3-(4,5- dimethylthiazol-2yl)-2,5-diphenyl-tetrazolium bromide assay. The expression level of VEGF was measured using reverse transcription-polymerase chain reaction (RT-PCR), and enzyme-linked immunosorbent assay. Messenger RNA (mRNA) expression level of TLR4 were determined by RT-PCR. Small interfering RNA (siRNA) for TLR4 was transfected to suppress TLR4 expression. Activation of reactive oxygen species (ROS) was analyzed by using dichlorodihydro-fluorescein diacetate assay. Mitogen-activated protein kinase (MAPK) and NF-kappaB activations were determined by using western blot and/or luciferase assay. Results CSE had no significant cytotoxic effect in nasal fibroblast up to 5%. CSE significantly increased both VEGF mRNA and protein expression dose-dependently. The down-regulation of TLR4 transcription by siRNA treatment suppressed CSE-induced expressions of both TLR4 and VEGF. Pretreatment with ROS scavengers, specific inhibitors of each MAPK, and NF-kappaB inhibitor significantly decreased CSE-induced VEGF expression. Conclusions CSE has a stimulatory effect on VEGF expression through the TLR4, ROS, MAPK, and NF-kappaB signaling pathway in nasal fibroblasts.

scholarly journals The role of vascular endothelial growth factor in predicting the tumor dynamics of meningiomas

2021 ◽  
Vol 9 (11) ◽  
pp. 3397
Author(s):  
Shristi Butta ◽  
Mallika Pal ◽  
Suman Ghosh ◽  
Manoj Kumar Gupta
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Vascular Endothelial ◽  
Vegf Expression ◽  
Who Grade ◽  
Grade Ii ◽  
Endothelial Growth Factor ◽  
Grade Iii

Background: Meningiomas are the most common tumors of the central nervous system with variable tumor dynamics. Histopathology is the gold standard but has its own constraints in predicting the tumor behavior. As intra- tumoral hypoxia leads to neo angio angiogenesis and subsequent tumor growth we envisage to establish the role of vascular endothelial growth factor (VEGF) in predicting the tumor dynamics of meningiomas.Methods: This observational, descriptive, longitudinal follow up study included 38 patients and spanned over a period of 2 years. Surgical samples were grossed and histo-pathologically analyzed and subsequently immune-histochemically categorized. Cases showing VEGF positivity were subjected to yearly follow up to ascertain the number of recurrent cases.Results: Majority of our cases belonged to WHO grade I (84.21%). The 73.68% were females. The 63.16% were aged >50 years. The 42.1 % of the total cases revealed moderate to strong VEGF expression. Majority of grade II and grade III meningiomas showed moderate to strong VEGF expression. However, a subgroup of grade I meningiomas also revealed a high immune-expression of VEGF (31.25%). Statistically significant association was found between VEGF expression and WHO grade (p=0.0001). On follow up 34.21% of the cases showed recurrence. Significant association was found between VEGF expression and recurrence of the tumor s (p=0.0005).Conclusions: VEGF has a role in ascertaining the high-risk grade I meningiomas that have a potential to recur as well as grade II and grade III meningiomas that show adverse patient prognosis. 

scholarly journals New insights on the role of vascular endothelial growth factor in biliary pathophysiology

JHEP Reports ◽  
2021 ◽  
Vol 3 (3) ◽  
pp. 100251
Author(s):  
Valeria Mariotti ◽  
Romina Fiorotto ◽  
Massimiliano Cadamuro ◽  
Luca Fabris ◽  
Mario Strazzabosco
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor

scholarly journals Role of Vascular Endothelial Growth Factor (VEGF) in Human Embryo Implantation: Clinical Implications

Biomolecules ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 253
Author(s):  
Xi Guo ◽  
Hong Yi ◽  
Tin Chiu Li ◽  
Yu Wang ◽  
Huilin Wang ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Recurrent Miscarriage ◽  
Embryo Implantation ◽  
Critical Role ◽  
Angiogenic Factor ◽  
Vascular Endothelial ◽  
Underlying Mechanisms ◽  
Endothelial Growth Factor

Vascular endothelial growth factor (VEGF) is a well-known angiogenic factor that plays a critical role in various physiological and pathological processes. VEGF also contributes to the process of embryo implantation by enhancing embryo development, improving endometrial receptivity, and facilitating the interactions between the developing embryo and the endometrium. There is a correlation between the alteration of VEGF expression and reproductive failure, including recurrent implantation failure (RIF) and recurrent miscarriage (RM). In order to clarify the role of VEGF in embryo implantation, we reviewed recent literature concerning the expression and function of VEGF in the reproductive system around the time of embryo implantation and we provide a summary of the findings reported so far. We also explored the effects and the possible underlying mechanisms of action of VEGF in embryo implantation.

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