Anemia and Elevated Systemic Levels of Vascular Endothelial Growth Factor (VEGF)

Dunst, Juergen; Becker, Axel; Lautenschläger, Christine; Markau, Silke; Becker, Heike E. F.; Fischer, Kersten; Haensgen, G.

doi:10.1007/s00066-002-0925-8

Cited by 63 publications

(50 citation statements)

References 22 publications

(32 reference statements)

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“…This observation was initially surprising and unexpected because in humans, anemia is frequently associated with high levels of VEGF in the plasma. 16 However, it is generally believed that elevation of VEGF is secondary to anemia or hypoxia as opposed to directly causing anemia. Nevertheless, the occurrence of large hemangiomas is frequently associated with thrombocytopenia, hemolytic anemia and splenomegaly (called Kasabach-Merritt syndrome) in human beings.…”

Section: Discussionmentioning

confidence: 99%

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Transgenic rabbits with increased VEGF expression develop hemangiomas in the liver: a new model for Kasabach–Merritt syndrome

Kitajima

Liu

Morimoto

et al. 2005

Laboratory Investigation

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Clinical studies have provided ample evidence that high (either systemic or local) levels of vascular endothelial growth factor (VEGF) are associated with several pathophysiological disorders, including hemangiomas. To investigate whether elevated VEGF expression could directly affect these disorders, we created a transgenic (Tg) rabbit model with increased hepatic expression of the human VEGF 165 transgene under the control of the human a-antitrypsin promoter. Tg rabbits exhibited marked hepatomegaly, with livers 2.5-fold heavier than those of control rabbits. Histological analysis revealed that the livers of Tg rabbits showed prominent dilation of the sinusoids and formed various-sized blood vessel networks, a feature of diffuse hemangiomas. Immunohistochemical staining revealed that the hepatocytes produced VEGF 165 , whereas plasma VEGF 165 was not detected. Furthermore, Tg rabbits suffered from hemolytic anemia, thrombocytopenia and splenomegaly, which was associated with marked extramedullary hematopoiesis. The manifestations of Tg rabbits mimic many of the features of hemangiomatous disorders in humans such as the Kasabach-Merritt syndrome, and therefore this model may be potentially useful for the study of the pathogenesis and complications of hemangiomas as well as the investigation of angiogenesis inhibitors.

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Section: Discussionmentioning

confidence: 99%

“…15 On the other hand, clinical studies also revealed that high plasma levels of VEGF were associated with rheumatoid arthritis, 13 hemangioma 5,6 and anemia. 16 However, it is unknown whether the increased VEGF in the plasma in these patients is causative or a consequence, or both of these disorders.…”

mentioning

confidence: 99%

Transgenic rabbits with increased VEGF expression develop hemangiomas in the liver: a new model for Kasabach–Merritt syndrome

Kitajima

Liu

Morimoto

et al. 2005

Laboratory Investigation

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“…Previous experimental studies have provided evidence of VEGF up-regulation, 12,33 angiogenesis, and increased capillary density in anemic animals and humans. [33][34][35] Our previous studies have demonstrated evidence of increased vascular endothelial growth factor (VEGF) RNA and protein in brain homogenates from anemic rats, suggesting that angiogenesis may be acutely activated.…”

Section: Genes Involved In Angiogenesismentioning

confidence: 99%

“…[33][34][35] Our previous studies have demonstrated evidence of increased vascular endothelial growth factor (VEGF) RNA and protein in brain homogenates from anemic rats, suggesting that angiogenesis may be acutely activated. The current microarray data demonstrated that angiopoietin 2 (angiogenic factor) increased progressively after 6 and 24 hr of anemia.…”

Section: Genes Involved In Angiogenesismentioning

confidence: 99%

L’expression génique dans le cortex cérébral de rats anémiques aigus: une analyse par microarray

Briet

Mazer

Tsui

et al. 2009

Can J Anesth/J Can Anesth

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Purpose Hemodilution in perioperative patients has been associated with neurological morbidity and increased mortality by undefined mechanisms. This study assesses whether hemodilutional anemia up-regulated inflammatory cerebral gene expression (microarray) to help define the mechanism. Methods Hemodilution was performed in anesthetized rats by exchanging 50% of the estimated blood volume (30 mL kg -1 ) with pentastarch. Two groups of control animals were utilized, i.e., a non-anesthetized control (Normal Control) and an anesthetized control group (Anesthesia Control). Blood pressure, hemoglobin concentration, and arterial blood gas analysis were performed before and after hemodilution. Cerebral cortex was harvested from isoflurane-anesthetized rats (n = 6) after 6 and 24 hr of recovery and was used to perform complimentary DNA (cDNA) microarray analyses. Pro-inflammatory chemokine and cytokine protein levels were also measured.Results Microarray analysis demonstrated up-regulation of 72 and 27 genes (6 and 24 hr, respectively) in anemic cerebral cortex. These genes were involved in a number of biological functions, including (1) inflammatory responses; (2) angiogenesis; (3) vascular homeostasis; (4) cellular biology; and (5) apoptosis. Chemokine ribonucleic acid (RNA) expression (CXCL-1, -10, and -11) was highest in anemic brain tissue (P \ 0.0125 for each). Protein measurements demonstrated a significant increase in interleukin-6, tumor necrosis factor a, and monocyte chemoattractant protein-1 (P \ 0.05 for each). Conclusion This study utilizes microarray technology to elucidate changes in cerebral cortical gene expression in response to acute hemodilution. These findings demonstrate an increase in pro-inflammatory chemokines (RNA, protein) and cytokines (protein). An improved understanding of the inflammatory response to anemia may help to minimize associated morbidity and mortality. RésuméObjectif L'he´modilution en pe´riope´ratoire chez les patients a e´te´associe´e à une morbidite´neurologique et une mortalite´accrue en raison de me´canismes inde´termine´s. Cette e´tude examine si l'ane´mie par he´modilution re´gule al a hausse l'expression ge´nique ce´re´brale inflammatoire (microarray) afin d'aider a`de´finir ce me´canisme. Méthode Une he´modilution a e´te´re´alise´e chez des rats anesthe´sie´s en e´changeant 50 % du volume sanguin estime( 30 mLÁkg -1 ) avec du pentastarch. Deux groupes d'animaux te´moins ont e´te´utilise´s, soit un groupe te´moin non anesthe´sie´(te´moin normal) et un groupe te´moin anesthe´sie( te´moin anesthe´sie´). La pression arte´rielle, la concentration d'he´moglobine et une gazome´trie sanguine arte´rielle

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“…This suggests that anemia might impact on the progression of angeiogenesis in malignant and benign diseases [6] .…”

Section: Introductionmentioning

confidence: 99%

Serum Vascular Endothelial Growth Factor in Children with Beta Thalassemia Major

Aziz¹

2016

jmscr

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Anemia and Elevated Systemic Levels of Vascular Endothelial Growth Factor (VEGF)

Abstract: Anemic patients have elevated levels of VEGF. The data suggest that anemia might impact on the progression of angiogenesis in malignant and benign diseases.

Cited by 63 publications

References 22 publications

Transgenic rabbits with increased VEGF expression develop hemangiomas in the liver: a new model for Kasabach–Merritt syndrome

Transgenic rabbits with increased VEGF expression develop hemangiomas in the liver: a new model for Kasabach–Merritt syndrome

L’expression génique dans le cortex cérébral de rats anémiques aigus: une analyse par microarray

Serum Vascular Endothelial Growth Factor in Children with Beta Thalassemia Major

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