scholarly journals Peran Eritropoietin pada Stroke Iskemik Akut

2020 ◽  
Vol 9 (2) ◽  
pp. 117-25
Author(s):  
Lisda Amalia ◽  
Gilang Nispu Saputra
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Ischemic Stroke ◽  
Growth Factor ◽  
Blood Vessels ◽  
Vascular Occlusion ◽  
Vascular Endothelial ◽  
Cerebral Ischemic ◽  
Cerebral Vascular Occlusion ◽  
Endothelial Growth Factor ◽  
The Brain

Stroke iskemik merupakan salah satu penyebab stroke tersering, disebabkan oleh oklusi pembuluh darah serebral dan penyebab kematian ketiga. Iskemik otak akan menghasilkan penghasilan mediator inflamasi yang dapat berpartisipasi dalam jejas iskemik di otak. Saat awitan stroke iskemik terjadi, area otak yang diperdarahi oleh pembuluh darah akan kekurangan oksigen dan nutrisi sehingga sel otak terutama neuron berada dalam risiko, neuron ini masih dapat berfungsi yang dikenal sebagai penumbra. Hipoksia jaringan dan iskemik serebral mengaktivasi HIF-1α, yang kemudian mengaktivasi transkripsi gen eritropoietin (EPO) dan Vascular Endothelial Growth Factor (VEGF). Eritropoietin (EPO) merupakan peptida yang juga memiliki efek non–hematopoiesis yaitu berperan mendorong neuroproteksi. Eritropoietin (EPO)  dikeluarkan dalam hitungan menit dari proses iskemik dan mencapai puncak dalam 24 jam dari awitan stroke iskemik. Efek neuroproteksi dari  EPO yaitu sebagai anti apoptosis, anti oksidan, anti inflamasi, anti eksitoksisitas, neurogenesis, angiogenesis dan neurotropik. Dengan kata lain bahwa EPO dapat mengurangi derajat keparahan akibat oklusi pembuluh darah otak. Role of Eritropoietin in Acute Ischemic StrokeAbstractIschemic stroke is one of the most common causes of stroke, caused by cerebral vascular occlusion and the third cause of death. . Ischemic brain will generate income of inflammatory mediators who can participate in ischemic lesions in the brain. When the recitation of an ischemic stroke occurs, areas of the brain that are obscurated by blood vessels will lack oxygen and nutrients so that brain cells, especially neurons, are at risk, these neurons can still function known as penumbra. Tissue hypoxia and cerebral ischemic activate HIF-1α, which then activates the transcription of the Eritropietin (EPO) and Vascular Endothelial Growth Factor (VEGF) genes. Eritropoietin (EPO) is a peptide that also has the effect of non-hematopoiesis which is responsible for encouraging neuroprotection. Eritropietin (EPO) is issued in minutes of an ischemic process and reaches its peak within 24 hours of the onset ischemic stroke. The neuroprotection effect of EPO is as anti-apoptosis, anti-oxidant, anti-inflammatory, anti-excitation, neurogenesis, angiogenesis and neurotropic. In other words, EPO can reduce the severity due to occlusion of brain blood vessels.

scholarly journals Hypoxia Inducible Factor (HIF) 1-Α dan Vascular Endothelial Growth Factor (VEGF) pada Stroke Iskemik Fase Akut

2019 ◽  
Vol 8 (3) ◽  
pp. 226-32
Author(s):  
Lisda Amalia ◽  
Ida Parwati ◽  
Ahmad Rizal ◽  
Ramdan Panigoro ◽  
Uni Gamayani ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Blood Vessels ◽  
Hypoxia Inducible Factor ◽  
Vascular Occlusion ◽  
Ischemic Precondition ◽  
Vascular Endothelial ◽  
Common Causes ◽  
Cerebral Vascular Occlusion ◽  
Endothelial Growth Factor

Stroke iskemik merupakan salah satu penyebab stroke tersering, disebabkan oleh oklusi pembuluh darah serebral dan penyebab kematian ketiga. Saat awitan stroke iskemik terjadi, area otak yang diperdarahi oleh pembuluh darah akan kekurangan oksigen dan nutrisi sehingga sel otak terutama neuron berada dalam risiko, neuron ini masih dapat berfungsi yang dikenal sebagai penumbra. Hipoksik, salah satu karakteristik penumbra merupakan stimulus utama regulasi protein HIF-1α. Hipoksik sendiri merupakan stimulus utama prekondisi iskemik. Prekondisi iskemik akan menghasilkan fenotipe tahan hipoksia yakni protein hypoxia inducible factor (HIF)-1α. HIF-1α merupakan satu-satunya zat yang dikeluarkan oleh jaringan yang mengalami hipoksia. HIF-1α bertindak sebagai protein sinyal yang dapat meregulasi gen protein lain. Efektor HIF-1α antara lain eritropoitin dan vascular endothelial growth factor (VEGF). Pertumbuhan, diferensiasi dan ketahanan sel endotel diregulasi oleh VEGF yang distimulasi dari HIF-1α. Selama iskemik serebral, jaringan yang rusak mencoba untuk meningkatkan pengiriman oksigen melalui induksi angiogenesis melalui produksi VEGF. Hal ini ditandai dengan adanya peningkatan jumlah pembuluh-pembuluh darah mikro di area infark. VEGF dan reseptornya diregulasi oleh HIF-1α dalam hari pertama iskemik.Hypoxia Inducible Factor (HIF) 1-Α and Vascular Endothelial Growth Factor (VEGF) in Acute Ischemic StrokeAbstractIschemic stroke is one of the most common causes of stroke, caused by cerebral vascular occlusion and the third cause of death. When the onset of an ischemic stroke occurs, the area of the brain bleeding by blood vessels will lack oxygen and nutrients so that brain cells, especially neurons, are at risk, these neurons can still function known as penumbra. Hypoxic, one of the characteristics of penumbra is the main stimulus for regulation of HIF-1α protein. Hypoxia itself is the main stimulus of ischemic precondition. The ischemic precondition will produce a hypoxic-resistant phenotype namely protein hypoxia inducible factor (HIF) -1α. HIF-1αis the only substance released by tissue that experiences hypoxia. HIF-1α acts as a signaling protein that can regulate other protein genes. Effectors of HIF-1αinclude erythropoitin and vascular endothelial growth factor (VEGF). Growth, differentiation and endurance of endothelial cells are regulated by VEGF stimulated from HIF-1α. During cerebral ischemia, damaged tissue tries to increase oxygen delivery through induction of angiogenesis through VEGF production. This is characterized by an increase in the number of micro blood vessels in the infarct area. VEGF and its receptors are regulated by HIF-1α in the first day of ischemia.

scholarly journals The Involvement of Angiotensin Type 1 and Type 2 Receptors in Estrogen-Induced Cell Proliferation and Vascular Endothelial Growth Factor Expression in the Rat Anterior Pituitary

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Hanna Lawnicka ◽  
Dorota Ptasinska-Wnuk ◽  
Slawomir Mucha ◽  
Jolanta Kunert-Radek ◽  
Marek Pawlikowski ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Cell Proliferation ◽  
Growth Factor ◽  
Blood Vessels ◽  
Proliferation Index ◽  
Pituitary Cells ◽  
Vascular Endothelial ◽  
Vegf Expression ◽  
Rat Pituitary ◽  
Endothelial Growth Factor

The aim of our study was to examine the involvement of renin-angiotensin system (RAS) in estrogen-induced lactotropes proliferation and vascular endothelial growth factor (VEGF) expression in rat pituitary. The study was performed on Fisher 344 rats underwent 8-day treatment with diethylstilboestrol (DES). The proliferation index (PCNA) and VEGF expression in pituitary sections were estimated using immunohistochemical methods. Treatment with DES increased the number of PCNA-positive cells, VEGF-positive cells, and VEGF-positive blood vessels in pituitary. Stimulatory effect of estrogen on cell proliferation and VEGF expression in blood vessels was attenuated by losartan, PD123319, and captopril. VEGF immunoreactivity in pituitary cells of DES-treated rats was decreased by AT1 antagonist and not changed by AT2 blocker and ACE inhibitor. Our findings suggest the involvement of RAS in DES-induced cell proliferation and VEGF expression in pituitary. Both the AT1 and AT2 receptors appear to mediate the estrogen-dependent mitogenic and proangiogenic effects in rat pituitary.

scholarly journals Vascular Permeability Factor/Vascular Endothelial Growth Factor Induces Lymphangiogenesis as well as Angiogenesis

2002 ◽  
Vol 196 (11) ◽  
pp. 1497-1506 ◽  
Author(s):  
Janice A. Nagy ◽  
Eliza Vasile ◽  
Dian Feng ◽  
Christian Sundberg ◽  
Lawrence F. Brown ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Blood Vessels ◽  
Vascular Permeability ◽  
Malignant Tumors ◽  
Vascular Endothelial ◽  
Vascular Permeability Factor ◽  
Immunodeficient Mice ◽  
Permeability Factor ◽  
Endothelial Growth Factor

Vascular permeability factor/vascular endothelial growth factor (VPF/VEGF, VEGF-A) is a multifunctional cytokine with important roles in pathological angiogenesis. Using an adenoviral vector engineered to express murine VEGF-A164, we previously investigated the steps and mechanisms by which this cytokine induced the formation of new blood vessels in adult immunodeficient mice and demonstrated that the newly formed blood vessels closely resembled those found in VEGF-A–expressing tumors. We now report that, in addition to inducing angiogenesis, VEGF-A164 also induces a strong lymphangiogenic response. This finding was unanticipated because lymphangiogenesis has been thought to be mediated by other members of the VPF/VEGF family, namely, VEGF-C and VEGF-D. The new “giant” lymphatics generated by VEGF-A164 were structurally and functionally abnormal: greatly enlarged with incompetent valves, sluggish flow, and delayed lymph clearance. They closely resembled the large lymphatics found in lymphangiomas/lymphatic malformations, perhaps implicating VEGF-A in the pathogenesis of these lesions. Whereas the angiogenic response was maintained only as long as VEGF-A was expressed, giant lymphatics, once formed, became VEGF-A independent and persisted indefinitely, long after VEGF-A expression ceased. These findings raise the possibility that similar, abnormal lymphatics develop in other pathologies in which VEGF-A is overexpressed, e.g., malignant tumors and chronic inflammation.

Knockdown of Nrf2 inhibits angiogenesis by downregulating VEGF expression through PI3K/Akt signaling pathway in cerebral microvascular endothelial cells under hypoxic conditions

2018 ◽  
Vol 96 (4) ◽  
pp. 475-482 ◽  
Author(s):  
Yujing Huang ◽  
Ying Mao ◽  
Huiying Li ◽  
Guangxun Shen ◽  
Guangxian Nan
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Ischemic Stroke ◽  
Growth Factor ◽  
Signaling Pathway ◽  
Akt Signaling ◽  
Tube Formation ◽  
Vascular Endothelial ◽  
Akt Signaling Pathway ◽  
Microvascular Endothelial ◽  
Endothelial Growth Factor

Ischemic stroke is a major cerebrovascular disease resulting from a transient or permanent local reduction of cerebral blood flow. Angiogenesis plays an important role in cerebral microvascular repair after ischemic stroke. This study aimed at investigating the effect of NF-E2-related factor 2 (Nrf2) on the angiogenesis of mouse cerebral microvascular endothelial bEnd.3 cells in a hypoxic environment. We found that Nrf2 expression was temporarily increased in hypoxia-induced bEnd.3 cells. Knockdown of Nrf2 inhibited the proliferation, migration, as well as tube formation in hypoxia-induced bEnd.3 cells. Meanwhile, vascular endothelial growth factor and PI3K/Akt signaling pathways were identified to be regulated by Nrf2 in hypoxia-induced bEnd.3 cells. It was found that silencing of Nrf2 downregulated the expression levels of NAD(P)H:quinine oxidoreductase-1, vascular endothelial growth factor, p-Akt, and heme oxygenase-1 in hypoxia-induced bEnd.3 cells. Data suggested that hypoxia induced the transient increase of Nrf2, which plays a key role in the angiogenesis of cerebral microangiogenesis, and that Nrf2 regulates the proliferation, migration, as well as tube formation likely through PI3K/Akt signaling pathway in hypoxia-induced bEnd.3 cells. Our study provides proof of concept for the modulation of Nrf2, so as to tilt the balance toward angiogenesis, representing a therapeutic strategy for hypoxia or ischemia disorders such as stroke.

scholarly journals Thrombospondin-1 Is Downregulated by Anoxia and Suppresses Tumorigenicity of Human Glioblastoma Cells

2000 ◽  
Vol 191 (10) ◽  
pp. 1789-1798 ◽  
Author(s):  
Mirna Tenan ◽  
Giulia Fulci ◽  
Michele Albertoni ◽  
Annie-Claire Diserens ◽  
Marie-France Hamou ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Blood Vessels ◽  
Vascular Endothelial ◽  
Glioblastoma Cell ◽  
Glioblastoma Cells ◽  
Thrombospondin 1 ◽  
Natural Inhibitor ◽  
Endothelial Growth Factor

Angiogenesis, the sprouting of new capillaries from preexisting blood vessels, results from a disruption of the balance between stimulatory and inhibitory factors. Here, we show that anoxia reduces expression of thrombospondin-1 (TSP-1), a natural inhibitor of angiogenesis, in glioblastoma cells. This suggests that reduced oxygen tension can promote angiogenesis not only by stimulating the production of inducers, such as vascular endothelial growth factor, but also by reducing the production of inhibitors. This downregulation may significantly contribute to glioblastoma development, since we show that an increase in TSP-1 expression is sufficient to strongly suppress glioblastoma cell tumorigenicity in vivo.

Effects of vascular endothelial growth factor in ischemic stroke

2012 ◽  
Vol 90 (10) ◽  
pp. 1873-1882 ◽  
Author(s):  
Yihui Ma ◽  
Anil Zechariah ◽  
Yan Qu ◽  
Dirk M. Hermann
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Ischemic Stroke ◽  
Growth Factor ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor
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