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Receptor-Mediated Endocytosis of VEGF-A in Rat Liver Sinusoidal Endothelial Cells
المؤلفون المشاركون
Mousavi, Seyed Ali
Skjeldal, Frode
Fønhus, Marita Sporstøl
Haugen, Linda Hofstad
Eskild, Winnie
Berg, Trond
Bakke, Oddmund
المصدر
العدد
المجلد 2019، العدد 2019 (31 ديسمبر/كانون الأول 2019)، ص ص. 1-12، 12ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2019-09-10
دولة النشر
مصر
عدد الصفحات
12
التخصصات الرئيسية
الملخص EN
Background and Aims.
Vascular endothelial growth factor (VEGF) receptors (VEGFR1 and VEGFR2) bind VEGF-A with high affinity.
This study sought to determine the relative contributions of these two receptors to receptor-mediated endocytosis of VEGF-A and to clarify their endocytic itineraries in rat liver sinusoidal endothelial cells (LSECs).
Methods.
Isolated LSECs and radiolabeled VEGF-A were used to examine surface binding and receptor-mediated endocytosis.
Quantitative real time RT-PCR (Q-RT-PCR) and Western blotting were applied to demonstrate receptor expression.
Results.
Q-RT-PCR analysis showed that VEGFR1 and VEGFR2 mRNA were expressed in LSECs.
Ligand saturation analysis at 4°C indicated two different classes of [125I]-VEGFA binding sites on LSECs with apparent dissociation constants of 8 and 210 pM.
At 37°C, LSECs efficiently took up and degraded [125I]-VEGF-A for at least 2 hours.
Uptake of [125I]-VEGF-A by LSECs was blocked by dynasore that inhibits dynamin-dependent internalization, whereas inhibition of cysteine proteases by leupeptin inhibited degradation without affecting the uptake of [125I]-VEGF-A, suggesting that it is degraded following transport to lysosomes.
Incubation of LSECs in the continued presence of a saturating concentration of unlabeled VEGF-A at 37°C was associated with a loss of as much as 75% of the total VEGFR2 within 30 min as shown by Western blot analysis, whereas there was no appreciable decrease in protein levels for VEGFR1 after 120 min incubation, suggesting that VEGF-A stimulation downregulates VEGFR2, but not VEGFR1, in LSECs.
This possibility was supported by the observation that a hexapeptide that specifically blocks VEGF-A binding to VEGFR1 caused a marked reduction in the uptake of [125I]-VEGF-A, whereas a control peptide had no effect.
Finally, live cell imaging studies using a fluorescently labeled anti-VEGFR2 antibody showed that VEGFR2 was transported via early and late endosomes to reach endolysosomes where degradation of the VEGFR2 takes place.
Conclusion.
Our studies suggest that, subsequent to VEGF-A binding and internalization, the unoccupied VEGFR1 may recycle to the cell surface allowing its reutilization, whereas the majority of the internalized VEGFR2 is targeted for degradation.
نمط استشهاد جمعية علماء النفس الأمريكية (APA)
Mousavi, Seyed Ali& Skjeldal, Frode& Fønhus, Marita Sporstøl& Haugen, Linda Hofstad& Eskild, Winnie& Berg, Trond…[et al.]. 2019. Receptor-Mediated Endocytosis of VEGF-A in Rat Liver Sinusoidal Endothelial Cells. BioMed Research International،Vol. 2019, no. 2019, pp.1-12.
https://search.emarefa.net/detail/BIM-1126089
نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)
Mousavi, Seyed Ali…[et al.]. Receptor-Mediated Endocytosis of VEGF-A in Rat Liver Sinusoidal Endothelial Cells. BioMed Research International No. 2019 (2019), pp.1-12.
https://search.emarefa.net/detail/BIM-1126089
نمط استشهاد الجمعية الطبية الأمريكية (AMA)
Mousavi, Seyed Ali& Skjeldal, Frode& Fønhus, Marita Sporstøl& Haugen, Linda Hofstad& Eskild, Winnie& Berg, Trond…[et al.]. Receptor-Mediated Endocytosis of VEGF-A in Rat Liver Sinusoidal Endothelial Cells. BioMed Research International. 2019. Vol. 2019, no. 2019, pp.1-12.
https://search.emarefa.net/detail/BIM-1126089
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-1126089
قاعدة معامل التأثير والاستشهادات المرجعية العربي "ارسيف Arcif"
أضخم قاعدة بيانات عربية للاستشهادات المرجعية للمجلات العلمية المحكمة الصادرة في العالم العربي
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