03026nas a2200121   4500008004100000245006000041210005800101260001200159300001000171490000700181520265600188856006002844       2013                        eng d00aDie lymphangiogenen Wachstumsfaktoren VEGF-C und VEGF-D0 aDie lymphangiogenen Wachstumsfaktoren VEGFC und VEGFD  c06/2013  a30-370 v173 aVEGF-C und VEGF-D sind die zwei zentralen Signalmoleküle, die für die Entwicklung und das Wachstum des Lymphgefäßsystems verantwortlich sind. Beide gehören zur VEGF-Proteinfamilie, deren Mitglieder hauptsächlich im Wachstum von Blutgefässen (Angiogenese) und Lymphgefässen (Lymphangiogenese) ihre Funktionen haben. Die VEGF-Familie umfasst in Säugetieren fünf Mitglieder: VEGF, PlGF, VEGF-B, VEGF-C und VEGF-D. Benannt wurde diese Familie nach ihrem zuerst entdeckten Mitglied VEGF („Vascular Endothelial Growth Factor”). VEGF-C und VEGF-D bilden funktionell und strukturell eine Untergruppe innerhalb der VEGF-Familie. Sie unterscheiden sich von den anderen VEGFs durch ihre besondere Biosynthese: sie werden als inaktive Vorgängermoleküle produziert, für deren Aktivierung ihre langen N- und C-terminalen Propeptide enzymatisch abgespalten werden müssen. Im Gegensatz zu den anderen VEGFs sind VEGF-C und VEGF-D direkte Stimulatoren für das Wachstum lymphatischer Gefäße. Ihre lymphangiogene Wirkung enfalten VEGF-C und VEGF-D über den VEGF-Rezeptor-3 (VEGFR-3), der im erwachsenen Organismus fast nur auf den Endothelzellen der Lymphvaskulatur zu finden ist.
In diesem Artikel geben wir einen Überblick über die VEGF-Proteinfamilie und deren Rezeptoren mit dem Schwerpunkt auf den lymphangiogenen Mitgliedern VEGF-C und VEGF-D, über ihre Biosynthese und ihre Rolle in der Embryonalentwicklung.

VEGF-C and VEGF-D are the two central signaling molecules that stimulate the development and the growth of lymphatic system. Both belong to the VEGF protein family which plays important roles in the growth of blood vessels (angiogenesis) and lymphatic vessels (lymphangiogenesis).
In mammals the VEGF family comprises five members: VEGF, PlGF, VEGF-B, VEGF-C and VEGF-D. The family was named after its first discovered member VEGF (“Vascular Endothelial Growth Factor”). VEGF-C and VEGF-D form functionally and structurally a subgroup within this family. They differ from the other VEGFs by their peculiar biosynthesis: they are produced as inactive precursors and need to be activated by proteolytic removal of their long N- and C-terminal propeptides. Unlike the other VEGFs, VEGF-C and VEGF-D are direct stimulators of lymphatic growth. They exert their lymphangiogenic function via VEGF receptor 3, which is expressed in the adult organism almost exclusively on lymphatic endothelial cells.
In this review we give an overview of the VEGF protein family and their receptors with the emphasis on the lymphangiogenic VEGF-C and VEGF-D, and we discuss their biosynthesis and their role in embryonic lymphangiogenesis.
  uhttps://www.jeltsch.org/Krebs%26Jeltsch2013?language=hu01999nas a2200217   4500008004100000245016300041210006900204260001200273300001300285490000700298520124700305653001901552653002201571653001501593653002701608653001101635653001101646100001801657700002101675856008501696       2013                        eng d00aDie lymphangiogenic growth factors VEGF-C and VEGF-D. Part 2: The role of VEGF-C and VEGF-D in diseases of the lymphatic system. [bilingual: English, German].0 aDie lymphangiogenic growth factors VEGFC and VEGFD Part 2 The ro  c11/2013  a96 - 1040 v173 aVEGF-C and VEGF-D are the two central signaling molecules that stimulate the develop- ment and growth of the lymphatic system. Both belong to the vascular endothelial growth factor (VEGF) protein family, which plays important roles in the growth of blood vessels (angiogenesis) and lymphatic vessels (lymphangiogenesis). In mammals, the VEGF family comprises five members: VEGF-A, PlGF, VEGF-B, VEGF-C and VEGF-D. The family was named after VEGF-A, the first member to be discovered. VEGF-C and VEGF-D form a subgroup within this family in terms of function and structure. Their distinctive biosynthesis differentiates them from the other VEGFs: they are produced as inactive precursors and need to be activated by proteolytic removal of their long N- and C-terminal propeptides. Unlike the other VEGFs, VEGF-C and VEGF-D are direct stimulators of lymphatic vessel growth. They exert their lymphangiogenic function via VEGF receptor 3, which is expressed in the adult organism almost exclusively on lymphatic endothelial cells. In this review, we provide an overview of the VEGF protein family and their receptors. We focus on the lymphangiogenic VEGF-C and VEGF-D, discussing their biosynthesis and their role in embryonic lymphangiogenesis.10agrowth factors10aLymphangiogenesis10alymphedema10alymphogenic metastasis10aVEGF-C10aVEGF-D1 aKrebs, Rainer1 aJeltsch, Michael  uhttp://jeltsch.org/sites/jeltsch.org/files/JeltschMichael_Lymphforsch2013_96.pdf01909nas a2200193   4500008004100000245014000041210006900181260001200250300001200262490000700274520124700281653001901528653002201547653001101569653001101580100001801591700002101609856008501630       2013                        eng d00aThe lymphangiogenic growth factors VEGF-C and VEGF-D. Part 1: Basic principles and embryonic development. [bilingual: English, German].0 alymphangiogenic growth factors VEGFC and VEGFD Part 1 Basic prin  c05/2013  a30 - 370 v173 aVEGF-C and VEGF-D are the two central signaling molecules that stimulate the develop- ment and growth of the lymphatic system. Both belong to the vascular endothelial growth factor (VEGF) protein family, which plays important roles in the growth of blood vessels (angiogenesis) and lymphatic vessels (lymphangiogenesis). In mammals, the VEGF family comprises five members: VEGF-A, PlGF, VEGF-B, VEGF-C and VEGF-D. The family was named after VEGF-A, the first member to be discovered. VEGF-C and VEGF-D form a subgroup within this family in terms of function and structure. Their distinctive biosynthesis differentiates them from the other VEGFs: they are produced as inactive precursors and need to be activated by proteolytic removal of their long N- and C-terminal propeptides. Unlike the other VEGFs, VEGF-C and VEGF-D are direct stimulators of lymphatic vessel growth. They exert their lymphangiogenic function via VEGF receptor 3, which is expressed in the adult organism almost exclusively on lymphatic endothelial cells. In this review, we provide an overview of the VEGF protein family and their receptors. We focus on the lymphangiogenic VEGF-C and VEGF-D, discussing their biosynthesis and their role in embryonic lymphangiogenesis.10agrowth factors10aLymphangiogenesis10aVEGF-C10aVEGF-D1 aKrebs, Rainer1 aJeltsch, Michael  uhttp://jeltsch.org/sites/jeltsch.org/files/JeltschMichael_Lymphforsch2013_30.pdf02099nas a2200133   4500008004100000022001400041245013000055210006900185260001300254300001200267490000800279520162800287856005001915       2012                        eng d  a1525-219100aCritical role of VEGF-C/VEGFR-3 signaling in innate and adaptive immune responses in experimental obliterative bronchiolitis.0 aCritical role of VEGFCVEGFR3 signaling in innate and adaptive im  c2012 Nov  a1607-200 v1813 a<p>Chronic inflammation, a hallmark of obliterative bronchiolitis, is known to induce lymphangiogenesis. We therefore studied the role of lymphangiogenic vascular endothelial growth factor C (VEGF-C), its receptor VEGFR-3, and lymphangiogenesis during development of experimental obliterative bronchiolitis [ie, obliterative airway disease (OAD)] in rat tracheal allografts. The functional importance of VEGF-C was investigated by adenovirus-mediated overexpression of VEGF-C (AdVEGF-C), and by inhibition of VEGF-C activity with VEGFR-3-Ig (AdVEGFR-3-Ig). Analyses included histology, immunohistochemistry, and real-time RT-PCR 10 and 30 days after transplantation. In the course of OAD development, lymphangiogenesis was induced in the airway wall during the alloimmune response, which was reversed by cyclosporine A in a dose-dependent fashion. VEGF-C overexpression in tracheal allografts induced epithelial activation, neutrophil chemotaxis, and a shift toward a Th17 adaptive immune response, followed by enhanced lymphangiogenesis and the development of OAD. In contrast, inhibition of VEGF-C activity with VEGFR-3-Ig inhibited lymphangiogenesis and angiogenesis and reduced infiltration of CD4(+) T cells and the development of OAD. Lymphangiogenesis was linked to T-cell responses during the development of OAD, and VEGF-C/VEGFR-3 signaling modulated innate and adaptive immune responses in the development of OAD in rat tracheal allografts. Our results thus suggest VEGFR-3-signaling as a novel strategy to regulate T-cell responses in the development of obliterative bronchiolitis after lung transplantation.</p>  uhttps://www.jeltsch.org/Krebs2012?language=hu