1,478 research outputs found
The Expression of Prolactin and its Cathepsin D-mediated Cleavage in the bovine Corpus luteum vary with the Oestrous cycle
No full textCopyright © 2007 by the American Physiological Society.In the corpus luteum (CL), blood vessels develop, stabilize, and regress. This depends on the ratio of pro- and anti-angiogenic factors, which change during the ovarian cycle. The present study focuses on the possible roles of 23-K prolactin (PRL) in the bovine CL and its anti-angiogenic N-terminal fragments after extracellular cleavage by cathepsin D (Cath D). Prolactin RNA and protein were demonstrated in the CL tissue, in luteal endothelial cells and steroidogenic cells. Cath D was detected in CL tissue, cell extracts and corresponding cell supernatants. In the intact CL, 23-K PRL levels decreased gradually, whereas Cath D levels concomitantly increased between early to late luteal stages. In vitro, PRL cleavage occurred in the presence of acidified homogenates of CL tissue, cells and corresponding cell supernatants. Similar fragments were obtained with purified Cath D, and their appearance was inhibited by pepstatin A. The aspartic protease specific substrate MOCAc-GKPILF~FRLK(Dnp)-D-R-NH2 was cleaved by CL cell supernatants, providing further evidence for Cath D activity. 16-K PRL inhibited proliferation of luteal endothelial cells accompanied by an increase in cleaved caspase-3. In conclusion: (1) The bovine CL is able to produce PRL and to process it into anti-angiogenic fragments by Cath D activity. (2) PRL cleavage might mediate angioregression during luteolysis.Sabine Erdmann, Albert Markus Ricken, Claudia Merkwitz, Ingrid Struman, Castino Roberta, Katja Hummitzsch, Frank Gaunitz, Ciro Isidoro, Joseph Martial and Katharina Spanel-Borowsk
Ingrid Ylva och tornet i Bjälbo
No full textThe article discusses the background to the erection of the huge church tower in Bjälbo, Östergötland, Sweden. It also focuses on medieval women as founders of churches. The author maintains that new dendrochronological dating of the tower could mean that founder of this building piece was not one of the male members of the important Bjälbo dynasty, but Ingrid Ylva the mother of Birger Jarl
Antiangiogenic peptides
No full textpublication date: 2008-02-14; filing date: 2005-08-11The present invention refers to a pharmaceutical composition comprising an isolated antiangiogenic peptide or a recombinant protein comprising the antiangiogenic peptide, wherein the peptide is between 11 and 40 amino acids in length and having antiangiogenic activity, the peptide comprising the amino acid sequence: X1-X2-X3-X4-X5-X6-X7-X8-X9-X10-X11-X12-X13-X14, wherein X1 is any amino acid residue comptabile with forming a helix; X2 is an amino acid redisue of : Leu, Ile, Val; X3 is an amino acid residue of: Arg, Lys, His, Ser, Thr; X4 is an amino acid residue of: Ile, Leu, Val; X5 is any amino acid residue compatible with forming a helix; X6 is an amino acid residue of: Leu, Ile, Val; X7 is an amino acid residue of: Leu, Ile, Val, Ser, Thr; X8 is any amino acid residue compatible with forming a helix; X9 is any amino acid residue compatible with forming a helix; X10 is an amino acid residue of: Gln, Glu, Asp, Arg, His, Lys, Asn; X11 is an amino acid residue of: Ser, Thr; X12 is an amino acid residue of: Trp, Tyr, Phe; X13 is an animo acid residue of Leu, Ile, Val, Asn, Gln; X14 is an amino acid residue of: Glu, Gln, Asp, Asn
Ingrid Winterbach: Novelist (Interview)
No full textWinner of the prestigious Hertzog Prize for Literature for Niggie (2002)Ingrid Winterbach is the author of eight novels, three of which have been translated into English and two into Dutch. The translation of her fourth novel, Karolina Ferreira (1993) as The Elusive Moth (2005), and subsequently, Niggie as To Hell with Cronjé (2007) and Die boek van toeval en toeverlaat (2006) as The Book of Happenstance (2008), have brought this author to the attention of a wider South African readership
Etude de l'effet antiangiogène de la prolactine 16K sur la progression tumorale et métastatique et identification de nouveaux peptides antiangiogènes
No full textAngiogenesis, the formation of new blood vessels from pre-existing ones, is a crucial step in many pathologies, including tumor growth and metastasis. We developed an adenovirus vector allowing the 16K hPRL expression, an antiangiogenic factor, in situ. We show 16K hPRL inhibits oxygen-induced retinopathy in mice.Then, using the 16K-Ad vector, we investigated the ability of 16K hPRL to prevent metastatic spread through inhibition of angiogenesis. We show that 16K hPRL administered via adenovirus-mediated gene transfer inhibits tumor growth in a subcutaneous B16-F10 mouse melanoma model by reducing the size and width of tumor vessels. We also show, for the first time, that 16K hPRL considerably reduces the establishment of B16-F10 metastases in an experimental lung metastasis model. These results highlight a potential role for 16K hPRL in anticancer therapy for both primary tumors and metastases.In parallel, we have sought to identify in human 16K PRL (16K hPRL) a peptide that might be responsible for its antiangiogenic activity. Although the 16K fragments of the other three human PRL/GH-family members are also potently antiangiogenic, the sequence similarity of these fragments is low (around 35% similarity between all mammalian PRL/GH sequences). This led us to seek a peculiar common structural feature rather than a similar sequence. We demonstrate that all these fragments possess a 14-amino-acid sequence having the characteristics of a tilted peptide. We show for the first time that tilted peptides exert antiangiogenic activity. The tilted peptides of hPRL and hGH induce endothelial cell apoptosis, inhibit endothelial cell proliferation, and inhibit capillary formation both in vitro and in vivo. These antiangiogenic effects are abolished when the peptides’ hydrophobicity gradient is altered by mutation. We further demonstrate for the first time that the well-known tilted peptides of SIV gp32 and Alzheimer’s beta-amyloid peptide are also angiogenesis inhibitors. Taken together these results point to a potential new role for tilted peptides in regulating angiogenesis. L’angiogenèse, la formation de nouveaux vaisseaux à partir de vaisseaux préexistants, joue un rôle important dans de nombreuses pathologies incluant la croissance tumorale et la dissémination des métastases.Nous avons développé un vecteur adénoviral (16K-Ad) nous permettant de produire le facteur antiangiogène hPRL 16K directement in situ. Une première analyse permettant d’étudier les effets de la hPRL 16K produite par l’approche adénovirale a été réalisée in vivo. Nous montrons tout d’abord que la hPRL 16K produite est capable de prévenir la néovascularisation rétinienne dans un modèle murin de rétinopathie. Par la suite, en utilisant le vecteur 16K-Ad, nous montrons que la hPRL 16K peut inhiber le développement tumoral dans un modèle murin développant des tumeurs formées par les cellules de mélanome B16-F10 dans le tissu sous-cutané. Cette inhibition de la croissance tumorale est corrélée avec une diminution de la taille des vaisseaux. Nous montrons aussi, pour la première fois, que la hPRL 16K peut considérablement réduire l’établissement des métastases B16-F10 dans un modèle expérimental de métastases se développant dans le poumon. Ces résultats soulignent le rôle potentiel de la hPRL 16K dans la thérapie anticancéreuse dirigée contre les tumeurs primaires et les métastases.Parallèlement à ces travaux, nous nous sommes attachés à identifier une région responsable de l’activité de la hPRL 16K. Partant du fait que les fragments 16K des trois autres membres de la famille humaine PRL/GH sont aussi de puissants facteurs antiangiogènes, malgré que leur similarité de séquence soit faible (environ 35% de similarité entre les séquences de la PRL et de la GH), nous avons recherché une caractéristique structurale commune partagée par ces différents fragments. Nous avons identifié un domaine susceptible d'adopter une structure en peptide oblique dans les séquences protéiques des fragments de 16 kDa de la famille PRL/GH. L’effet antiangiogène des peptides obliques de la hPRL 16K et de la hGH 16K est montré dans des expériences menées in vitro et in vivo. Nous montrons également l’effet antiangiogène des peptides obliques du peptide de fusion gp 32 du virus SIV et du peptide b-amyloïde
7. When They Left
No full textFigure 7.1 The author, Ingrid Griffith (right) with her sister Dawn (left) and brother Oliver (center) in December 1968. Their maternal grandmother had taken them to Skevelair’s Photo Studio in Georgetown, Guyana to pose in the church outfits their parents, who had recently migrated to the United States, had sent for Christmas. © Griffith Family Collection. Courtesy of Ingrid Griffith. CC BY 4.0. It was one of the worst days of my life. I was seven years old, my sist..
270 - Ingrid Jane Slette
No full textGlobal climate change is causing more extreme droughts, as well as subtler chronic changes in precipitation patterns. Both chronic and extreme precipitation change can alter ecosystem structure and function, and these alterations may affect how systems respond to future extreme climatic events. Understanding how legacies of various past precipitation changes may alter the effects of future extreme droughts will be important for predicting ecosystem responses to climate change. We investigated how ecological legacies of experimentally-imposed chronic and extreme precipitation changes altered the impact of an extreme drought on an economically-important grassland ecosystem.Top Scholars for University-Wide Graduate Programs
Funktionelle Analyse von potententiell aktivierenden FGFR3 Mutationen
No full textAuthor Ingrid Hartl, MScAbweichender Titel laut Übersetzung der Verfasserin/des VerfassersDissertation Johannes Kepler Universität Linz 2022Arbeit nach Ablauf der Sperre auf den öffentlichen PCs in den Bibliotheken der JKU+Medizin abrufba
Resensies: Vlam in die sneeu. Die liefdesbriewe van André P. Brink en Ingrid Jonker
No full textBook Title: Vlam in die sneeu. Die liefdesbriewe van André P. Brink en Ingrid JonkerBook Author: Francis Galloway (red.)Kaapstad: Umuzi, 2015. 450 pp. ISBN: 978-1-4152-0881-6. Spesiale uitgawe ISBN: 978-1-4152-0893-9
Evidence for a role of microRNA-21 and microRNA-125b in negatively regulating angiogenic processes
No full textRecently discovered, miRNAs have quickly become strong regulators of biological processes. These small non-coding RNAs of about 22 nucleotides partially base pair to the 3’UTR of the targeted mRNAs and repress them. Due to their wide range effects, microRNAs were extensively studied in various diseases and were rapidly demonstrated to be deregulated
in pathologies such as cancer. More recently, they have been shown to be implicated in
vascular network formation (angiogenesis) and were proposed to be used in anti-angiogenic
therapies. Nowadays about twenty angiomiRs have been discovered including the endothelial
specific miR-126. As observed in several miRNA profiling of endothelial cells and confirmed
in our laboratory in HUVECs (human umbilical veins endothelial cells), miR-21 and miR-
125b are highly expressed in this cell type suggesting that these miRNAs could play a role in
vascular network formation. We then studied the implication of miR-21 and miR-125b in in
vitro as well as in vivo angiogenesis.
One of the most studied miRNA in cancer progression is miR-21 as it was shown to modify proliferating properties of numerous tumor cells. Our experiments revealed that miR-21 overexpression and inhibition have no direct effect on endothelial cells proliferation rate.
However, miR-21 overexpression leads to the inhibition of HUVECs migration and tube formation as demonstrated in in vitro angiogenic assays. Moreover, opposite effects were
observed upon miR-21 inhibition. We also confirmed that RhoB, a small Rho-GTPase implicated in stress fibers formation, is involved in these phenomena as RhoB inhibition using siRNA mimics miR-21 overexpression in endothelial cells. Moreover, miR-21 modulation affects RhoB mRNA and protein expressions. We further demonstrated a direct interaction between miR-21 and the RhoB 3’UTR confirming that miR-21 modulates angiogenesis partially through its effect on RhoB expression.
A similar approach was used to study the implication of miR-125b in vascular network formation. In vivo, miR-125b expression was modulated in the zebrafish revealing that miR-125b expression needs to be controlled for proper intersomitic blood vessels establishment. In
vitro, miR-125b overexpression decreases HUVECs migration and tube formation whereas
miR-125b inhibition increases these functions. A transcriptomic analysis suggests that numerous adhesion molecules such as VE-cadherin or MCAM are involved in these processes.
Furthermore, other proteins known to regulate angiogenesis such as the transcription factor
ETS1 and the VEGFA receptor, VEGFR2 were also shown to be regulated by miR-125b. This
observation confirms that miR-125b modulates angiogenic properties of endothelial cells.
Finally, we investigated the impact of miR-21 and miR-125b overexpression in an in vivo pathological model of angiogenesis. In a mouse model of choroïdal neovascularization we
demonstrated that miR-21 or miR-125b overexpression in the eyes of these mice decreases
blood vessel establishment suggesting that these microRNAs could be used as therapeutic antiangiogenic agents.
Taken together, the results presented in this thesis show that miR-21 and miR-125b regulate angiogenesis in vitro and in vivo
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