Wilting, Jörg

[["dc.bibliographiccitation.artnumber","157"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Cell & Bioscience"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Wilting, Jörg"],["dc.contributor.author","Becker, Jürgen"],["dc.date.accessioned","2022-09-19T07:17:59Z"],["dc.date.available","2022-09-19T07:17:59Z"],["dc.date.issued","2022-09-15"],["dc.date.updated","2022-09-18T03:12:12Z"],["dc.description.abstract","Abstract\r\n Almost 400 years after the (re)discovery of the lymphatic vascular system (LVS) by Gaspare Aselli (Asellius G. De lactibus, sive lacteis venis, quarto vasorum mesaraicorum genere, novo invento Gasparis Asellii Cremo. Dissertatio. (MDCXXIIX), Milan; 1628.), structure, function, development and evolution of this so-called ‘second’ vascular system are still enigmatic. Interest in the LVS was low because it was (and is) hardly visible, and its diseases are not as life-threatening as those of the blood vascular system. It is not uncommon for patients with lymphedema to be told that yes, they can live with it. Usually, the functions of the LVS are discussed in terms of fluid homeostasis, uptake of chylomicrons from the gut, and immune cell circulation. However, the broad molecular equipment of lymphatic endothelial cells suggests that they possess many more functions, which are also reflected in the pathophysiology of the system. With some specific exceptions, lymphatics develop in all organs. Although basic structure and function are the same regardless their position in the body wall or the internal organs, there are important site-specific characteristics. We discuss common structure and function of lymphatics; and point to important functions for hyaluronan turn-over, salt balance, coagulation, extracellular matrix production, adipose tissue development and potential appetite regulation, and the influence of hypoxia on the regulation of these functions. Differences with respect to the embryonic origin and molecular equipment between somatic and splanchnic lymphatics are discussed with a side-view on the phylogeny of the LVS. The functions of the lymphatic vasculature are much broader than generally thought, and lymphatic research will have many interesting and surprising aspects to offer in the future."],["dc.identifier.citation","Cell & Bioscience. 2022 Sep 15;12(1):157"],["dc.identifier.doi","10.1186/s13578-022-00898-0"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/114251"],["dc.language.iso","en"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","CC BY 4.0"],["dc.rights.holder","The Author(s)"],["dc.subject","Initial lymphatics"],["dc.subject","Lymphatic collector"],["dc.subject","Lymphangiogenesis"],["dc.subject","Circulating endothelial precursor cells"],["dc.subject","Pacemaker cell"],["dc.subject","Smooth muscle cell origin"],["dc.subject","Sphingosine-1-phosphate"],["dc.subject","Melanocortin-2 receptor accessory protein-2"],["dc.title","The lymphatic vascular system: much more than just a sewer"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","084653712110038"],["dc.bibliographiccitation.journal","Canadian Association of Radiologists Journal"],["dc.contributor.author","Qazi, Emmad"],["dc.contributor.author","Wilting, Joerg"],["dc.contributor.author","Patel, Neeral R."],["dc.contributor.author","Alenezi, Abdullah O."],["dc.contributor.author","Kennedy, Sean A."],["dc.contributor.author","Tan, Kong T."],["dc.contributor.author","Jaberi, Arash"],["dc.contributor.author","Mafeld, Sebastian"],["dc.date.accessioned","2021-06-01T10:47:54Z"],["dc.date.available","2021-06-01T10:47:54Z"],["dc.date.issued","2021"],["dc.description.abstract","Objectives: The purpose of this article is to review the embryology of the lower limb arterial anatomy along with common variants and their clinical relevance. Design: Embryologic variations of the lower limb arterial system may be explained by i.) persistence of primordial arterial segments, ii.) abnormal fusion, iii.) segmental hypoplasia/absence, or a combination of both. Persistent sciatic artery, corona mortis, and popliteal entrapment syndrome will also be discussed with associated symptoms, and potential complications. Conclusion: Knowledge of these variations is essential for surgical and endovascular management as failure to recognize them can result in complications."],["dc.identifier.doi","10.1177/08465371211003860"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/85761"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation.eissn","1488-2361"],["dc.relation.issn","0846-5371"],["dc.title","Arteries of the Lower Limb—Embryology, Variations, and Clinical Significance"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","278"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","The Anatomical Record"],["dc.bibliographiccitation.lastpage","287"],["dc.bibliographiccitation.volume","302"],["dc.contributor.author","Fukuoka, Kenichiro"],["dc.contributor.author","Wilting, Joerg"],["dc.contributor.author","Rodríguez‐Vázquez, Jose Francisco"],["dc.contributor.author","Murakami, Gen"],["dc.contributor.author","Ishizawa, Akimitsu"],["dc.contributor.author","Matsubara, Akio"],["dc.date.accessioned","2020-12-10T14:05:41Z"],["dc.date.available","2020-12-10T14:05:41Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1002/ar.v302.2"],["dc.identifier.eissn","1932-8494"],["dc.identifier.issn","1932-8486"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/69618"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","The Embryonic Ascent of the Kidney Revisited"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.journal","Journal of Cellular and Molecular Medicine"],["dc.bibliographiccitation.lastpage","9"],["dc.contributor.author","Malik, Gesa"],["dc.contributor.author","Wilting, Jörg"],["dc.contributor.author","Hess, Clemens Friedrich"],["dc.contributor.author","Ramadori, Giuliano"],["dc.contributor.author","Malik, Ihtzaz Ahmed"],["dc.date.accessioned","2019-07-09T11:50:04Z"],["dc.date.available","2019-07-09T11:50:04Z"],["dc.date.issued","2019"],["dc.description.abstract","The mechanisms of radiation-induced liver damage are poorly understood. We investigated if tumour necrosis factor (TNF)-α acts synergistically with irradiation, and how its activity is influenced by platelet endothelial cell adhesion molecule-1 (PECAM-1). We studied murine models of selective single-dose (25 Gy) liver irradiation with and without TNF-α application (2 μg/mouse; i.p.). In serum of wild-type (wt)-mice, irradiation induced a mild increase in hepatic damage marker aspartate aminotransferase (AST) in comparison to sham-irradiated controls. AST levels further increased in mice treated with both irradiation and TNF-α. Accordingly, elevated numbers of leucocytes and increased expression of the macrophage marker CD68 were observed in the liver of these mice. In parallel to hepatic damage, a consecutive decrease in expression of hepatic PECAM-1 was found in mice that received radiation or TNF-α treatment alone. The combination of radiation and TNF-α induced an additional significant decline of PECAM-1. Furthermore, increased expression of hepatic lipocalin-2 (LCN-2), a hepatoprotective protein, was detected at mRNA and protein levels after irradiation or TNF-α treatment alone and the combination of both. Signal transducer and activator of transcription-3 (STAT-3) seems to be involved in the signalling cascade. To study the involvement of PECAM-1 in hepatic damage more deeply, the liver of both wt- and PECAM-1-knock-out-mice were selectively irradiated (25 Gy). Thereby, ko-mice showed higher liver damage as revealed by elevated AST levels, but also increased hepatoprotective LCN-2 expression. Our studies show that TNF-α has a pivotal role in radiation-induced hepatic damage. It acts in concert with irradiation and its activity is modulated by PECAM-1, which mediates pro- and anti-inflammatory signalling."],["dc.identifier.doi","10.1111/jcmm.14224"],["dc.identifier.pmid","30761739"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15851"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59695"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1582-4934"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","PECAM-1 modulates liver damage induced by synergistic effects of TNF-α and irradiation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.issue","105"],["dc.bibliographiccitation.journal","BMC cancer"],["dc.bibliographiccitation.lastpage","17"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Norgall, Susanne"],["dc.contributor.author","Papoutsi, Maria"],["dc.contributor.author","Rössler, Jochen"],["dc.contributor.author","Schweigerer, Lothar"],["dc.contributor.author","Wilting, Jörg"],["dc.contributor.author","Weich, Herbert A."],["dc.date.accessioned","2019-07-10T08:13:00Z"],["dc.date.available","2019-07-10T08:13:00Z"],["dc.date.issued","2007"],["dc.description.abstract","Background: Lymphangiomas are neoplasias of childhood. Their etiology is unknown and a causal therapy does not exist. The recent discovery of highly specific markers for lymphatic endothelial cells (LECs) has permitted their isolation and characterization, but expression levels and stability of molecular markers on LECs from healthy and lymphangioma tissues have not been studied yet. We addressed this problem by profiling LECs from normal dermis and two children suffering from lymphangioma, and also compared them with blood endothelial cells (BECs) from umbilical vein, aorta and myometrial microvessels. Methods: Lymphangioma tissue samples were obtained from two young patients suffering from lymphangioma in the axillary and upper arm region. Initially isolated with anti-CD31 (PECAM-1) antibodies, the cells were separated by FACS sorting and magnetic beads using anti-podoplanin and/or LYVE-1 antibodies. Characterization was performed by FACS analysis, immunofluorescence staining, ELISA and micro-array gene analysis. Results: LECs from foreskin and lymphangioma had an almost identical pattern of lymphendothelial markers such as podoplanin, Prox1, reelin, cMaf and integrin-a1 and -a9. However, LYVE-1 was down-regulated and VEGFR-2 and R-3 were up-regulated in lymphangiomas. Prox1 was constantly expressed in LECs but not in any of the BECs. Conclusion: LECs from different sources express slightly variable molecular markers, but can always be distinguished from BECs by their Prox1 expression. High levels of VEGFR-3 and -2 seem to contribute to the etiology of lymphangiomas."],["dc.identifier.fs","171198"],["dc.identifier.ppn","560267541"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/4366"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/61096"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","610"],["dc.title","Elevated expression of VEGFR-3 in lymphatic endothelial cells from lymphangiomas"],["dc.title.alternative","Research article"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","5519"],["dc.bibliographiccitation.issue","36"],["dc.bibliographiccitation.journal","Current Medicinal Chemistry"],["dc.bibliographiccitation.lastpage","5527"],["dc.bibliographiccitation.volume","18"],["dc.contributor.author","Wilting, J."],["dc.contributor.author","Hagedorn, M."],["dc.date.accessioned","2021-06-01T10:48:34Z"],["dc.date.available","2021-06-01T10:48:34Z"],["dc.date.issued","2011"],["dc.identifier.doi","10.2174/092986711798347252"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/85980"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation.issn","0929-8673"],["dc.title","Left-Right Asymmetry in Embryonic Development and Breast Cancer: Common Molecular Determinants?"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","583"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Clinical Anatomy"],["dc.bibliographiccitation.lastpage","592"],["dc.bibliographiccitation.volume","31"],["dc.contributor.author","Cho, Baik Hwan"],["dc.contributor.author","Kim, Ji Hyun"],["dc.contributor.author","Jin, Zhe Wu"],["dc.contributor.author","Wilting, Joerg"],["dc.contributor.author","Rodríguez-Vázquez, José Francisco"],["dc.contributor.author","Murakami, Gen"],["dc.date.accessioned","2020-12-10T14:05:43Z"],["dc.date.available","2020-12-10T14:05:43Z"],["dc.date.issued","2017"],["dc.identifier.doi","10.1002/ca.v31.4"],["dc.identifier.issn","0897-3806"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/69633"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Topographical anatomy of the intestines during in utero physiological herniation"],["dc.title.alternative","Rotation of the Intestine and Colon"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","163"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Angiogenesis"],["dc.bibliographiccitation.lastpage","172"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Hemmen, Katherina"],["dc.contributor.author","Reinl, Tobias"],["dc.contributor.author","Buttler, Kerstin"],["dc.contributor.author","Behler, Friederike"],["dc.contributor.author","Dieken, Hauke"],["dc.contributor.author","Jaensch, Lothar"],["dc.contributor.author","Wilting, Joerg"],["dc.contributor.author","Weich, Herbert A."],["dc.date.accessioned","2018-11-07T08:56:20Z"],["dc.date.available","2018-11-07T08:56:20Z"],["dc.date.issued","2011"],["dc.description.abstract","Recently, we isolated and characterized resident endothelial progenitor cells from the lungs of adult mice. These cells have a high proliferation potential, are not transformed and can differentiate into blood- and lymph-vascular endothelial cells under in vitro and in vivo conditions. Here we studied the secretome of these cells by nanoflow liquid chromatographic mass spectrometry (LC-MS). For analysis, 3-day conditioned serum-free media were used. We found 133 proteins belonging to the categories of membrane-bound or secreted proteins. Thereby, several of the membrane-bound proteins also existed as released variants. Thirty-five proteins from this group are well known as endothelial cell- or angiogenesis-related proteins. The MS analysis of the secretome was supplemented and confirmed by fluorescence activated cell sorting analyses, ELISA measurements and immunocytological studies of selected proteins. The secretome data presented in this study provides a platform for the in-depth analysis of endothelial progenitor cells and characterizes potential cellular markers and signaling components in hem- and lymphangiogeneis."],["dc.identifier.doi","10.1007/s10456-011-9200-x"],["dc.identifier.isi","000291038200006"],["dc.identifier.pmid","21234671"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/23121"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0969-6970"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","High-resolution mass spectrometric analysis of the secretome from mouse lung endothelial progenitor cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","5"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Investigative Ophthalmology & Visual Science"],["dc.bibliographiccitation.volume","61"],["dc.contributor.author","Kim, Ji Hyun"],["dc.contributor.author","Hayashi, Shogo"],["dc.contributor.author","Yamamoto, Masahito"],["dc.contributor.author","Murakami, Gen"],["dc.contributor.author","Wilting, Jorg"],["dc.contributor.author","Rodríguez-Vázquez, José Francisco"],["dc.date.accessioned","2021-04-14T08:31:22Z"],["dc.date.available","2021-04-14T08:31:22Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1167/iovs.61.12.5"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/83572"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.issn","1552-5783"],["dc.title","Examination of the Annular Tendon (Annulus of Zinn) as a Common Origin of the Extraocular Rectus Muscles: 2. Embryological Basis of Extraocular Muscles Anomalies"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2302"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Oncotarget"],["dc.bibliographiccitation.lastpage","2316"],["dc.bibliographiccitation.volume","4"],["dc.contributor.author","Exertier, Prisca"],["dc.contributor.author","Javerzat, Sophie"],["dc.contributor.author","Wang, Baigang"],["dc.contributor.author","Franco, Mélanie"],["dc.contributor.author","Herbert, John"],["dc.contributor.author","Platonova, Natalia"],["dc.contributor.author","Winandy, Marie"],["dc.contributor.author","Pujol, Nadège"],["dc.contributor.author","Nivelles, Olivier"],["dc.contributor.author","Ormenese, Sandra"],["dc.contributor.author","Godard, Virginie"],["dc.contributor.author","Becker, Jürgen"],["dc.contributor.author","Bicknell, Roy"],["dc.contributor.author","Pineau, Raphael"],["dc.contributor.author","Wilting, Jörg"],["dc.contributor.author","Bikfalvi, Andreas"],["dc.contributor.author","Hagedorn, Martin"],["dc.date.accessioned","2019-07-10T08:11:46Z"],["dc.date.available","2019-07-10T08:11:46Z"],["dc.date.issued","2013-12-01"],["dc.description.abstract","Kinesin motor proteins exert essential cellular functions in all eukaryotes. They control mitosis, migration and intracellular transport through interaction with microtubules. Small molecule inhibitors of the mitotic kinesin KiF11/Eg5 are a promising new class of anti-neoplastic agents currently evaluated in clinical cancer trials for solid tumors and hematological malignancies. Here we report induction of Eg5 and four other mitotic kinesins including KIF20A/Mklp2 upon stimulation of in vivo angiogenesis with vascular endothelial growth factor-A (VEGF-A). Expression analyses indicate up-regulation of several kinesin-encoding genes predominantly in lymphoblasts and endothelial cells. Chemical blockade of Eg5 inhibits endothelial cell proliferation and migration in vitro. Mitosis-independent vascular outgrowth in aortic ring cultures is strongly impaired after Eg5 or Mklp2 protein inhibition. In vivo, interfering with KIF11/Eg5 function causes developmental and vascular defects in zebrafish and chick embryos and potent inhibition of tumor angiogenesis in experimental tumor models. Besides blocking tumor cell proliferation, impairing endothelial function is a novel mechanism of action of kinesin inhibitors."],["dc.identifier.fs","603240"],["dc.identifier.pmid","24327603"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10759"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60793"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1949-2553"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","CC BY 3.0"],["dc.rights.uri","http://creativecommons.org/licenses/by/3.0"],["dc.title","Impaired angiogenesis and tumor development by inhibition of the mitotic kinesin Eg5."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]