Articles by Marion Ludwig in JoVE
Microscopia intravital de la microcirculación en el músculo de ratón Cremaster para el análisis de la migración de la célula madre periféricas Peter Donndorf1, Marion Ludwig1, Fabian Wildschütz1, Dritan Useini1, Alexander Kaminski1, Brigitte Vollmar2, Gustav Steinhoff1 1Reference and Translation Centre for Cardiac Stem Cell Therapy (RTC), Department of Cardiac Surgery, University Rostock, 2Institute for Experimental Surgery, University of Rostock Microscopía intravital del cremáster microcirculación ratón M. ofrece un único y bien estandarizada-modelo in vivo para el análisis de médula ósea periférica migración de células madre en.
Other articles by Marion Ludwig on PubMed
Whole-body Analysis of a Viral Infection: Vascular Endothelium is a Primary Target of Infectious Hematopoietic Necrosis Virus in Zebrafish Larvae PLoS Pathogens. 2011 | Pubmed ID: 21304884 The progression of viral infections is notoriously difficult to follow in whole organisms. The small, transparent zebrafish larva constitutes a valuable system to study how pathogens spread. We describe here the course of infection of zebrafish early larvae with a heat-adapted variant of the Infectious Hematopoietic Necrosis Virus (IHNV), a rhabdovirus that represents an important threat to the salmonid culture industry. When incubated at 24 °C, a permissive temperature for virus replication, larvae infected by intravenous injection died within three to four days. Macroscopic signs of infection followed a highly predictable course, with a slowdown then arrest of blood flow despite continuing heartbeat, followed by a loss of reactivity to touch and ultimately by death. Using whole-mount in situ hybridization, patterns of infection were imaged in whole larvae. The first infected cells were detectable as early as 6 hours post infection, and a steady increase in infected cell number and staining intensity occurred with time. Venous endothelium appeared as a primary target of infection, as could be confirmed in fli1:GFP transgenic larvae by live imaging and immunohistochemistry. Disruption of the first vessels took place before arrest of blood circulation, and hemorrhages could be observed in various places. Our data suggest that infection spread from the damaged vessels to underlying tissue. By shifting infected fish to a temperature of 28 °C that is non-permissive for viral propagation, it was possible to establish when virus-generated damage became irreversible. This stage was reached many hours before any detectable induction of the host response. Zebrafish larvae infected with IHNV constitute a vertebrate model of an hemorrhagic viral disease. This tractable system will allow the in vivo dissection of host-virus interactions at the whole organism scale, a feature unrivalled by other vertebrate models.
The Regenerative Potential of Angiotensin AT2 Receptor in Cardiac Repair Canadian Journal of Physiology and Pharmacology. Mar, 2012 | Pubmed ID: 22364522 Angiotensin II, the main effector peptide of the renin-angiotensin system, interferes with cardiac remodeling and repair through its receptors, including AT(1) and AT(2) receptor (R). The functional relevance of the previously neglected AT(2)R is currently intensively studied. Pharmacological therapies with AT(1)R blockers have improved outcomes in patients with ischemic heart injury, probably involving an indirect stimulation of AT(2)R. Previous experimental studies have clearly shown a protective action of AT(2)R in tissue repair and regeneration. We have recently identified the c-kit(+)AT(2)R(+) progenitor cell population in rat heart and bone marrow, which increases after induction of myocardial infarction. Further experimental evidence demonstrates that AT(2)R mediates cardiac homing and repair process of the c-kit(+) progenitor cells. AT(2)R stimulation through AT(1)R blockers or directly by AT(2)R agonist or both in combination may potentially offer the translational options to improve the regenerative potentials of stem/progenitor cells derived from patients with cardiovascular disease.