Increased local delivery of antagomir therapeutics to the rodent myocardium using ultrasound and microbubbles

Autor: Maike A.D. Brans, Rick F. J. Kwekkeboom, Corina H.G. Metz, Joost P.G. Sluijter, René J. P. Musters, Ben van Middelaar, Otto Kamp, Walter J Paulus

Publikováno v: Journal of Controlled Release, 222, 18-31. Elsevier
Journal of Controlled Release, 222, 18. Elsevier
Kwekkeboom, R F J, Sluijter, J P G, van Middelaar, B J, Metz, C H, Brans, M A, Kamp, O, Paulus, W J & Musters, R J P 2016, ' Increased local delivery of antagomir therapeutics to the rodent myocardium using ultrasound and microbubbles ', Journal of Controlled Release, vol. 222, pp. 18-31 . https://doi.org/10.1016/j.jconrel.2015.11.020

Recent developments in microRNA (miRNA) research have identified these as important mediators in the pathophysiological response upon myocardial infarction (MI). Specific miRNAs can inhibit the translation of entire groups of mRNAs, which are involve

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::0b1e060e8120aba34d7024a75cadcd91
https://dspace.library.uu.nl/handle/1874/332949

Leucocyte expression of complement C5a receptors exacerbates infarct size after myocardial reperfusion injury

Autor: Leo Timmers, Vince C. de Hoog, Amerik van Duijvenvoorde, Mirjam B. Smeets, Dominique P.V. de Kleijn, Pieter A. Doevendans, Saskia C.A. de Jager, Ben van Middelaar, Gerard Pasterkamp, C. Erik Hack, Trent M. Woodruff

Publikováno v: Cardiovascular research. 103(4)

Aims Early reperfusion is mandatory for the treatment of acute myocardial infarction. This process, however, also induces additional loss of viable myocardium, called ischaemia–reperfusion (IR) injury. Complement activation plays an important role

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::b7834cd8c8be50f0af377edb99be2045
https://pubmed.ncbi.nlm.nih.gov/24935433

Inhibition of RIP1-dependent necrosis prevents adverse cardiac remodeling after myocardial ischemia-reperfusion in vivo

Autor: Joost P.G. Sluijter, Martinus I. F. J. Oerlemans, Jia Liu, Fatih Arslan, Krista den Ouden, Ben van Middelaar, Pieter A. Doevendans

Publikováno v: Basic research in cardiology. 107(4)

Accumulating evidence indicatesthat programmed necrosis plays a critical role in cell death during ischemia–reperfusion. Necrostatin-1 (Nec-1), a small molecule capable of inhibiting a key regulator of programmed necrosis (RIP1), was shown to preve

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::e1c64f29bf66c26a9fc8bb8aab53b69a
https://pubmed.ncbi.nlm.nih.gov/22553001

Abstract 350: Toll-like Receptor 2 Activation, Especially In Circulating Leukocytes, Mediates Myocardial Ischemia/Reperfusion Injury In Mice

Autor: Fatih Arslan, Gerard Pasterkamp, Leo Timmers, Ben van Middelaar, Pieter A Doevendans, Dominique P de Kleijn

Publikováno v: Circulation. 118

OBJECTIVES. Myocardial ischemia/reperfusion (MI/R) injury is characterized by an inflammatory response through NF-κB, increase of infarct size and worsening of cardiac function. Toll-like receptors (TLRs) are part of innate immunity and initiate the

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_________::bac0f8354563aee511835535d2a59b06
https://doi.org/10.1161/circ.118.suppl_18.s_288

Toll-like receptor 4 is involved in outward arterial remodeling

Autor: Arjan H. Schoneveld, Chaylendra Strijder, Margreet R. de Vries, J. Karlijn van Keulen, Dominique P.V. de Kleijn, Paul H.A. Quax, Saskia C.G. Hollestelle, Aryan Vink, Ben van Middelaar, Gerard Pasterkamp

Publikováno v: Circulation, 109(3), 393-398. LIPPINCOTT WILLIAMS & WILKINS
Circulation, 3, 109, 393-398

Background— Toll-like receptor 4 (Tlr4) is the receptor for exogenous lipopolysaccharides (LPS). Expression of endogenous Tlr4 ligands, heat shock protein 60 (Hsp60) and extra domain A of fibronectin, has been observed in arthritic and oncological

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::f6367118ae25600fd6f090179f91ee9b
https://pubmed.ncbi.nlm.nih.gov/14699006