Universität zu Köln

Goltz, Diane, Hittetiya, Kanishka, Gevensleben, Heidrun, Kirfel, Jutta, Diehl, Linda, Meyer, Rainer and Buettner, Reinhard (2016). Loss of the LIM-only protein Fhl2 impairs inflammatory reaction and scar formation after cardiac ischemia leading to better hemodynamic performance. Life Sci., 151. S. 348 - 359. OXFORD: PERGAMON-ELSEVIER SCIENCE LTD. ISSN 1879-0631

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Abstract

Aims: The pathogenesis of myocardial ischemia-reperfusion injury (MI/R) involves an inflammatory response. Since the four-and-a-half LIM domain-containing protein 2 (Fhl2) has been observed to modulate immune cell migration, we aimed to study the consequences of Fhl2(-/-) under MI/R with respect to immune reaction, scar formation, and hemodynamic performance. Material and methods: In a closed chest model of 1 h MI/R, immune cell invasion of phagocytic monocytes was characterized by flow cytometry and immunohistochemistry. In addition, infarct size was assessed by triphenyltetrazolium chloride/Masson trichrome staining 24 h/21 days after reperfusion and a set of hemodynamic parameters was recorded by catheterisation in Fhl2(-/-) mice and controls. Key findings: While flow cytometry did not reveal differences in myocardial CD45(high) immune cell infiltrate, histological analysis showed that infiltrating immune cells in Fhl2(-/-) animals were preferentially located in the perivascular area, whereas in wild type, immune cells were well dispersed within the area at risk. After 24 h and 21 days of reperfusion, infarct size was significantly reduced in Fhl2(-/-) compared to WT animals. In addition, hemodynamic performance was better in Fhl2(-/-) mice, compared to WT mice up to day 21 of reperfusion. The loss of Fhl2 leads to an altered immune response to myocardial ischemia, which results in smaller infarcts and better hemodynamic performance up to 21 days after myocardial ischemia reperfusion. Significance: Immune cell invasion plays a pivotal role in the context of MI/R. Fhl2 significantly influences immune cell function and immune cell interaction with injured cardiac tissue leading to altered scar composition. (C) 2016 Elsevier Inc. All rights reserved.

Item Type:	Journal Article
Creators:	Creators Email ORCID ORCID Put Code Goltz, Diane UNSPECIFIED UNSPECIFIED UNSPECIFIED Hittetiya, Kanishka UNSPECIFIED UNSPECIFIED UNSPECIFIED Gevensleben, Heidrun UNSPECIFIED UNSPECIFIED UNSPECIFIED Kirfel, Jutta UNSPECIFIED UNSPECIFIED UNSPECIFIED Diehl, Linda UNSPECIFIED UNSPECIFIED UNSPECIFIED Meyer, Rainer UNSPECIFIED UNSPECIFIED UNSPECIFIED Buettner, Reinhard UNSPECIFIED UNSPECIFIED UNSPECIFIED
URN:	urn:nbn:de:hbz:38-278600
DOI:	10.1016/j.lfs.2016.02.084
Journal or Publication Title:	Life Sci.
Volume:	151
Page Range:	S. 348 - 359
Date:	2016
Publisher:	PERGAMON-ELSEVIER SCIENCE LTD
Place of Publication:	OXFORD
ISSN:	1879-0631
Language:	English
Faculty:	Unspecified
Divisions:	Unspecified
Subjects:	no entry
Uncontrolled Keywords:	Keywords Language MYOCARDIAL-INFARCTION; SPLENIC RESERVOIR; MONOCYTES; MICE; HETEROGENEITY; HEART; DEFICIENCY; DISEASE; REPAIR; CELLS Multiple languages Medicine, Research & Experimental; Pharmacology & Pharmacy Multiple languages
Refereed:	Yes
URI:	http://kups.ub.uni-koeln.de/id/eprint/27860