Tlr2 deficiency does not limit the development of left ventricular hypertrophy in a model of transverse aortic constriction induced pressure overload.
BACKGROUND
Toll-like receptors (TLRs) are involved in a variety of cardiovascular disorders, including septic cardiomyopathy, ischemia/reperfusion, heart failure, and cardiac hypertrophy. Previous research revealed that TLR4 promotes cardiac hypertrophy in vivo. Therefore, we investigated whether TLR2 is also involved in the development of cardiac hypertrophy.


METHODS
Tlr2 deficient and wild type mice were subjected to transverse aortic constriction (TAC) or sham operation procedure. Left ventricular, heart and lung weights as well as hemodynamic parameters were determined after 3, 14 or 28 days. Real-time RT PCR was used to evaluate left ventricular gene expression. Protein content was determined via ELISA.


RESULTS
TAC increased systolic left ventricular pressure, contraction and relaxations velocities as well as the heart weight in both genotypes. Tlr2 deficiency significantly enhanced cardiac hypertrophy after 14 and 28 days of TAC. Left ventricular end-diastolic pressure and heart rate increased in Tlr2(-/-) TAC mice only. Fourteen days of TAC led to a significant elevation of ANP, BNP, TGFβ and TLR4 mRNA levels in Tlr2(-/-) left ventricular tissue.


CONCLUSIONS
These data suggest that Tlr2 deficiency may promote the development of cardiac hypertrophy and ventricular remodeling after transverse aortic constriction.
Physiology Department, Medical Science Faculty, Naresuan University, Phitsanulok, 65000, Thailand.|Institute of Physiology II, University Hospital Bonn, Nussallee 11, 53115, Bonn, Germany.
Tippaporn
T
Bualeong
Institute of Physiology II, University Hospital Bonn, Nussallee 11, 53115, Bonn, Germany.|Department of Neurology, University Hospital Bonn, Sigmund-Freud-Str. 25, 53127, Bonn, Germany.
Sied
S
Kebir
Institute of Physiology II, University Hospital Bonn, Nussallee 11, 53115, Bonn, Germany.
Dorothea
D
Hof
Institute of Physiology II, University Hospital Bonn, Nussallee 11, 53115, Bonn, Germany.|Polyclinic of Orthodontics, University of Bonn, Welschnonnenstraße 17, 53111, Bonn, Germany.
Lina
L
Goelz
Institute of Physiology II, University Hospital Bonn, Nussallee 11, 53115, Bonn, Germany.
Mathias
M
Graewe
Department of Anaesthesiology and Intensive Care Medicine, University Hospital Bonn, Sigmund-Freud-Straße 25, 53127, Bonn, Germany.
Stefan Felix
SF
Ehrentraut
Department of Anaesthesiology and Intensive Care Medicine, University Hospital Bonn, Sigmund-Freud-Straße 25, 53127, Bonn, Germany.
Pascal
P
Knuefermann
Department of Anaesthesiology and Intensive Care Medicine, University Hospital Bonn, Sigmund-Freud-Straße 25, 53127, Bonn, Germany.
Georg
G
Baumgarten
Institute of Physiology II, University Hospital Bonn, Nussallee 11, 53115, Bonn, Germany.
Rainer
R
Meyer
Department of Anaesthesiology and Intensive Care Medicine, University Hospital Bonn, Sigmund-Freud-Straße 25, 53127, Bonn, Germany. heidi.ehrentraut@ukb.uni-bonn.de.
Heidi
H
Ehrentraut
D000818:Animals; D001024:Aortic Valve Stenosis / Q000235:genetics / Q000503:physiopathology*; D005109:Extracellular Matrix / Q000378:metabolism; D005786:Gene Expression Regulation; D017379:Hypertrophy, Left Ventricular / Q000235:genetics / Q000503:physiopathology*; D008297:Male; D051379:Mice; D011312:Pressure; D012333:RNA, Messenger / Q000235:genetics; D051195:Toll-Like Receptor 2 / Q000235:genetics / Q000502:physiology*
D012333:RNA, Messenger; C493486:Tlr2 protein, mouse; D051195:Toll-Like Receptor 2
Aortic constriction; Cardiac hypertrophy; Innate immunity; TLR2