No effect of thymosin beta-4 on the expression of the transcription factor Islet-1 in the adult murine heart
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No effect of thymosin beta-4 on the expression of the transcription factor Islet-1 in the adult murine heart. / Weinberger, Florian; Nicol, Philipp; Starbatty, Jutta; Stubbendorff, Mandy; Becher, Peter M; Schrepfer, Sonja; Eschenhagen, Thomas.
in: PHARMACOL RES PERSPE, Jahrgang 6, Nr. 3, 03.06.2018, S. e00407.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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TY - JOUR
T1 - No effect of thymosin beta-4 on the expression of the transcription factor Islet-1 in the adult murine heart
AU - Weinberger, Florian
AU - Nicol, Philipp
AU - Starbatty, Jutta
AU - Stubbendorff, Mandy
AU - Becher, Peter M
AU - Schrepfer, Sonja
AU - Eschenhagen, Thomas
N1 - © 2018 The Authors. Pharmacology Research & Perspectives published by John Wiley & Sons Ltd, British Pharmacological Society and American Society for Pharmacology and Experimental Therapeutics.
PY - 2018/6/3
Y1 - 2018/6/3
N2 - The transcription factor Islet-1 marks a progenitor cell population of the second heart field during cardiogenesis. In the adult heart Islet-1 expression is limited to the sinoatrial node, the ventricular outflow tract, and parasympathetic ganglia. The regenerative effect in the injured mouse ventricle of thymosin beta-4 (TB4), a 43-aminoacid peptide, was associated with increased Islet-1 immunostaining, suggesting the induction of an Islet-1-positive progenitor state by TB4. Here we aimed to reassess this effect in a genetic model. Mice from the reporter mouse line Isl1-nLacZ were primed with TB4 and subsequently underwent myocardial infarction. Islet-1 expression was assessed 2, 7, and 14 days after infarction. We detected only a single Islet-1+ cell in 8 TB4 treated and infarcted hearts which located outside of the sinoatrial node, the outflow tract or cardiac ganglia (in ~2500 sections). Two cells were identified in 5 control infarcted hearts. TB4 did not induce LacZ positivity in ventricular explants cultures of Isl1-nLacZ mice nor did it affect the density of LacZ+ cells in explant cultures of nLacZ+ regions of the heart. In summary, we found no evidence that TB4 reactivates Islet-1 expression in adult mouse ventricle.
AB - The transcription factor Islet-1 marks a progenitor cell population of the second heart field during cardiogenesis. In the adult heart Islet-1 expression is limited to the sinoatrial node, the ventricular outflow tract, and parasympathetic ganglia. The regenerative effect in the injured mouse ventricle of thymosin beta-4 (TB4), a 43-aminoacid peptide, was associated with increased Islet-1 immunostaining, suggesting the induction of an Islet-1-positive progenitor state by TB4. Here we aimed to reassess this effect in a genetic model. Mice from the reporter mouse line Isl1-nLacZ were primed with TB4 and subsequently underwent myocardial infarction. Islet-1 expression was assessed 2, 7, and 14 days after infarction. We detected only a single Islet-1+ cell in 8 TB4 treated and infarcted hearts which located outside of the sinoatrial node, the outflow tract or cardiac ganglia (in ~2500 sections). Two cells were identified in 5 control infarcted hearts. TB4 did not induce LacZ positivity in ventricular explants cultures of Isl1-nLacZ mice nor did it affect the density of LacZ+ cells in explant cultures of nLacZ+ regions of the heart. In summary, we found no evidence that TB4 reactivates Islet-1 expression in adult mouse ventricle.
KW - Animals
KW - Cells, Cultured
KW - Disease Models, Animal
KW - Gene Expression Regulation
KW - Heart Ventricles
KW - LIM-Homeodomain Proteins
KW - Mice
KW - Mice, Transgenic
KW - Myocardial Infarction
KW - Sinoatrial Node
KW - Stem Cells
KW - Thymosin
KW - Transcription Factors
KW - Journal Article
KW - Research Support, Non-U.S. Gov't
U2 - 10.1002/prp2.407
DO - 10.1002/prp2.407
M3 - SCORING: Journal article
C2 - 29864245
VL - 6
SP - e00407
JO - PHARMACOL RES PERSPE
JF - PHARMACOL RES PERSPE
SN - 2052-1707
IS - 3
ER -