Literature DB >> 17399693

Post-infarction remodeling is independent of mitogen-activated protein kinase kinase 3 (MKK3).

James E Clark1, Richard A Flavell, Matthew E Faircloth, Roger J Davis, Richard J Heads, Michael S Marber.   

Abstract

OBJECTIVES: Our aim was to examine the role of mitogen-activated protein kinase kinase 3 (MKK3) in the development of left ventricular (LV) remodeling following myocardial infarction (MI).
METHODS: MKK3-null mice were subjected to permanent coronary artery ligation. Twenty-eight days after MI, haemodynamics in male mkk3+/+(WT) and mkk3-/-(KO) littermates were assessed using a pressure-conductance catheter. MI groups were compared to un-operated time-matched WT and KO controls.
RESULTS: MI caused significant LV contractile dysfunction and dilatation which did not differ by genotype. Detailed morphometric analysis of excised hearts confirmed these similar global indices of remodeling and also demonstrated that pathological changes within remote myocardium and scar did not differ between KO and WT hearts.
CONCLUSIONS: Despite numerous lines of evidence suggesting MKK3 is the relevant kinase upstream of p38 mitogen-activated protein kinase in LV remodeling these processes can continue in its absence.

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Year:  2007        PMID: 17399693     DOI: 10.1016/j.cardiores.2007.02.027

Source DB:  PubMed          Journal:  Cardiovasc Res        ISSN: 0008-6363            Impact factor:   10.787


  4 in total

1.  Characterization of a novel MK3 splice variant from murine ventricular myocardium.

Authors:  Nadège Moïse; Dharmendra Dingar; Aida M Mamarbachi; Louis R Villeneuve; Nada Farhat; Matthias Gaestel; Maya Khairallah; Bruce G Allen
Journal:  Cell Signal       Date:  2010-06-04       Impact factor: 4.315

2.  Myocardial stress remodelling after regional infarction is independent of glycogen synthase kinase-3 inactivation.

Authors:  Ian G Webb; Pierre Sicard; James E Clark; Simon Redwood; Michael S Marber
Journal:  J Mol Cell Cardiol       Date:  2010-08-06       Impact factor: 5.000

3.  Co-expression of POU4F2/Brn-3b with p53 may be important for controlling expression of pro-apoptotic genes in cardiomyocytes following ischaemic/hypoxic insults.

Authors:  V Budhram-Mahadeo; R Fujita; S Bitsi; P Sicard; R Heads
Journal:  Cell Death Dis       Date:  2014-10-30       Impact factor: 8.469

4.  Non-Invasive whole-body detection of complement activation using radionuclide imaging in a mouse model of myocardial ischaemia-reperfusion injury.

Authors:  Ehsan Sharif-Paghaleh; May Lin Yap; Sarah-Lena Puhl; Adam Badar; Julia Baguña Torres; Krisanat Chuamsaamarkkee; Florian Kampmeier; Richard A Smith; James Clark; Philip J Blower; Steven Sacks; Gregory E Mullen
Journal:  Sci Rep       Date:  2017-11-23       Impact factor: 4.379

  4 in total

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