Shortening of the elastic tandem immunoglobulin segment of titin leads to diastolic dysfunction.

ABSTRACT:

Background

Diastolic dysfunction is a poorly understood but clinically pervasive syndrome that is characterized by increased diastolic stiffness. Titin is the main determinant of cellular passive stiffness. However, the physiological role that the tandem immunoglobulin (Ig) segment of titin plays in stiffness generation and whether shortening this segment is sufficient to cause diastolic dysfunction need to be established.

Methods and results

We generated a mouse model in which 9 Ig-like domains (Ig3-Ig11) were deleted from the proximal tandem Ig segment of the spring region of titin (IG KO). Exon microarray analysis revealed no adaptations in titin splicing, whereas novel phospho-specific antibodies did not detect changes in titin phosphorylation. Passive myocyte stiffness

SUBMITTER: Chung CS 

PROVIDER: S-EPMC3822017 | biostudies-literature | 2013 Jul

REPOSITORIES: biostudies-literature