• No results found

VU Research Portal

N/A
N/A
Protected

Academic year: 2021

Share "VU Research Portal"

Copied!
3
0
0

Bezig met laden.... (Bekijk nu de volledige tekst)

Hele tekst

(1)

VU Research Portal

Interactions between thyroid hormone and microRNAs in the heart:

Janssen, J.A.

2016

document version

Publisher's PDF, also known as Version of record

Link to publication in VU Research Portal

citation for published version (APA)

Janssen, J. A. (2016). Interactions between thyroid hormone and microRNAs in the heart: implications for

pathological ventricular remodeling.

General rights

Copyright and moral rights for the publications made accessible in the public portal are retained by the authors and/or other copyright owners and it is a condition of accessing publications that users recognise and abide by the legal requirements associated with these rights. • Users may download and print one copy of any publication from the public portal for the purpose of private study or research. • You may not further distribute the material or use it for any profit-making activity or commercial gain

• You may freely distribute the URL identifying the publication in the public portal ?

Take down policy

If you believe that this document breaches copyright please contact us providing details, and we will remove access to the work immediately and investigate your claim.

E-mail address:

vuresearchportal.ub@vu.nl

(2)

Chapter 1

General Introduction

— 9 Part I Cardiac Remodeling and Chronic Heart Failure — 11 Part II Thyroid Hormone and the Heart — 18

Part III A Evidence for a local hypothyroid condition — 24 Part III B Focus on DIO3 — 27

Aims and outline of the study — 29

Chapter 2

Thyroid hormone- regulated

cardiac microRNAs are

predicted to suppress

pathological hypertrophic

signaling

— 31

Abstract — 32 Introduction — 33

Materials and methods — 35 Results — 37

Discussion — 42

Supplementary data — 45

Chapter 3

Cardiac expression of

deiodinase type 3 (Dio3)

following myocardial

infarction is associated

with the induction of a

pluripotency microRNA

signature from the

Dlk1-Dio3 genomic region

— 49 Abstract — 50

Introduction — 51

Methods and methods — 52 Results — 54

Discussion — 57

Supplementary data — 59

(3)

Chapter 4

MicroRNA 214 is a

potential regulator of

thyroid hormone levels

in the mouse heart

following myocardial

infarction, by targeting

the thyroid- hormone

inactivating enzyme

deiodinase type III

— 63 Abstract — 64

Introduction — 65

Materials and methods — 67 Results — 71 Discussion — 77 Supplementary data — 80 Chapter 5

Cardiac induction of

the thyroid-hormone

degrading enzyme type III

deiodinase in human

ischemic heart failure

— 83 Abstract — 84

Introduction — 85

Methods and materials — 87 Results — 90

Discussion — 93

Chapter 6

Referenties

GERELATEERDE DOCUMENTEN

Copyright and moral rights for the publications made accessible in the public portal are retained by the authors and/or other copyright owners and it is a condition of

Copyright and moral rights for the publications made accessible in the public portal are retained by the authors and/or other copyright owners and it is a condition of

Copyright and moral rights for the publications made accessible in the public portal are retained by the authors and/or other copyright owners and it is a condition of

Copyright and moral rights for the publications made accessible in the public portal are retained by the authors and/or other copyright owners and it is a condition of

Copyright and moral rights for the publications made accessible in the public portal are retained by the authors and/or other copyright owners and it is a condition of

Copyright and moral rights for the publications made accessible in the public portal are retained by the authors and/or other copyright owners and it is a condition of

Copyright and moral rights for the publications made accessible in the public portal are retained by the authors and/or other copyright owners and it is a condition of

Copyright and moral rights for the publications made accessible in the public portal are retained by the authors and/or other copyright owners and it is a condition of