scholarly journals Lysosomal integral membrane protein 2 is a novel component of the cardiac intercalated disc and vital for load-induced cardiac myocyte hypertrophy

2007 ◽  
Vol 177 (4) ◽  
pp. i5-i5
Author(s):  
Blanche Schroen ◽  
Joost J. Leenders ◽  
Arie van Erk ◽  
Anne T. Bertrand ◽  
Mirjam van Loon ◽  
...  
Keyword(s):  
Membrane Protein ◽  
Cardiac Myocyte ◽  
Integral Membrane Protein ◽  
Intercalated Disc ◽  
Myocyte Hypertrophy ◽  
Cardiac Myocyte Hypertrophy ◽  
Cardiac Intercalated Disc

scholarly journals Lysosomal integral membrane protein 2 is a novel component of the cardiac intercalated disc and vital for load-induced cardiac myocyte hypertrophy

2007 ◽  
Vol 204 (5) ◽  
pp. 1227-1235 ◽  
Author(s):  
Blanche Schroen ◽  
Joost J. Leenders ◽  
Arie van Erk ◽  
Anne T. Bertrand ◽  
Mirjam van Loon ◽  
...  
Keyword(s):  
Membrane Protein ◽  
Cardiac Myocyte ◽  
Cardiac Development ◽  
Integral Membrane Protein ◽  
Genetically Engineered ◽  
Intercalated Disc ◽  
Hypertrophic Response ◽  
Id Proteins ◽  
Genetically Engineered Mice ◽  
Cardiac Myocyte Hypertrophy

The intercalated disc (ID) of cardiac myocytes is emerging as a crucial structure in the heart. Loss of ID proteins like N-cadherin causes lethal cardiac abnormalities, and mutations in ID proteins cause human cardiomyopathy. A comprehensive screen for novel mechanisms in failing hearts demonstrated that expression of the lysosomal integral membrane protein 2 (LIMP-2) is increased in cardiac hypertrophy and heart failure in both rat and human myocardium. Complete loss of LIMP-2 in genetically engineered mice did not affect cardiac development; however, these LIMP-2 null mice failed to mount a hypertrophic response to increased blood pressure but developed cardiomyopathy. Disturbed cadherin localization in these hearts suggested that LIMP-2 has important functions outside lysosomes. Indeed, we also find LIMP-2 in the ID, where it associates with cadherin. RNAi-mediated knockdown of LIMP-2 decreases the binding of phosphorylated β-catenin to cadherin, whereas overexpression of LIMP-2 has the opposite effect. Collectively, our data show that LIMP-2 is crucial to mount the adaptive hypertrophic response to cardiac loading. We demonstrate a novel role for LIMP-2 as an important mediator of the ID.

Heart Fatty Acid Binding Protein Is a Novel Regulator of Cardiac Myocyte Hypertrophy

1994 ◽  
Vol 205 (3) ◽  
pp. 1822-1828 ◽  
Author(s):  
P.B.J. Burton ◽  
C.E. Hogben ◽  
C.L. Joannou ◽  
A.G.B. Clark ◽  
J.J. Hsuan ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Binding Protein ◽  
Cardiac Myocyte ◽  
Binding Protein ◽  
Fatty Acid Binding ◽  
Myocyte Hypertrophy ◽  
Acid Binding Protein ◽  
Cardiac Myocyte Hypertrophy

scholarly journals P126The role of MIP1 in cardiac myocyte hypertrophy and survival

2014 ◽  
Vol 103 (suppl 1) ◽  
pp. S22.2-S22
Author(s):  
C Mansfield ◽  
B Buyandelger ◽  
S Kostin ◽  
G Knoell ◽  
MR Toliat ◽  
...  
Keyword(s):  
Cardiac Myocyte ◽  
Myocyte Hypertrophy ◽  
Cardiac Myocyte Hypertrophy

Sphingolipids induce cardiac myocyte hypertrophy through Gi protein-coupled receptor and MAPK cascade

1999 ◽  
Vol 5 (3) ◽  
pp. 78
Author(s):  
Kenichi Sekiguchi ◽  
Tomoyuki Yokoyama ◽  
Masashi Arai ◽  
Masahiko Kurabayashi ◽  
Ryozo Nagai
Keyword(s):  
Cardiac Myocyte ◽  
Mapk Cascade ◽  
Myocyte Hypertrophy ◽  
Gi Protein ◽  
Cardiac Myocyte Hypertrophy

Aldosterone directly stimulates cardiac myocyte hypertrophy

2004 ◽  
Vol 10 (6) ◽  
pp. 511-518 ◽  
Author(s):  
Marina P. Okoshi ◽  
Xinhua Yan ◽  
Katashi Okoshi ◽  
Masaharu Nakayama ◽  
Adam J.T. Schuldt ◽  
...  
Keyword(s):  
Cardiac Myocyte ◽  
Myocyte Hypertrophy ◽  
Cardiac Myocyte Hypertrophy

scholarly journals Emodin and emodin-rich rhubarb inhibits histone deacetylase (HDAC) activity and cardiac myocyte hypertrophy

2020 ◽  
Vol 79 ◽  
pp. 108339 ◽  
Author(s):  
Levi W. Evans ◽  
Abigail Bender ◽  
Leah Burnett ◽  
Luis Godoy ◽  
Yi Shen ◽  
...  
Keyword(s):  
Histone Deacetylase ◽  
Cardiac Myocyte ◽  
Hdac Activity ◽  
Myocyte Hypertrophy ◽  
Cardiac Myocyte Hypertrophy
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