You are here

Energy metabolism and slow skeletal troponin I phosphorylation in cardiac troponin I null mouse heart

Download pdf | Full Screen View

Date Issued:
2003
Summary:
Troponin I (TnI) plays an important role in cardiac muscle contraction. Two TnI genes (cardiac and slow skeletal TnI) are predominantly expressed in the heart. In cTnI knockout mice, myocardial TnI deficiency results in a diastolic dysfunction and a sudden death in homozygous mutants. In the present studies, energy metabolism has been analyzed in myocardial cells from cTnI null hearts. Our results have demonstrated that damaged relaxation and increased Ca2+-independent force production in cTnI null hearts stimulated myofibril MgATPase activities accompanied by the increase of mitochondria quantity and ATPase activities. In addition, an increase of ssTnI phosphorylation level has been observed in cTnI null hearts. The results indicate that TnI deficiency can cause the disturbance of energy metabolism and some protein overphosphorylation.
Title: Energy metabolism and slow skeletal troponin I phosphorylation in cardiac troponin I null mouse heart.
124 views
34 downloads
Name(s): Jia, Yuanyuan
Florida Atlantic University, Degree grantor
Huang, Xupei, Thesis advisor
Charles E. Schmidt College of Medicine
Department of Biomedical Science
Type of Resource: text
Genre: Electronic Thesis Or Dissertation
Issuance: monographic
Date Issued: 2003
Publisher: Florida Atlantic University
Place of Publication: Boca Raton, FL
Physical Form: application/pdf
Extent: 64 p.
Language(s): English
Summary: Troponin I (TnI) plays an important role in cardiac muscle contraction. Two TnI genes (cardiac and slow skeletal TnI) are predominantly expressed in the heart. In cTnI knockout mice, myocardial TnI deficiency results in a diastolic dysfunction and a sudden death in homozygous mutants. In the present studies, energy metabolism has been analyzed in myocardial cells from cTnI null hearts. Our results have demonstrated that damaged relaxation and increased Ca2+-independent force production in cTnI null hearts stimulated myofibril MgATPase activities accompanied by the increase of mitochondria quantity and ATPase activities. In addition, an increase of ssTnI phosphorylation level has been observed in cTnI null hearts. The results indicate that TnI deficiency can cause the disturbance of energy metabolism and some protein overphosphorylation.
Identifier: 9780496181629 (isbn), 12998 (digitool), FADT12998 (IID), fau:9865 (fedora)
Degree granted: Thesis (M.S.)--Florida Atlantic University, 2003.
Collection: FAU Electronic Theses and Dissertations Collection
Note(s): Charles E. Schmidt College of Science
Subject(s): Mice as laboratory animals
Mice--Metabolism
Energy metabolism
Mitochondria
Held by: Florida Atlantic University Libraries
Persistent Link to This Record: http://purl.flvc.org/fcla/dt/12998
Sublocation: Digital Library
Use and Reproduction: Copyright © is held by the author with permission granted to Florida Atlantic University to digitize, archive and distribute this item for non-profit research and educational purposes. Any reuse of this item in excess of fair use or other copyright exemptions requires permission of the copyright holder.
Use and Reproduction: http://rightsstatements.org/vocab/InC/1.0/
Host Institution: FAU
Is Part of Series: Florida Atlantic University Digital Library Collections.