Localization and quantitation of cardiac annexins II, V, and VI in hypertensive guinea pigs
1 Institut National de la Santé et de la Recherche Médicale U-127, IFR Circulation, Hôpital Lariboisière, and 3 Institut National de la Santé et de la Recherche Médicale U-332, ICGM, UFR Cochin Port-Royal 75475 Paris Cedex 10, France; and 2 Cardiology Research Center, 121552 Moscow, Russia Annexi...
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Veröffentlicht in: | American journal of physiology. Heart and circulatory physiology 1999-04, Vol.276 (4), p.H1159-H1166 |
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Zusammenfassung: | 1 Institut National de la
Santé et de la Recherche Médicale U-127, IFR Circulation,
Hôpital Lariboisière, and
3 Institut National de la
Santé et de la Recherche Médicale U-332, ICGM, UFR
Cochin Port-Royal 75475 Paris Cedex 10, France; and
2 Cardiology Research Center,
121552 Moscow, Russia
Annexins are characterized by
Ca 2+ -dependent binding to
phospholipids. Annexin II mainly participates in cell-cell adhesion and
signal transduction, whereas annexins V and VI also seem to regulate
intracellular calcium cycling. Their abundance and localization were
determined in left ventricle (LV) and right ventricle (RV) from
hypertensive guinea pigs, during the transition from compensatory hypertrophy to heart failure. Immunoblot analysis of annexins II, V,
and VI revealed an increased accumulation (2.6-, 1.45-, and 2.3-fold,
respectively) in LV from hypertensive guinea pigs and no modification
in RV. Immunofluorescent labeling of annexins II, V, and VI; of
Na + -K + -ATPase;
and of sarcomeric -actinin showed that in control LV and RV,
1 ) annexin II is present in
nonmuscle cells; 2 ) annexins V and
VI are mainly observed in the sarcolemma and intercalated disks of
myocytes; 3 ) annexins II, V, and VI
strongly label endothelial cells and adventitia of coronary arteries;
and 4 ) annexin VI is present in the
media. At the onset of heart failure, the most striking changes are the
increased protein accumulation in LV and the very strong labeling of
annexins II, V, and VI in interstitial tissue, suggesting a role in
fibrosis development and cardiac remodeling.
hypertrophy and heart failure; remodeling |
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ISSN: | 0363-6135 0002-9513 1522-1539 |
DOI: | 10.1152/ajpheart.1999.276.4.h1159 |