α‐Actin isoform distribution in normal and failing human heart: a morphological, morphometric, and biochemical study

Journal of Pathology - Tập 199 Số 3 - Trang 387-397 - 2003
Albert J.H. Suurmeijer1,2, Sophie Clément1,3, Arianna Francesconi4, Leonardo Bocchi3, Annalisa Angelini5, Dirk J. van Veldhuisen6, Luigi Giusto Spagnoli4, Giulio Gabbiani3, Augusto Orlandi4
1Both AJHS and SC contributed equally to this work
2Department of Pathology University Hospital Groningen, Groningen The Netherlands
3Department of Pathology, University of Geneva, Geneva, Switzerland
4Institute of Anatomic Pathology, Tor Vergata University of Rome, Rome, Italy
5Institute of Anatomic Pathology, University of Padua, Padua, Italy
6Thoraxcenter/Cardiology, University Hospital Groningen, Groningen, The Netherlands

Tóm tắt

AbstractWe investigated the distribution of α‐skeletal, α‐cardiac, and α‐smooth muscle actin isoforms in human heart during development, hypertrophy, and failure. At 20 weeks of fetal life, α‐skeletal actin was localized in a small proportion of subendocardial and papillary muscle cardiomyocytes. At this gestation time, diffuse α‐cardiac actin staining was observed, associated with focal expression of α‐smooth muscle actin. In normal adult subjects, α‐skeletal actin positive cardiomyocytes were distributed in a transmural gradient with the highest proportion located subendocardially. In myocardial hypertrophy and cardiomyopathies, the amount of α‐skeletal actin was increased and diffuse staining was seen in all layers of ventricular myocardium, with the exception of idiopathic dilated cardiomyopathies. Cardiomyocytes were negative for α‐smooth muscle actin in all pathological situations studied. As expected, fibroblasts in post‐infarct scars expressed α‐smooth muscle actin and transforming growth factor‐β1 but, surprisingly, were negative for these proteins in interstitial fibrosis. Our results demonstrate that increased expression of α‐skeletal actin in the diseased human heart is associated with increased myocyte stretch, increased wall stress, and pressure overload, but not with idiopathic dilated cardiomyopathies. They also suggest that fibrotic changes develop with different mechanisms in scars versus interstitial fibrosis. Copyright © 2003 John Wiley & Sons, Ltd.

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Tài liệu tham khảo

10.1016/S0021-9258(17)36017-9

10.1161/01.RES.59.5.551

10.1073/pnas.87.7.2456

10.1161/01.RES.70.5.999

10.1172/JCI113951

Swynghedauw B, 1990, Cardiac Hypertrophy and Failure

10.1172/JCI115295

10.1016/S0024-3205(98)00452-4

10.1161/01.RES.85.10.e51

Clement S, Actin isoform pattern expression: a tool for the diagnosis and biological characterization of human rhabdomyosarcoma, Virchows Archiv

10.1083/jcb.103.6.2787

10.1111/j.1462-5822.2007.00901.x

10.1073/pnas.76.9.4350

10.1016/0021-9150(91)90003-L

Vracko R, 1991, Contractile cells in rat myocardial scar tissue, Lab Invest, 65, 214

Willems IE, 1994, The alpha‐smooth muscle actin‐positive cells in healing human myocardial scars, Am J Pathol, 145, 868

10.1006/excr.1999.4543

10.1093/eurheartj/16.suppl_N.3

Tokuyasu KT, 1990, Developmental Cardiology: Morphogenesis and Function, 205

10.1111/j.1432-0436.1988.tb00091.x

10.1083/jcb.107.6.2575

10.1002/aja.1001930203

10.1002/(SICI)1097-0185(199712)249:4<495::AID-AR9>3.0.CO;2-Q

10.1152/ajpheart.1981.240.6.H920

10.1161/01.CIR.100.17.1770

10.1007/s003950170002

10.1007/s003950170005

10.1016/0735-1097(95)00145-P

10.1161/01.RES.74.4.740

10.1016/S0735-1097(99)00522-7

10.1016/0735-1097(94)90740-4

10.1046/j.1432-0436.2001.690107.x

10.1097/00004872-200018090-00016

10.1016/0012-1606(90)90296-U

10.1046/j.1365-2613.1996.d01-214.x

10.1016/S0192-0561(99)00056-9

10.1007/s004080000051

Villarreal FJ, 1992, Cardiac hypertrophy‐induced changes in mRNA levels for TGF‐beta 1, fibronectin, and collagen, Am J Physiol, 262, H1861

10.1016/S0008-6363(98)00305-8

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Journal of Pathology

Tập 199 Số 3

387-397

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