Advances in understanding the molecular regulation of cardiac development

Current Opinion in Pediatrics

Volumn 11, Issue 5, 1999, Pages 413-418

  Baldwin, H Scott ^a  

^a CHILDREN S HOSPITAL OF PHILADELPHIA   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

AORTA ARCH; CELL REGENERATION; CONGENITAL HEART DISEASE; GENE THERAPY; HEART DEVELOPMENT; HEART MUSCLE CELL; HUMAN; NEURAL CREST; NONHUMAN; PRIORITY JOURNAL; REVIEW; STEM CELL;

ANIMALS; CHROMOSOME MAPPING; HEART; HEART DEFECTS, CONGENITAL; HUMANS; MICE; MICE, KNOCKOUT; NEURAL CREST; STEM CELLS;

EID: 0032883605     PISSN: 10408703     EISSN: None     Source Type: Journal    
DOI: 10.1097/00008480-199910000-00008     Document Type: Review

References (39)

1. Logan M, Pagán-Westphal SM, Smith DM, Paganessi L, Tabin CJ: The transcription factor Pitx2 mediates situs-specific morphogenesis in response to left-right asymmetric signals. Cell 1998, 94:307-317. This is the first and most detailed description of the role that Pitx2 plays in the mechanistic pathways that define left-right pattern formation in the embryo.
2. Ryan AK, Blumberg B, Rodriguez-Esteban C, Yonei-Tamura S, Tamura K, Tsukui T, et al.: Pitx2 determines left-right asymmetry of internal organs in vertebrates. Nature 1998, 394:545-551. This is a brief but informative initial description of the importance of Pitx2 in defining left right developmental fields before heart tube formation.
3. Yoshioka H, Meno C, Koshiba K, Sugihara M, Itoh H, Ishimaru Y, et al.: Pitx2, a bicoid-type homeobox gene, is involved in a lefty-signaling pathway in determination of left-right asymmetry. Cell 1998, 94:299-305.
4. Campione M, Steinbeisser H, Schweikert A, Deissler K, van Bebber F, Lowe L, et al.: The homeobox gene Pitx2: mediator of asymmetric left-right signaling in vertebrate heart and gut looping. Development 1999, 126:1225-1234.
5. Nonaka S, Tanaka Y, Okada Y, Takeda S, Harada A, Kanai Y, et al.: Randomization of left-right asymmetry due to loss of nodal cilia generating leftward flow of extraembryonic fluid in mice lacking KIF38 motor protein. Cell 1998, 95:829-837. This is a thorough analysis of how cilliary proteins may be important in establishing the direction of cardiac looping as well as determining visceral organ location.
6. Takeda S, Yonekawa Y, Tanaka Y, Okada Y, Nonaka S, Hirokawa N: Left-right asymmetry and kinesin superfamily protein KIF3A: new insights in determination of laterality and mesoderm induction by kif3A-/- mice analysis. J Cell Biol 1999, 17:825-836.
7. Chen J, Knowles HJ, Hebert JL, Hackett BP: Mutation of the mouse hepatocyte nuclear factor/forkhead homologue 4 gene results in an absence of cilia and random left-right asymmetry. J Clin Invest 1998, 15:1077-1082.
8. Supp DM, Witte DP, Potter SS, Brueckner M: Mutation of an axonemal dynein affects left-right asymmetry in inversus viscerum mice. Nature 1977, 389:963-966.
9. Kurihara H, Kurihawa Y, Maemura K, Yazaki Y: The role of endothelin-1 in cardiovascular development. Ann N Y Acad Sci 1997, 811:168-177.
10. Brand M, Le Moullec JM, Corvol P, Gasc JM: Ontogeny of endothelins-1 and -3, their receptors, and endothelin converting enzyme-1 in the early human embryo. J Clin Invest 1998, 101:549-559. Using these in situ hybridization experiments, the authors document the expression pattern of critical components of the endothelin signaling cascade in human embryos.
11. Clouthier DE, Hosada K, Richardson JA, Williams SC, Yanagisawa H, Kuwaki T, et al.: Cranial and cardiac neural crest defects in endothelin-A receptor-deficient mice. Development 1998, 125:813-84.
12. Yanagisawa H, Yanagisawa M, Kapur RP, Richardson JA, Williams SC, Clouthier DE, et al.: Dual genetic pathways of endothelin-mediated intercellular signaling revealed by targeted disruption of endothelin converting enzyme-1 gene. Development 1998, 125:825-836.
13. Yanagisawa H, Hammer RE, Richardson JA, Williams SC, Clouthier DE, Yanagisawa M: Role of Endothelin-1/Endothelin-A receptor-mediated signaling pathway in the aortic arch patterning in mice [comments]. J Clin Invest 1998, 102:22-33.
14. Iida K, Koseki H, Kakinuma H, Kato N, Mizutani-Koseki Y, Ohuchi H, et al.: Essential roles of the winged helix transcription factor MFH-1 in aortic arch patterning and skeletogenesis. Development 1997, 124:4627-4638.
15. Goldmuntz E, Emanuel BS: Genetic disorders of cardiac morphogenesis: the DiGeorge and velocardiofacial syndromes [comments]. Circ Res 1997, 80:437-443.
16. Thomas T, Kurihara H, Yamagishi H, Kurihara Y, Yazaki Y, Olsen EN, et al.: A signaling cascade involving endothelin-1, dHand and msx1 regulates development of neural-crest-derived branchial arch mesenchyme. Development 1998, 125:3005-3014.
17. Yamagishi H, Garg V, Matsuoka R, Thomas T, Srivastava D: A molecular pathway revealing a genetic basis for human cardiac and craniofacial defects [comments]. Science 1999, 283:1158-1161. The authors of this article present a potential candidate gene within the DiGeorge syndrome critical region that might explain the conotruncal cardiac defects. The article also represents an example of basic science investigation that can be directly translated into clinical relevance.
18. Thomas T, Yamagishi H, Overbeek PA, Olsen EN, Srivastava D: The bHLH factors, dHand and eHand, specify pulmonary and systemic cardiac ventricles independent of left-right sidedness. Dev Biol 1998, 196:228-236. In this article, the authors document a systematic, genetic approach to defining the role of the transcription factors dHand and eHand ventricular formation.
19. Wang HU, Chen ZF, Anderson DJ: Molecular distinction and angiogenic interaction between embryonic arteries and veins revealed by ephrin-B2 and its receptor Eph-B4 [comments]. Cell 1998, 93:741-753. This seminal article is the first to describe molecular markers that distinguish arterial endothelial cells from venous endothelium. The receptor/ligand interactions described provide an important pathway involved in establishing the pattern of the developing vascular system, and delineate a potential role for these genes in cardiac trabeculation.
20. Holder N, Klein R: Eph receptors and ephrins: effectors of morphogenesis. Development 1999, 126:2033-2044. This is an excellent, in-depth review by two leaders in the field.
21. Adams RH, et al.: Roles of ephrin B ligands and EphB receptors in cardiovascular development: demarcation of arterial/venous domains, vascular morphogenesis, and sprouting angiogenesis. Genes Dev 1999, 13:295-306.
22. Ranger AM, Grusby MJ, Hodge MR, Gravallese EM, de la Brousse FC, Hoey T, et al.: The transcription factor NF-ATc is essential for cardiac valve formation [comments]. Nature 1998, 392:186-190. This article is one of the first to define an endocardial-specific transcription factor and to demonstrate a developmental pathway preferentially required for a semilunar valve formation. These results were quite surpising given that before these experiments, NFATc was not even known to be expressed in the embryo.
23. de la Pompa JL, Timmerman LA, Takimoto H, Yoshida H, Elia AJ, Samper E, et al.: Role of the NF-ATc transcription factor in morphogenesis of cardiac valves and septum. Nature 1998, 12:182-186. This article appeared simultaneously with Ranger AM, et al. (Nature 1998, 392:186-190), and confirmed and collaborated the major findings observed. However, these investigators observed subtle abnormalities in mitral and tricuspid valve formation not documented by the previous researchers.
24. Brown CB, Boyer AS, Runyan RB, Barnett JV: Requirement of type III TGF- beta receptor for endocardial cell transformation in the heart. Science 1999, 283:2080-2082. This article represents an important breakthrough in our understanding of how valve formation is initiated. It provides a molecular marker for a subset of endocardial cells uniquely specified to form valve tissue.
25. Asahara T, et al.: Isolation of putative progenitor endothelial cells for angiogenesis. Science 1997, 275:964-967.
26. Shi O, et al.: Evidence for circulating bone marrow-derived endothelial cells. Blood 1998, 92:362-367. These authors present the first convincing data that indogenous roving endothelial progenitors reside within normal bone marrow and serve as a cell source for neovasculogenesis.
27. Takahashi T, et al.: Ischemia- and cytokine-induced mobilization of bone marrow-derived endothelial progenitor cells for neovascularization. Nat Med 1999, 5:434-438. This important article documents that endothelial progenitors can be artificially mobilized as potential therapeutic agents.
28. Isner JM, Asahara T: Angiogenesis and vasculogenesis as therapeutic strategies for postnatal neovascularization, J Clin Invest 1999, 103:1231-1236. This is an excellent review of several experiments that define the unique potential of the endothelial progenitor population of cells.
29. Makino S, et al.: Cardiomyocytes can be generated from marrow stromal cells in vitro. J Clin Invest 1999, 103:697-705. This authors of this landmark article document successful acquisition of one of the "holy grails" of cardiac development: an immortalized myocardial cell line.
30. Leiden JM: Beating the odds: a cardiomyocyte cell line at last. J Clin Invest 1999, 103:591-592.
31. Thomson JA, et al.: Embryonic stem cell lines derived from human blastocysts. Science 1998, 282:1145-1147. [published erratum appears in Science 1998, 282:1827.] This article documents the derivation of pluripotent stem cells from human blastocysts. It should serve as the foundation for new avenues of research that most likely will result in important therapeutic interventions. In addition, it will serve to stimulate significant ethical debate and challenges.
32. Shamblott MJ, et al.: Derivation of pluripotent stem cells from cultured human primordial germ cells. Proc Natl Acad Sci USA 1998. 95:13726-13731. As with Thomas JA et al. (Science 1998, 282:1145-1147), these investigators derived pluripotent stem cells but used a different cell source, namely primordial germ cells isolated from human fetal gonadal ridges. The potential and ethical challenges of these experiments with be a matter of much discussion and investigation over the next several years.
33. Keller G, Snodgrass HR: Human embryonic stem cells: the future is now. Nat Med 1999, 5:151-152.
34. Mason CA, et al.: Gene transfer in utero biologically engineers a patent ductus arteriosus in lambs by arresting fibroneclin-dependent neointimal formation. Nat Med 1999, 5: 176-182. This article presents an intriguing application of basic science observations used to direct gene therapy strategies.
35. Nabel EG: Gene therapy for cardiovascular diseases. J Nucl Cardiol 1999, 6:69-75.
36. Nabel EG: Delivering genes to the heart-right where it counts [comment]! Nat Med 1999, 5:141-142.
37. Schachtner SK, Buck CA, Baldwin HS: Intravascular delivery of adenovirus in utero during cardiovascular development. Gene Ther 1999, 6:1249-1257.
38. Schneider H, Coutelle C: In utero gene therapy: the case for. Nat Med 1999, 5:256-257. In this article, the authors present preliminary evidence that the cardiovascular system may be particularly susceptible to viral mediated gene therapy strategies.
39. Billings PR: In utero gene therapy: the case against. Nat Med 1999, 5:255-256.