Onset of expression and regional deposition of alpha‐smooth and sarcomeric actin during avian heart development

Sugi, Yukiko; Lough, John

doi:10.1002/aja.1001930203

Cited by 57 publications

(44 citation statements)

References 24 publications

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“…All four muscle actins can incorporate into the thin filaments of cultured adult rat cardiomyocytes (41), and vascular smooth muscle ␣-actin is normally present in the sarcomeres of the developing heart (15,17). Similarly, both vascular smooth muscle and skeletal muscle ␣-actins can be detected in myofibrils (Fig.…”

Section: Discussionmentioning

confidence: 99%

“…There is coexpression of cardiac and skeletal ␣-actin genes in the developing heart of chicken (4,11), mouse (12,13), rat (8), and human (9). Moreover, transient expression of the vascular smooth muscle ␣-actin gene is observed during early cardiogenesis in Xenopus (14), chicken (11,15), mouse (16), and rat (17,18). In contrast, the enteric smooth muscle ␥-actin (SMGA) gene is not expressed in the myocardium at any stage (8,16,17).…”

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confidence: 99%

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Rescue of cardiac α-actin-deficient mice by enteric smooth muscle γ-actin

Kumar

Crawford

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

176

166

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The muscle actins in higher vertebrates display highly conserved amino acid sequences, yet they show distinct expression patterns. Thus, cardiac ␣-actin, skeletal ␣-actin, vascular smooth muscle ␣-actin, and enteric smooth muscle ␥-actin comprise the major actins in their respective tissues. To assess the functional and developmental significance of cardiac ␣-actin, the murine (129͞SvJ) cardiac ␣-actin gene was disrupted by homologous recombination. The majority (Ϸ56%) of the mice lacking cardiac ␣-actin do not survive to term, and the remainder generally die within 2 weeks of birth. Increased expression of vascular smooth muscle and skeletal ␣-actins is observed in the hearts of newborn homozygous mutants and also heterozygotes but apparently is insufficient to maintain myofibrillar integrity in the homozygous mutants. Mice lacking cardiac ␣-actin can be rescued to adulthood by the ectopic expression of enteric smooth muscle ␥-actin using the cardiac ␣-myosin heavy chain promoter. However, the hearts of such rescued cardiac ␣-actin-deficient mice are extremely hypodynamic, considerably enlarged, and hypertrophied. Furthermore, the transgenically expressed enteric smooth muscle ␥-actin reduces cardiac contractility in wild-type and heterozygous mice. These results demonstrate that alterations in actin composition in the fetal and adult heart are associated with severe structural and functional perturbations.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Rescue of cardiac α-actin-deficient mice by enteric smooth muscle γ-actin

Kumar

Crawford

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

176

166

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“…Is terminal cardiogenesis completely halted in the absence of anterior endoderm, or is the process merely slowed? Although no above-background fluorescence was detected in these explants, it must nonetheless be considered these explants express cardiogenic traits that are below the level of detection by immunostaining for the sarcomeric actins, which appear relatively late in the cardiogenic sequence in vivo (Sugi and Lough, 1992). This question could be resolved by immunostaining for markers that appear earlier in the cardiogenic sequence, such as ventricular myosin heavy chain 1 (Bisaha and Bader, 1991) or sarcomeric myosin heavy chain (Han et al, 1992).…”

Section: Discussionmentioning

confidence: 99%

“…When cultured in isolation without supplements, mesoderm explants do not survive, up to 4 days (Sugi and Lough, unpublished results.) Explants were observed daily for contractility; expression of sarcomeric alpha-actin, which appears in the early myocardium at stage 9 (Sugi and Lough, 1992), was assessed after 4 days in culture. Figure 1 depicts the results of experiments in which contiguous germ layers of anterior endoderm/mesoderm (Fig.…”

Section: Resultsmentioning

confidence: 99%

Anterior endoderm is a specific effector of terminal cardiac myocyte differentiation of cells from the embryonic heart forming region

Sugi

Lough

1994

Developmental Dynamics

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135

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The ability of anterior lateral plate mesoderm cells in the heart-forming region (HFR) of stage 6 chicken embryos to respond to cardiogenic stimuli from cells in adjacent germ layers has been investigated using explants cultured under defined conditions. Two types of explantation were evaluated: those in which two germ layers were explanted in contiguity, and those in which germ layers were isolated and cocultured. Two parameters-contractility and expression of sarcomeric alpha-actin-were monitored to evaluate the terminal differentiation of cardiac myocytes. Contiguously explanted anterior endoderm/mesoderm became multilayered and underwent terminal differentiation within 2 days. By contrast, although contiguous anterior ectoderm/mesoderm or posterior endoderm/mesoderm co-explants also became multilayered, these explants did not differentiate, up to 5 days. To ascertain the cardiogenic potential of cells from different regions of the embryo, individual germ layers were isolated and co-cultured by placing the explants in separate areas of the culture chamber. These determinations demonstrated that anterior, but not posterior, endoderm effected differentiation of anterior mesoderm. As before, mesoderm in both types of co-culture survived and became multilayered; by contrast, mesoderm did not survive when cultured in isolation. These experiments provide evidence that anterior endoderm regulates the terminal differentiation, as opposed to growth, of presumptive cardiac myocytes in mesoderm cells from the anterior lateral plate. Finally, anterior endoderm was co-cultured with mesoderm from the posterior half of the embryo, which does not contain an HFR. The failure of these co-cultured explants to differentiate infers that pre-cardiac myoblasts in stage 6 anterior mesoderm are previously specified to respond to the terminal cardiogenic effects of endoderm.0 1994 Wiley-Liss, Inc.

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“…Stages of embryonic development were determined using the criteria of Hamburger and Hamilton (1951). Embryos were fixed by cryopreservation (Kitten et al, 1987) to preserve antigenicity; details of this procedure are provided in a previous communication (Sugi and Lough, 1992). Alternatively, where indicated, 4% paraformaldehyde in phosphate buffered saline (pH 7.4) was used for fixation.…”

Section: Experimental Procedures Embryos Fixation and Embeddingmentioning

confidence: 99%

Developmental expression of fibroblast growth factor receptor‐1 (cek‐1; flg) during heart development

Sugi

Sasse

Barron

et al. 1995

Developmental Dynamics

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Previous work in this laboratory has indicated that fibroblast growth factor-2 (FGF-2; bFGF) regulates the initial stages of avian heart development in paracrine and autocrine fashion (Parlow et al. [19911 Dev. Biol. 146:139-147; Sugi et al. [19931 Dev. Biol. 157:28-37). Because these findings inferred the presence of a functional receptor for fibroblast growth factor (FGFR), we have immunochemically assessed the appearance of FGFR-1 (cek-I; flg) during development. Using a peptide-generated antibody, Western blots of total embryonic proteins revealed that FGFR-1 was barely detectable at pre-heart stages, followed by sequential increases in relative abundance that peaked at stage 24, followed by a decline at days 7-14. Western blots of proteins from isolated embryonic hearts demonstrated a similar developmental pattern, except that FGFR-1 expression was not decreased at later stages. The presence of FGFR-1 mRNA was verified by reverse transcriptiodpolymerase chain reaction (RT/PCR) amplification. Immunohistochemical examination revealed punctate deposits of FGFR-1 in the precardiac endoderm at stage 6, followed by detection in the endoderm, foregut, and pre-cardiac splanchnic mesoderm at stage 8 and in the newly formed myocardium at the heart tube stage (9/10). By stage 13, FGFR-1 staining was observed only in the myocardium, a pattern which persisted at least until stage 30 (day 7), after which only isolated hearts were examined. After stage 30, staining was diminished in the ventricle, but not in the atrium. Staining of cardiac endothelial cells was not observed at any stage. A functional role for FGFR-1 was indicated by experiments in which anti-FGFR-1, but not pre-absorbed antiserum, retarded proliferation and multilayering of cardiogenie cells in an in vitro model of cardiac morphogenesis.

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Onset of expression and regional deposition of alpha‐smooth and sarcomeric actin during avian heart development

Cited by 57 publications

References 24 publications

Rescue of cardiac α-actin-deficient mice by enteric smooth muscle γ-actin

Rescue of cardiac α-actin-deficient mice by enteric smooth muscle γ-actin

Anterior endoderm is a specific effector of terminal cardiac myocyte differentiation of cells from the embryonic heart forming region

Developmental expression of fibroblast growth factor receptor‐1 (cek‐1; flg) during heart development

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