Localization of bFGF-like proteins as punctate inclusions in the preseptation myocardium of the chicken embryo

Parlow, M.; Bolender, David L.; Kokan-Moore, Nighat P.; Lough, John

doi:10.1016/0012-1606(91)90454-b

Cited by 69 publications

(55 citation statements)

References 26 publications

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“…mechanism is consistent with our observations that stage 6 endoderm cells, which potently effect the terminal differentiation of pre-cardiac cells (Sugi and Lough, 19941, contain FGF-like proteins (Parlow et al, 1991); in addition, we have observed that physiologic stage 30 day 7 levels (0.5-50 ng/ml) of FGF-2 can support the differentiation of pre-cardiac myocytes in vitro (Sugi and Lough, manuscript in preparation). In response to paracrine signalling, it is proposed that step 2-the synthesis of an autocrine supply of FGF-2-is initiated to support the differentiation and proliferation of cardiac myocytes in the developing heart.…”

Section: Discussionsupporting

confidence: 91%

“…In response to paracrine signalling, it is proposed that step 2-the synthesis of an autocrine supply of FGF-2-is initiated to support the differentiation and proliferation of cardiac myocytes in the developing heart. The existence of an autocrine FGF loop in the developing heart is indicated by the abrupt appearance of FGF-like protein at the heart tube stage (st. 10; Parlow et al, 1991) and by observations that myocardial cell proliferation and contractility are inhibited by antisense OdN-mediated inhibition of FGF-2 synthesis (Sugi et al, 1993).…”

Section: Discussionmentioning

confidence: 99%

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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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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

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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“…proteins in anterior endoderm at stage 5t6 during chicken embryogenesis (Parlow et al, 1991). More recently, we determined that physiologic concentrations (< 5 ng/ml) of purified activin-A or FGF-2 mimic the cardiogenic effects of endoderm on cultured anterior lateral plate mesoderm (Sugi and Lough, manuscript in preparation).…”

Section: Discussionmentioning

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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“…FGF (13)(14)(15)(16) and the FGF receptor (FGFR) (17,18) are expressed at high levels early in cardiogenesis and exhibit a later decline as mitotic indices of the myocytes fall off (13,19). To examine the role of FGF signaling during chicken cardiogenesis in vivo, we have constructed replication-defective retroviral expression vectors capable of altering (i) levels of FGFR or (ii) the functional properties of its receptor.…”

mentioning

confidence: 99%

Fibroblast growth factor receptor is required for in vivo cardiac myocyte proliferation at early embryonic stages of heart development.

Mima

Ueno

Fischman

et al. 1995

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

171

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In In bird embryos, cardiac myocytes are derived from mesoderm lateral to Hensen's node (1, 2). Soon after gastrulation starts, these cells become committed to a myocyte lineage (3), begin to express muscle-specific genes (4, 5), and exhibit rhythmic contractile activity several hours later (Hamburger-Hamilton stage 10) (6, 7). The functioning myocytes proliferate actively early in development, but mitotic activity decreases later in embryogenesis and is completely lost after birth (8 MATERIALS AND METHODSRetroviral Vectors. The retroviruses used for the present study are replication-defective variants based on the spleen necrosis virus (26). Although the truncated FGFR1 inhibits FGF signaling (23)(24)(25), neither the population of dimeric receptors containing recombinant FGFR1 nor the level of FGFR1 mRNA can be monitored in individual cells in vivo. To identify cells expressing viral transgenes, the vectors were designed to coexpress the bacterial ,B-galactosidase (13-gal) gene lacZ and the FGFR1 sequence (Fig. 1). To equivalently express both FGFR1 and ,B-gal from dicistronic messages, the vector contained an internal ribosome entry sequence (IRES) derived from the 5' noncoding region of the encephalomyocarditis virus genome (28) between the FGFR1 and lacZ genes. An Xba I-Nco I fragment of pLZIC2 (29) encoding an IRES was inserted into pCXLp-(30); this was designated pCXIL. The Xba I-Sst I fragment of pCXIL encoding the IRES and 5' lacZ and a Sst I-Sal I fragment of pMC1871 (Pharmacia) were coligated into pSN(31) and designated pSNIZ. After removal of the poly(A) signal from FGFR1, full-length and truncated FGFR1 of pSVcFR and pSVcTR (23) were transferred into the Xba I site of pSNIZ, and these vectors were designated pSNFRIZ and pSNAFRIZ, respectively. The construct encoding AFGFR1 in antisense orientation has been termed pSNaFRIZ. By using a packaging cell line, D17.2G, we generated replication-defective virions as described (27). Viral propagation, proof of helper virus-free stocks, and the evidence for clonality in studies of myocardial development have Abbreviations: FGF, fibroblast growth factor; FGFR, FGF receptor;

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Localization of bFGF-like proteins as punctate inclusions in the preseptation myocardium of the chicken embryo

Cited by 69 publications

References 26 publications

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

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

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

Fibroblast growth factor receptor is required for in vivo cardiac myocyte proliferation at early embryonic stages of heart development.

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