[10] Isolation and culture of whole postimplantation embryos and germ layer derivatives

Sturm, Karin S.; Tam, Patrick

doi:10.1016/0076-6879(93)25013-r

Cited by 108 publications

(76 citation statements)

References 23 publications

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“…For these studies, we used the mesodermal stem cell line QCE6, which in previous studies was shown to possess properties of a hematopoietic progenitor cell, as they will give rise to a broad range of differentiated hematopoietic cells when placed under conditions that promote blood differentiation (Eisenberg and Markwald, 1997;Brandon et al, 2000). In these more recent experiments, labeled QCE6 cells were injected into the yolk sac vessel leading to the sinus venous of ED 9 whole mouse embryos and allowed to develop for 24 hr ex ovo, according to previously established procedures (Sturm and Tam, 1993;Eto and Osumi-Yamashita, 1995). Subsequent analysis of these embryos showed individual labeled cells that integrated into the myocardium and expressed cardiac proteins (Fig.…”

Section: Does the Precardiac Mesoderm Uniquely Contribute To The Myocmentioning

confidence: 99%

“…ED9 mouse embryos were dissected from the uterus with fetal placenta and yolk sac intact and then injected into the yolk sac vessel leading to the sinus venous with QCE6 cells labeled with either a ␤-galactosidase-positive retrovirus (Eisenberg and Markwald, 1997) (A-C) or the fluorescent cell marker DiI (1,1Ј-dioctadecyl-3, 3,3Ј, 3Ј-tetramethyl-indocarbocyanine perchlorate) (D-F). The injected embryos were allowed to develop for 24 hr ex ovo, according to established procedures (Sturm and Tam, 1993;Eto and Osumi-Yamashita, 1995). A-C: QCE6 cells in the outer myocardial wall overlying the AV canal.…”

Section: Stem Cell Plasticity-implications For Heart Formation In Thementioning

confidence: 99%

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Stem cells and the formation of the myocardium in the vertebrate embryo

2003

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A major goal in cardiovascular biology is to repair diseased or damaged hearts with newly generated myocardial tissue. Stem cells offer a potential source of replacement myocytes for restoring cardiac function. Yet little is known about the nature of the cells that are able to generate myocardium and the conditions they require to form heart tissue. A source of information that may be pertinent to addressing these issues is the study of how the myocardium arises from progenitor cells in the early vertebrate embryo. Accordingly, this review will examine the initial events of cardiac developmental biology for insights into the identity and characteristics of the stem cells that can be used to generate myocardial tissue for therapeutic purposes. Anat Rec Part A 276A:2-12, 2004.

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Section: Does the Precardiac Mesoderm Uniquely Contribute To The Myocmentioning

confidence: 99%

Section: Stem Cell Plasticity-implications For Heart Formation In Thementioning

confidence: 99%

Stem cells and the formation of the myocardium in the vertebrate embryo

2003

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“…The parietal yolk sac was removed by using a pair of fine forceps and the visceral yolk sac was left intact. Embryos (2-5/bottle) were cultured in 5 ml of rat serum at 38°C in 30 rev/min rotation in the roller bottle system (Sturm and Tam, 1993;Wei et al, 2001;Zhao and Rivkees, 2001). Embryos were treated with vehicle or Y27632 (Calbiochem), a selective ROCK kinase inhibitor Iwamoto et al, 2000;Narumiya et al, 2000).…”

Section: Experimental Procedures Embryo and Heart Culturementioning

confidence: 99%

Rho‐associated kinases play an essential role in cardiac morphogenesis and cardiomyocyte proliferation

Zhao

Rivkees

2002

Developmental Dynamics

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Rho-associated coiled-coil kinases (ROCKs), initially identified as effectors for Rho GTPases, play a role in cardiac cell physiology and are also expressed in the developing heart. However, their role in cardiac development is not known. To investigate the role of these kinases in cardiac development, we examined cardiac development in cultured murine embryos treated with the ROCK inhibitor Y27632. After inhibition of ROCK activity, we found disturbed cardiac chamber formation and trabeculation. To further examine the mechanisms by which ROCK blockade causes cardiac hypoplasia, we assessed programmed cell death and cell proliferation in the hearts. We found decreased cell proliferation in the Y27632-treated hearts, but no changes in programmed cell death. We further observed that ROCK inhibition decreased cardiac myocyte proliferation, suggesting that ROCK kinases regulate cardiomyocyte division. To identify factors involved in ROCK action in regulation of cardiac cell division, we examined expression of cell cycle proteins by using Western blot analysis. We found that ROCK blockade decreased expression of cell cycle proteins, cyclin D3, CDK6, and p27 KIP1 in the hearts and cardiomyocytes, which are required for initiation of cell cycle and G1/S phase transition. These observations show that ROCK kinases play a role in cardiac development and that ROCK kinases regulate cardiac cell proliferation and cell cycle protein expression. Developmental Dynamics 226:24 -32, 2003.

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“…This approach was used as it provides a means to directly examine the effects of agents on intact embryos without potential confounding influences of the placenta or the dam (Sturm and Tam, 1993).…”

Section: Effects Of A1ar Activation On Heart Development In Vitromentioning

confidence: 99%

“…Embryos (E7.0 and E10.5) were cultured in the roller system as described by Sturm and Tam (1993). Briefly, embryos (E7.0 or E10.5; n ϭ 2-5/bottle) were cultured with 5 ml rat serum that was prepared as described by Hogan et al (1994) at 38°C for 24 -48 hr.…”

Section: Embryo Culturesmentioning

confidence: 99%

Inhibition of cell proliferation in the embryonic myocardium by A1 adenosine receptor activation

Zhao

Rivkees

2001

Developmental Dynamics

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A1 adenosine receptors (A1ARs) are expressed in the embryonic heart and influence cardiac function at early developmental stages. To test if A1ARs also affect cardiac structural development, we examined the effects of A1AR activation on heart formation. When pregnant mice were treated with the A1AR agonist, N 6 -cyclopentyladenosine (CPA), fetuses showed marked reduction of ventricular size and manifested features of heart failure. Suggesting that these findings represent direct effects on embryos, CPA treatment of cultured whole murine embryos resulted in cardiac hypoplasia. When rates of cell division and cell death in the heart were examined, we found decreases in cardiac cell proliferation following A1AR activation. In contrast, no changes in numbers or distribution of apoptotic cells were seen. Collectively, these data show that A1AR activation inhibits cardiac cell proliferation and can lead to cardiac hypoplasia. These data identify adenosine as a potential regulator of cardiac cell division during early development.

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[10] Isolation and culture of whole postimplantation embryos and germ layer derivatives

Cited by 108 publications

References 23 publications

Stem cells and the formation of the myocardium in the vertebrate embryo

Stem cells and the formation of the myocardium in the vertebrate embryo

Rho‐associated kinases play an essential role in cardiac morphogenesis and cardiomyocyte proliferation

Inhibition of cell proliferation in the embryonic myocardium by A1 adenosine receptor activation

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