Cardiac specific expression of the green fluorescent protein during early murine embryonic development

Fleischmann, Michaela; Bloch, Wilhelm; Kolossov, Eugen; Andressen, Christian; Müller, Mathias; Brem, Gottfried; Hescheler, Jürgen; Addicks, Klaus; Fleischmann, Bernd K.

doi:10.1016/s0014-5793(98)01476-8

Cited by 81 publications

(64 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Cell Preparation-Murine embryonic cardiomyocytes were obtained from superovulated mice of the HIM:OF1 strain as described (18,19). Spontaneously beating neonatal Sprague-Dawley rat cardiomyocytes were isolated and purified as reported earlier (20).…”

Section: Methodsmentioning

confidence: 99%

S100A1 Enhances the L-type Ca2+ Current in Embryonic Mouse and Neonatal Rat Ventricular Cardiomyocytes

Reppel

Sasse

Piekorz

et al. 2005

Journal of Biological Chemistry

View full text Add to dashboard Cite

S100A1 is an EF-hand type Ca2؉ -binding protein with a musclespecific expression pattern. The highest S100A1 protein levels are found in cardiomyocytes, and it is expressed already at day 8 in the heart during embryonic development. Since S100A1 is known to be involved in the regulation of Ca 2؉ homeostasis, we tested whether extracellular S100A1 plays a role in regulating the L-type Ca 2؉ current (I Ca ) in ventricular cardiomyocytes. Murine embryonic (day 16.5 postcoitum) ventricular cardiomyocytes were incubated with S100A1 (0.001-10 M) for different time periods (20 min to 48 h). I Ca density was found to be significantly increased as early as 20 min (from ؊10.8 ؎ 1 pA/pF, n ‫؍‬ 18, to ؊22.9 ؎ 1.4 pA/pF; ؉112.5 ؎ 13%, n ‫؍‬ 9, p < 0.001) after the addition of S100A1 (1 M). S100A1 also enhanced I Ca current density in neonatal rat cardiomyocytes. Fluorescence and capacitance measurements evidenced a fast translocation of rhodamine-coupled S100A1 from the extracellular space into cardiomyocytes. S100A1 treatment did not affect cAMP levels. However, protein kinase inhibitor, a blocker of cAMP-dependent protein kinase A (PKA), abolished the S100A1-induced enhancement of I Ca . Accordingly, measurements of PKA activity yielded a significant increase in S100A1-treated cardiomyocytes. In vitro reconstitution assays further demonstrated that S100A1 enhanced PKA activity. We conclude that the Ca 2؉ -binding protein S100A1 augments transsarcolemmal Ca 2؉ influx via an increase of PKA activity in ventricular cardiomyocytes and hence represents an important regulator of cardiac function.In 1965, Moore (1) described a novel protein "soluble in 100% saturated ammonium sulfate solution" and therefore denoted it S100 protein. Today 21 different S100 proteins belonging to a multigene family of Ca 2ϩ -binding proteins of the EF-hand type are known to be differentially expressed in a large number of cell types (2). S100A1 is found in the cytosol, displays highest expression levels in the heart (3), and is already expressed at day 8 postcoitum in embryonic mouse hearts (4). Although the physiological relevance of S100 proteins in healthy tissue is still unclear, several findings point to a role of S100A1 in the diseased heart, since it is up-regulated during the course of myocardial hypertrophy (5) and markedly down-regulated in the left ventricle of patients with end stage heart failure (6). Recently, S100A1 was identified as a novel regulator of cardiac function based on the observation that overexpression of S100A1 led to a significant increase of contractility in adult cardiomyocytes (7). This was found to be related to an increased sarcoplasmic reticulum Ca 2ϩ -ATPase (8) and ryanodine receptor 2 activity (9) as well as to a decrease in myofilamental Ca 2ϩ sensitivity (8) and might be explained by enhancement of PKA 3 activity. The physiological relevance of S100A1 is further supported by data of Du and co-workers (10), who identified S100A1 as a regulator of cardiac reserve in a S100A1 mouse knock-out model. Accordingly, ...

show abstract

Section: Methodsmentioning

confidence: 99%

S100A1 Enhances the L-type Ca2+ Current in Embryonic Mouse and Neonatal Rat Ventricular Cardiomyocytes

Reppel

Sasse

Piekorz

et al. 2005

Journal of Biological Chemistry

View full text Add to dashboard Cite

show abstract

“…For harvesting embryonic cardiomyocytes from murine atria, mice of the strain HIM:OF1 were bred using superovulation for precise staging (33). For isolation of early-and late-stage cardiomyocytes, E10.5-E12.5 and E16.5-E18.5 embryos were used, respectively.…”

Section: Methodsmentioning

confidence: 99%

Differential subunit composition of the G protein–activated inward-rectifier potassium channel during cardiac development

Fleischmann¹,

Duan²,

Fan³

et al. 2004

J. Clin. Invest.

View full text Add to dashboard Cite

“…Murine embryos (E11.5 to E12.5) were obtained from Anxa7 Ϫ/Ϫ and control mice by using standard superovulation protocols (12). Embryonic hearts were dissected and enzymatically digested as described before (20).…”

Section: Methodsmentioning

confidence: 99%

Loss of Annexin A7 Leads to Alterations in Frequency-Induced Shortening of Isolated Murine Cardiomyocytes

Herr¹,

Smyth²,

Ullrich³

et al. 2001

Molecular and Cellular Biology

View full text Add to dashboard Cite

Annexin A7 has been proposed to function in the fusion of vesicles, acting as a Ca 2؉ channel and as Ca 2؉ -activated GTPase, thus inducing Ca 2؉ /GTP-dependent secretory events. To understand the function of annexin A7, we have performed targeted disruption of the Anxa7 gene in mice. Matings between heterozygous mice produced offspring showing a normal Mendelian pattern of inheritance, indicating that the loss of annexin A7 did not interfere with viability in utero. Mice lacking annexin A7 showed no obvious phenotype and were fertile. To assay for exocytosis, insulin secretion from isolated islets of Langerhans was examined. Ca 2؉ -induced and cyclic AMP-mediated potentiation of insulin secretion was unchanged in the absence of annexin A7, suggesting that it is not directly implicated in vesicle fusion. Ca 2؉ regulation studied in isolated cardiomyocytes, showed that while cells from early embryos displayed intact Ca 2؉ homeostasis and expressed all of the components required for excitation-contraction coupling, cardiomyocytes from adult Anxa7 ؊/؊ mice exhibited an altered cell shortening-frequency relationship when stimulated with high frequencies. This suggests a function for annexin A7 in electromechanical coupling, probably through Ca 2؉ homoeostasis.

show abstract

Cardiac specific expression of the green fluorescent protein during early murine embryonic development

Cited by 81 publications

References 24 publications

S100A1 Enhances the L-type Ca2+ Current in Embryonic Mouse and Neonatal Rat Ventricular Cardiomyocytes

S100A1 Enhances the L-type Ca2+ Current in Embryonic Mouse and Neonatal Rat Ventricular Cardiomyocytes

Differential subunit composition of the G protein–activated inward-rectifier potassium channel during cardiac development

Loss of Annexin A7 Leads to Alterations in Frequency-Induced Shortening of Isolated Murine Cardiomyocytes

Contact Info

Product

Resources

About