What is the clinical evidence from this study?

Study design: Other. Population: Heart development and function. Intervention: Targeted deletion of Ncx1 gene vs. Normal littermates. Primary outcome: Heartbeat and myofibrillar organization.

What question did this study set out to answer?

To determine the functional and structural role of the sodium-calcium exchanger (Ncx1) during mammalian cardiac development and excitation-contraction coupling.

March 12, 2001The FASEB Journal

Targeted inactivation of the sodium‐calcium exchanger (Ncx1) results in the lack of a heartbeat and abnormal myofibrillar organization

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Key result

Targeted deletion of the Ncx1 gene in mice resulted in embryos that lacked a spontaneously beating heart and had a complete lack of organized myofibrils and Z-lines compared with normal littermates.

Why the study?

Does targeted deletion of Ncx1 affect heart development and function in mouse embryos?

Population

Mouse embryos

Comparison

Targeted inactivation/deletion of the… vs Normal littermates

Design

Preclinical

Follow-up

up to 11.0 days postcoitum

Authors

SKSrinagesh V. KoushikNational Institutes of Health JWJian WangShanghai University RRRhonda RogersMichigan Department of Environment, Great Lakes, and Energy

Discussion

Member takes

Implication

Ncx1 is required for mouse embryonic cardiac function; leaves open its role in human cardiogenesis and congenital disease.

Key Points

To determine the functional and structural role of the sodium-calcium exchanger (Ncx1) during mammalian cardiac development and excitation-contraction coupling.
Generated an Ncx1 gene deletion model in mice via targeted gene knockout.
Assessed embryonic survival, spontaneous cardiac contractions, and organogenesis up to 11.0 days postcoitum.
Evaluated intracellular calcium transients upon electrical stimulation and cardiomyocyte ultrastructure using electron microscopy.
Ncx1-null mouse embryos survived up to 11.0 days postcoitum with growth retardation, exhibited relatively normal heart morphogenesis, but completely lacked a spontaneous heartbeat.
Cardiomyocytes from Ncx1-null embryos generated relatively normal transient Ca2+ signals during electrical stimulation, showing preserved intracellular Ca2+ regulation.
Ultrastructural examination revealed a total absence of organized myofibrils and Z-lines in Ncx1-deficient cardiomyocytes compared to normal littermates.

Structured PICO

Does targeted deletion of Ncx1 affect heart development and function in mouse embryos?

Population

Mouse embryos

Intervention

Targeted inactivation/deletion of the sodium-calcium exchanger (Ncx1) gene

Comparator

Normal littermates

Outcome

Heartbeat presence, heart morphogenesis, Ca2+ signals, and myofibrillar organizationsurrogate

The sodium-calcium exchanger (Ncx1) is essential for normal cardiomyocyte development, myofibrillar organization, and heartbeat in mice.

Cite This Study

Koushik et al. (2001) studied Heart development and function. Targeted deletion of Ncx1 gene vs. Normal littermates was evaluated on Heartbeat and myofibrillar organization. Targeted deletion of the Ncx1 gene in mice resulted in embryos that lacked a spontaneously beating heart and had a complete lack of organized myofibrils and Z-lines compared with normal littermates.

synapsesocial.com/papers/6a0ea12106ecbe833447a20d https://doi.org/10.1096/fj.00-0696fje

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Targeted inactivation of the sodium‐calcium exchanger (Ncx1) results in the lack of a heartbeat and abnormal myofibrillar organization

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Targeted inactivation of the sodium‐calcium exchanger (Ncx1) results in the lack of a heartbeat and abnormal myofibrillar organization

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Also Consider

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