ArticlePloS one2018
Rats deficient C-type natriuretic peptide suffer from impaired skeletal growth without early death.
Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
- Physiological and Pathophysiological Effects of C-Type Natriuretic Peptide on the Heart.Biology · 2022Review
- Molecular Mechanism of Induction of Bone Growth by the C-Type Natriuretic Peptide.International journal of molecular sciences · 2022Review
- The Natriuretic Peptides for Hypertension Treatment.High blood pressure & cardiovascular prevention : the official journal of the Italian Society of Hypertension · 2022Review
- Rat models of human diseases and related phenotypes: a systematic inventory of the causative genes.Journal of biomedical science · 2020Review
- Is C-type natriuretic peptide regulated by a feedback loop? A study on systemic and local autoregulatory effect.PloS one · 2020Article
- Exogenous C-type natriuretic peptide therapy for impaired skeletal growth in a murine model of glucocorticoid treatment.Scientific reports · 2019Article
- Translational science: Newly emerging science in biology and medicine - Lessons from translational research on the natriuretic peptide family and leptin.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2019Review
- Safety assessment of a novel C-type natriuretic peptide derivative and the mechanism of bone- and cartilage-specific toxicity.PloS one · 2019Article
- Article
- Exogenous C-type natriuretic peptide restores normal growth and prevents early growth plate closure in its deficient rats.PloS one · 2018Article
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Authors and funding
22 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have previously investigated the physiological role of C-type natriuretic peptide (CNP) on endochondral bone growth, mainly with mutant mouse models deficient in CNP, and reported that CNP is indispensable for physiological endochondral bone growth in mice. However, the survival rate of CNP knockout (KO) mice fell to as low as about 70% until 10 weeks after birth, and we could not sufficiently analyze the phenotype at the adult stage. Herein, we generated CNP KO rats by using zinc-finger nuclease-mediated genome editing technology. We established two lines of mutant rats completely deficient in CNP (CNP KO rats) that exhibited a phenotype identical to that observed in mice deficient in CNP, namely, a short stature with severely impaired endochondral bone growth. Histological analysis revealed that the width of the growth plate, especially that of the hypertrophic chondrocyte layer, was markedly lower and the proliferation of growth plate chondrocytes tended to be reduced in CNP KO rats. Notably, CNP KO rats did not have malocclusions and survived for over one year after birth. At 33 weeks of age, CNP KO rats persisted significantly shorter than wild-type rats, with closed growth plates of the femur in all samples, which were not observed in wild-type rats. Histologically, CNP deficiency affected only bones among all body tissues studied. Thus, CNP KO rats survive over one year, and exhibit a deficit in endochondral bone growth and growth retardation throughout life.
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