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| Status |
Public on Sep 01, 2019 |
| Title |
Impairment of cardiac natriuretic peptide signaling develops the excessive cardiac hypertrophy during lactation period |
| Organism |
Mus musculus |
| Experiment type |
Expression profiling by array
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| Summary |
Two natriuretic peptides, atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) act through the common receptor, guanylyl cyclase-A (GC-A) to lower blood pressure, induce diuresis/natriuresis and dilate blood vessels. Recently, we discovered that the excessive cardiac hypertrophy accompanied with cardiac dysfunction was induced in the lactating natriuretic peptide receptor 1 (Npr1, which encodes GC-A)-deficient mice. To clarify the cause of lactation-induced cardic hypertrophy in Npr1-/-, we performed the gene expressions analysis using nulliparous (NP) or postpartum lactating wild-type (Npr1+/+) and Npr1-/- mice.
Numerous genes were altered in the postpartum lactating period both in Npr1+/+ and Npr1-/-. Additionally, the involvement of inflammatory responce in the cardiac hypertrophy in lactating-Npr1-/- mice was clarified bythe gene ontology analysis.
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| Overall design |
Gene expressions of female mice heart were examined in nulliparous (NP) and lactating (Lactation) Npr1+/+ and Npr1-/- mice. Four independent mice were utilized for analysis.
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| Contributor(s) |
Hasegawa T |
| Citation missing |
Has this study been published? Please login to update or notify GEO. |
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| Submission date |
Jul 22, 2016 |
| Last update date |
Sep 02, 2019 |
| Contact name |
Kentaro Otani |
| E-mail(s) |
otani@ri.ncvc.go.jp
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| Organization name |
National Cerebral and Cardiovascular Center Research Institute
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| Department |
Department of Regenerative Medicine and Tissue Engineering
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| Street address |
5-7-1 Fujishiro-dai
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| City |
Suita |
| ZIP/Postal code |
5658565 |
| Country |
Japan |
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| Platforms (1) |
| GPL10787 |
Agilent-028005 SurePrint G3 Mouse GE 8x60K Microarray (Probe Name version) |
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| Samples (16)
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| Relations |
| BioProject |
PRJNA330981 |
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