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Updated: May 5, 2026
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Published on: May 24, 2024
Prdm6 is essential for cardiovascular development in vivo
Andreas Gewies1, Mercedes Castineiras-Vilarino, Uta Ferch
1Institut für Klinische Chemie und Pathobiochemie, Klinikum Rechts der Isar, Technische Universität München, Munich, Germany ; German Cancer Consortium (DKTK), Heidelberg, Germany ; German Cancer Research Center (DKFZ), Heidelberg, Germany ; Laboratory of Signaling in the Immune System, Helmholtz Zentrum München, German Research Center for Environmental Health, Neuherberg, Germany.
Insights
Prdm6 is essential for cardiovascular development. Its absence causes embryonic lethality due to vascular defects, and conditional loss in smooth muscle cells leads to perinatal lethality from lung hemorrhage.
Area of Science:
- Developmental Biology
- Cardiovascular Research
- Genetics
Background:
- The PRDM protein family is crucial for embryonic development.
- Previous studies suggested Prdm6 plays a role in vascular cells.
Purpose of the Study:
- To investigate the physiological functions of Prdm6 in cardiovascular development.
- To determine the consequences of Prdm6 deficiency in vivo.
Main Methods:
- Generation of conditional Prdm6-deficient mice.
- Analysis of cardiovascular development in Prdm6-deficient embryos.
- Conditional deletion of Prdm6 in smooth muscle cells using SM22-Cre.
Main Results:
- Complete Prdm6 deletion caused embryonic lethality with cardiovascular defects and vascular patterning aberrations.
- Smooth muscle cell differentiation and proliferation were normal in Prdm6-deficient embryonic stem cells and embryos.
- Conditional Prdm6 deletion in smooth muscle cells led to perinatal lethality due to lung hemorrhage.
Conclusions:
- Prdm6 is essential for the physiological control of cardiovascular development.
- Prdm6 plays a critical role in vascular integrity and function.
- Specific roles of Prdm6 in smooth muscle cells are vital for perinatal survival.
Abstract:
Members of the PRDM protein family have been shown to play important roles during embryonic development. Previous in vitro and in situ analyses indicated a function of Prdm6 in cells of the vascular system. To reveal physiological functions of Prdm6, we generated conditional Prdm6-deficient mice. Complete deletion of Prdm6 results in embryonic lethality due to cardiovascular defects associated with aberrations in vascular patterning. However, smooth muscle cells could be regularly differentiated from Prdm6-deficient embryonic stem cells and vascular smooth muscle cells were present and proliferated normally in Prdm6-deficient embryos. Conditional deletion of Prdm6 in the smooth muscle cell lineage using a SM22-Cre driver line resulted in perinatal lethality due to hemorrhage in the lungs. We thus identified Prdm6 as a factor that is essential for the physiological control of cardiovascular development.
