PKCδ deficiency inhibits fetal development and is associated with heart elastic fiber hyperplasia and lung inflammation in adult PKCδ knockout mice

التفاصيل البيبلوغرافية
العنوان: PKCδ deficiency inhibits fetal development and is associated with heart elastic fiber hyperplasia and lung inflammation in adult PKCδ knockout mice
المؤلفون: Hiroaki Kanda, Tomio Ono, Ikuo Kawashima, Yoshinobu Iguchi, Kiyotsugu Yoshida, Kiyoshi Ogura, Kaoru Mita-Yoshida, Kenji Sakimura, Yuko S. Niino, Satomi Yogosawa, Seiji Shioda, Takaya Gotoh, Maya Yamazaki
المصدر: PLoS ONE
PLoS ONE, Vol 16, Iss 7, p e0253912 (2021)
بيانات النشر: Public Library of Science, 2021.
سنة النشر: 2021
مصطلحات موضوعية: 0301 basic medicine, Male, Embryology, Physiology, Artificial Gene Amplification and Extension, Gene mutation, Polymerase Chain Reaction, Fetal Development, Mice, 0302 clinical medicine, Medicine and Health Sciences, Lung, Mice, Knockout, Multidisciplinary, Mammalian Genomics, Genetically Modified Organisms, Embryo, Heart, Animal Models, Genomics, Protein Kinase C-delta, Experimental Organism Systems, 030220 oncology & carcinogenesis, Knockout mouse, Medicine, Engineering and Technology, Female, medicine.symptom, Anatomy, Genetic Engineering, Research Article, Biotechnology, medicine.medical_specialty, Science, Inflammation, Mouse Models, Bioengineering, Biology, Research and Analysis Methods, Calcification, 03 medical and health sciences, Model Organisms, Internal medicine, medicine, Genetics, Animals, Humans, Protein kinase A, Molecular Biology Techniques, Molecular Biology, Fetus, Fetuses, Hyperplasia, Genetically Modified Animals, Alternative splicing, Embryos, Biology and Life Sciences, Pneumonia, Elastic Tissue, Disease Models, Animal, 030104 developmental biology, Endocrinology, Apoptosis, Animal Genomics, Animal Studies, Cardiovascular Anatomy, Physiological Processes, Developmental Biology
الوصف: Protein kinase C-delta (PKCδ) has a caspase-3 recognition sequence in its structure, suggesting its involvement in apoptosis. In addition, PKCδ was recently reported to function as an anti-cancer factor. The generation of a PKCδ knockout mouse model indicated that PKCδ plays a role in B cell homeostasis. However, the Pkcrd gene, which is regulated through complex transcription, produces multiple proteins via alternative splicing. Since gene mutations can result in the loss of function of molecular species required for each tissue, in the present study, conditional PKCδ knockout mice lacking PKCδI, II, IV, V, VI, and VII were generated to enable tissue-specific deletion of PKCδ using a suitable Cre mouse. We generated PKCδ-null mice that lacked whole-body expression of PKCδ. PKCδ+/- parental mice gave birth to only 3.4% PKCδ-/- offsprings that deviated significantly from the expected Mendelian ratio (χ2(2) = 101.7, P < 0.001). Examination of mice on embryonic day 11.5 (E11.5) showed the proportion of PKCδ-/- mice implanted in the uterus in accordance with Mendelian rules; however, approximately 70% of the fetuses did not survive at E11.5. PKCδ-/- mice that survived until adulthood showed enlarged spleens, with some having cardiac and pulmonary abnormalities. Our findings suggest that the lack of PKCδ may have harmful effects on fetal development, and heart and lung functions after birth. Furthermore, our study provides a reference for future studies on PKCδ deficient mice that would elucidate the effects of the multiple protein variants in mice and decipher the roles of PKCδ in various diseases.
اللغة: English
تدمد: 1932-6203
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::fa1a15be62dbb404bd4e556468975a72Test
http://europepmc.org/articles/PMC8248728Test
حقوق: OPEN
رقم الانضمام: edsair.doi.dedup.....fa1a15be62dbb404bd4e556468975a72
قاعدة البيانات: OpenAIRE