PKCδ deficiency inhibits fetal development and is associated with heart elastic fiber hyperplasia and lung inflammation in adult PKCδ knockout mice
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 homeost...
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| creator | Niino, Yuko S. Kawashima, Ikuo Iguchi, Yoshinobu Kanda, Hiroaki Ogura, Kiyoshi Mita-Yoshida, Kaoru Ono, Tomio Yamazaki, Maya Sakimura, Kenji Yogosawa, Satomi Yoshida, Kiyotsugu Shioda, Seiji Gotoh, Takaya |
| description | 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. |
| doi_str_mv | 10.1371/journal.pone.0253912 |
| format | Article |
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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.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0253912</identifier><identifier>PMID: 34197550</identifier><language>eng</language><publisher>San Francisco: Public Library of Science</publisher><subject>Abnormalities ; Alternative splicing ; Apoptosis ; Artificial chromosomes ; Biochemistry ; Biology and Life Sciences ; Birth ; Brain research ; Caspase-3 ; Cell growth ; Embryos ; Engineering and Technology ; Fetuses ; Genetic testing ; Genomes ; Homeostasis ; Hyperplasia ; Inflammation ; Kinases ; Laboratories ; Lungs ; Medicine ; Medicine and Health Sciences ; Mutation ; Neurobiology ; Neurosciences ; Polymerase chain reaction ; Protein kinase C ; Proteins ; Research and Analysis Methods ; Respiratory function ; Signal transduction ; Transcription ; Uterus</subject><ispartof>PloS one, 2021-07, Vol.16 (7), p.e0253912-e0253912</ispartof><rights>2021 Niino et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2021 Niino et al 2021 Niino et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c503t-ce511509daf7867a2ea20825c594a25af5dcfeee2910fb89d13c2bad5ceac2393</citedby><cites>FETCH-LOGICAL-c503t-ce511509daf7867a2ea20825c594a25af5dcfeee2910fb89d13c2bad5ceac2393</cites><orcidid>0000-0001-5270-8658</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8248728/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8248728/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,724,777,781,861,882,2096,2915,23847,27905,27906,53772,53774,79349,79350</link.rule.ids></links><search><contributor>Fraidenraich, Diego</contributor><creatorcontrib>Niino, Yuko S.</creatorcontrib><creatorcontrib>Kawashima, Ikuo</creatorcontrib><creatorcontrib>Iguchi, Yoshinobu</creatorcontrib><creatorcontrib>Kanda, Hiroaki</creatorcontrib><creatorcontrib>Ogura, Kiyoshi</creatorcontrib><creatorcontrib>Mita-Yoshida, Kaoru</creatorcontrib><creatorcontrib>Ono, Tomio</creatorcontrib><creatorcontrib>Yamazaki, Maya</creatorcontrib><creatorcontrib>Sakimura, Kenji</creatorcontrib><creatorcontrib>Yogosawa, Satomi</creatorcontrib><creatorcontrib>Yoshida, Kiyotsugu</creatorcontrib><creatorcontrib>Shioda, Seiji</creatorcontrib><creatorcontrib>Gotoh, Takaya</creatorcontrib><title>PKCδ deficiency inhibits fetal development and is associated with heart elastic fiber hyperplasia and lung inflammation in adult PKCδ knockout mice</title><title>PloS one</title><description>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.</description><subject>Abnormalities</subject><subject>Alternative splicing</subject><subject>Apoptosis</subject><subject>Artificial chromosomes</subject><subject>Biochemistry</subject><subject>Biology and Life Sciences</subject><subject>Birth</subject><subject>Brain research</subject><subject>Caspase-3</subject><subject>Cell growth</subject><subject>Embryos</subject><subject>Engineering and Technology</subject><subject>Fetuses</subject><subject>Genetic testing</subject><subject>Genomes</subject><subject>Homeostasis</subject><subject>Hyperplasia</subject><subject>Inflammation</subject><subject>Kinases</subject><subject>Laboratories</subject><subject>Lungs</subject><subject>Medicine</subject><subject>Medicine and Health 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Tomio</au><au>Yamazaki, Maya</au><au>Sakimura, Kenji</au><au>Yogosawa, Satomi</au><au>Yoshida, Kiyotsugu</au><au>Shioda, Seiji</au><au>Gotoh, Takaya</au><au>Fraidenraich, Diego</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>PKCδ deficiency inhibits fetal development and is associated with heart elastic fiber hyperplasia and lung inflammation in adult PKCδ knockout mice</atitle><jtitle>PloS one</jtitle><date>2021-07-01</date><risdate>2021</risdate><volume>16</volume><issue>7</issue><spage>e0253912</spage><epage>e0253912</epage><pages>e0253912-e0253912</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>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.</abstract><cop>San Francisco</cop><pub>Public Library of Science</pub><pmid>34197550</pmid><doi>10.1371/journal.pone.0253912</doi><orcidid>https://orcid.org/0000-0001-5270-8658</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | PloS one, 2021-07, Vol.16 (7), p.e0253912-e0253912 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_2547542148 |
| source | DOAJ Directory of Open Access Journals; Public Library of Science (PLoS); EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Abnormalities Alternative splicing Apoptosis Artificial chromosomes Biochemistry Biology and Life Sciences Birth Brain research Caspase-3 Cell growth Embryos Engineering and Technology Fetuses Genetic testing Genomes Homeostasis Hyperplasia Inflammation Kinases Laboratories Lungs Medicine Medicine and Health Sciences Mutation Neurobiology Neurosciences Polymerase chain reaction Protein kinase C Proteins Research and Analysis Methods Respiratory function Signal transduction Transcription Uterus |
| title | PKCδ deficiency inhibits fetal development and is associated with heart elastic fiber hyperplasia and lung inflammation in adult PKCδ knockout mice |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-20T09%3A06%3A24IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=PKC%CE%B4%20deficiency%20inhibits%20fetal%20development%20and%20is%20associated%20with%20heart%20elastic%20fiber%20hyperplasia%20and%20lung%20inflammation%20in%20adult%20PKC%CE%B4%20knockout%20mice&rft.jtitle=PloS%20one&rft.au=Niino,%20Yuko%20S.&rft.date=2021-07-01&rft.volume=16&rft.issue=7&rft.spage=e0253912&rft.epage=e0253912&rft.pages=e0253912-e0253912&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0253912&rft_dat=%3Cproquest_plos_%3E2548410044%3C/proquest_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2547542148&rft_id=info:pmid/34197550&rft_doaj_id=oai_doaj_org_article_9aeae0a7358643b3bccee12c21878958&rfr_iscdi=true |