For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
16
views
20
references
 Top references
cited by
6
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      143
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Deletion of Cdc42 in embryonic cardiomyocytes results in right ventricle hypoplasia

      research-article

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Background

          Cdc42 is a member of the Rho GTPase family and functions as a molecular switch in regulating cytoskeleton remodeling and cell polarity establishment. Inactivating Cdc42 in cardiomyocytes resulted in embryonic lethality with heart developmental defects, including ventricular septum defects and thin ventricle wall syndrome.

          Findings

          In this study, we have generated a Cdc42 cardiomyocyte knockout mouse line by crossing Cdc42/flox mice with myosin light chain 2a (MLC2a)-Cre mice. We found that the deletion of Cdc42 in embryonic cardiomyocytes resulted in an underdeveloped right ventricle. Microarray analysis and real-time PCR data analysis displayed that the deletion of Cdc42 decreased dHand expression level. In addition, we found evaginations in the ventricle walls of Cdc42 knockout hearts.

          Conclusion

          We concluded that Cdc42 plays an essential role in right ventricle growth.

          Related collections

          Most cited references20

          • Record: found
          • Abstract: found
          • Article: not found

          Making or breaking the heart: from lineage determination to morphogenesis.

          Deepak Srivastava (2006)
          The cues governing cardiac cell-fate decisions, cardiac differentiation, and three-dimensional morphogenesis are rapidly being elucidated. Several themes are emerging that are relevant for childhood and adult heart disease and the growing field of stem cell biology. This review will consider our current understanding of cardiac cell-fate determination and cardiogenesis--largely derived from developmental studies in model organisms and human genetic approaches--and examine future implications for diagnosis, prevention, and treatment of heart disease in the young and old.
          Article 0 comments Cited 162 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            The arterial pole of the mouse heart forms from Fgf10-expressing cells in pharyngeal mesoderm.

            R G Kelly, N Brown, M E Buckingham (2001)
            Development of the arterial pole of the heart is a critical step in cardiogenesis, yet its embryological origin remains obscure. We have analyzed a transgenic mouse line in which beta-galactosidase activity is observed in the embryonic right ventricle and outflow tract of the heart and in contiguous splanchnic and pharyngeal mesoderm. The nlacZ transgene has integrated upstream of the fibroblast growth factor 10 (Fgf10) gene and comparison with the expression pattern of Fgf10 in pharyngeal mesoderm indicates transgene control by Fgf10 regulatory sequences. Dil labeling shows a progressive movement of cells from the pharyngeal arch region into the growing heart tube between embryonic days 8.25 and 10.5. These data suggest that arterial pole myocardium originates outside the classical heart field.
            Article 0 comments Cited 155 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              A genetic blueprint for cardiac development.

              D. Srivastava, Janet Olson (2000)
              Congenital heart disease is the leading non-infectious cause of death in children. It is becoming increasingly clear that many cardiac abnormalities once thought to have multifactorial aetiologies are attributable to mutations in developmental control genes. The consequences of these mutations can be manifest at birth as life-threatening cardiac malformations or later as more subtle cardiac abnormalities. Understanding the genetic underpinnings of cardiac development has important implications not only for understanding congenital heart disease, but also for the possibility of cardiac repair through genetic reprogramming of non-cardiac cells to a cardiogenic fate.
              Article 0 comments Cited 94 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Contributors
                Yang Liu: Yang.Liu2@BSWHealth.org
                Jian Wang: jwan22@medicine.tamhsc.edu
                Jieli Li: shirleyli1220@gmail.com
                Rui Wang: wangruino1@sina.com
                Binu Tharakan: Binu.Tharakan@BSWHealth.org
                Shenyuan L. Zhang: Shenyuan.Zhang@medicine.tamhsc.edu
                Carl W. Tong: CTong@medicine.tamhsc.edu
                Xu Peng:
                ORCID: http://orcid.org/0000-0001-9068-102X
                (254) 742-7176 , xpeng@medicine.tamhsc.edu
                Journal
                Journal ID (nlm-ta): Clin Transl Med
                Journal ID (iso-abbrev): Clin Transl Med
                Title: Clinical and Translational Medicine
                Publisher: Springer Berlin Heidelberg (Berlin/Heidelberg )
                ISSN (Electronic): 2001-1326
                Publication date (Electronic): 3 November 2017
                Publication date PMC-release: 3 November 2017
                Publication date Collection: 2017
                Volume: 6
                Electronic Location Identifier: 40
                Affiliations
                [1 ]ISNI 0000 0004 4687 2082, GRID grid.264756.4, Department of Medical Physiology, College of Medicine, , Texas A&M University, ; Temple, USA
                [2 ]Department of Obstetrics and Gynecology, Baylor Scott & White Health, Temple, USA
                [3 ]ISNI 0000000123704535, GRID grid.24516.34, Yangpu District Central Hospital, , Tongji University, ; Shanghai, China
                [4 ]Department of Surgery, Baylor Scott & White Health, Temple, USA
                [5 ]Internal Medicine/Cardiology Division, Baylor Scott & White Health, Temple, USA
                Author information
                http://orcid.org/0000-0001-9068-102X
                Article
                Publisher ID: 171
                DOI: 10.1186/s40169-017-0171-4
                PMC ID: 5670094
                PubMed ID: 29101495
                SO-VID: d63df5f0-aa9b-4bf8-acf2-eec32bcf86ec
                Copyright © © The Author(s) 2017
                License:

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

                History
                Date received : 4 October 2017
                Date accepted : 17 October 2017
                Funding
                Funded by: FundRef http://dx.doi.org/10.13039/100000968, American Heart Association;
                Award ID: 13BGIA14470002
                Award Recipient :
                Categories
                Subject: Short Report
                Custom metadata
                issue-copyright-statement © The Author(s) 2017

                ScienceOpen disciplines: Medicine
                Keywords: gtpase,cdc42,heart development,right ventricle development
                Data availability:
                ScienceOpen disciplines: Medicine
                Keywords: gtpase, cdc42, heart development, right ventricle development

                Comments

                Comment on this article

                scite_

                Similar content143

                See all similar

                Cited by6

                See all cited by

                Most referenced authors458

                See all reference authors