scholarly journals Placental Mitochondrial DNA Content and Particulate Air Pollution during in Utero Life

2012 ◽  
Vol 120 (9) ◽  
pp. 1346-1352 ◽  
Author(s):  
Bram G. Janssen ◽  
Elke Munters ◽  
Nicky Pieters ◽  
Karen Smeets ◽  
Bianca Cox ◽  
...  
Keyword(s):  
Air Pollution ◽  
Mitochondrial Dna ◽  
Dna Content ◽  
In Utero ◽  
Particulate Air Pollution ◽  
Mitochondrial Dna Content

scholarly journals Identifying sensitive windows for prenatal particulate air pollution exposure and mitochondrial DNA content in cord blood

2017 ◽  
Vol 98 ◽  
pp. 198-203 ◽  
Author(s):  
Maria José Rosa ◽  
Allan C. Just ◽  
Marco Sánchez Guerra ◽  
Itai Kloog ◽  
Hsiao-Hsien Leon Hsu ◽  
...  
Keyword(s):  
Air Pollution ◽  
Mitochondrial Dna ◽  
Cord Blood ◽  
Dna Content ◽  
Particulate Air Pollution ◽  
Mitochondrial Dna Content ◽  
Air Pollution Exposure ◽  
Pollution Exposure

Prenatal exposure to ambient air pollution predicts telomere length and mitochondrial DNA content in 7-year old children

2016 ◽  
Vol 2016 (1) ◽  
Author(s):  
Diana B.P. Clemente* ◽  
Martine Vrijheid ◽  
Dries S. Martens ◽  
Regina Grazuleviciene ◽  
Asta Danileviciute ◽  
...  
Keyword(s):  
Air Pollution ◽  
Mitochondrial Dna ◽  
Telomere Length ◽  
Prenatal Exposure ◽  
Dna Content ◽  
Ambient Air ◽  
Ambient Air Pollution ◽  
Mitochondrial Dna Content

scholarly journals Prenatal Ambient Air Pollution, Placental Mitochondrial DNA Content, and Birth Weight in the INMA (Spain) and ENVIR ON AGE (Belgium) Birth Cohorts

2016 ◽  
Vol 124 (5) ◽  
pp. 659-665 ◽  
Author(s):  
Diana B.P. Clemente ◽  
Maribel Casas ◽  
Nadia Vilahur ◽  
Haizea Begiristain ◽  
Mariona Bustamante ◽  
...  
Keyword(s):  
Air Pollution ◽  
Mitochondrial Dna ◽  
Birth Weight ◽  
Dna Content ◽  
Ambient Air ◽  
Ambient Air Pollution ◽  
Birth Cohorts ◽  
Mitochondrial Dna Content

scholarly journals Child buccal telomere length and mitochondrial DNA content as biomolecular markers of ageing in association with air pollution

2021 ◽  
Vol 147 ◽  
pp. 106332
Author(s):  
Pauline Hautekiet ◽  
Tim S. Nawrot ◽  
Bram G. Janssen ◽  
Dries S. Martens ◽  
Eva M. De Clercq ◽  
...  
Keyword(s):  
Air Pollution ◽  
Mitochondrial Dna ◽  
Telomere Length ◽  
Dna Content ◽  
Mitochondrial Dna Content ◽  
Biomolecular Markers

scholarly journals Prenatal ambient air pollution exposure, infant growth and placental mitochondrial DNA content in the INMA birth cohort

2017 ◽  
Vol 157 ◽  
pp. 96-102 ◽  
Author(s):  
Diana B.P. Clemente ◽  
Maribel Casas ◽  
Bram G. Janssen ◽  
Aitana Lertxundi ◽  
Loreto Santa-Marina ◽  
...  
Keyword(s):  
Air Pollution ◽  
Mitochondrial Dna ◽  
Birth Cohort ◽  
Dna Content ◽  
Ambient Air ◽  
Infant Growth ◽  
Ambient Air Pollution ◽  
Mitochondrial Dna Content ◽  
Air Pollution Exposure ◽  
Pollution Exposure

Development of matured hiPSCs-derived 3D cardiac tissue using ERR gamma agonist and mechanical stress and application for Hypertrophic Cardiomyopathy (HCM) model

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
Y Fujiwara ◽  
K Deguchi ◽  
Y Naka ◽  
M Sasaki ◽  
T Nishimoto ◽  
...  
Keyword(s):  
Mitochondrial Dna ◽  
Hypertrophic Cardiomyopathy ◽  
Mechanical Stress ◽  
Cell Size ◽  
Dna Content ◽  
Disease Model ◽  
Heart Tissue ◽  
Funding Source ◽  
Mitochondrial Dna Content ◽  
Mechanical Stretching

Abstract Introduction Tissue engineering using human induced pluripotent stem cells-derived cardiomyocytes (hiPSCs-CMs) is one of the potential tools to replicate human heart in vitro. Although there are many publications on 3 dimensional (3D) heart tissues (1), these tissues show fetal like phenotypes. For that reason, several maturation methods such as electrical stimulation and mechanical stress have been investigated (2, 3). However, these methods have been inadequate in differentiating fetal like phenotype tissue from adult tissues. Previously, we identified a novel compound, T112, which induced hiPSCs-CMs maturation from approximately 9,000 compounds using Troponin I1-EmGFP and Troponin I3-mCherry double reporter hiPSCs-CMs. This compound enhanced morphological and metabolic maturation of hiPSCs-CMs via estrogen-rerated receptor gamma activation Purpose We hypothesized that our novel compound, T112, in combination with mechanical stress could result in further maturation of 3D heart tissue. Therefore, our specific aim is to develop a novel maturation method applicable to genetic disease model of HCM using 3D heart tissue combined with T112. Methods We constructed 3D heart tissue mixed with fibroblast and double reporter hiPSCs-CMs by the hydrogel methods using Flex cell system®. We added T112 with or without mechanical stretching to 3D tissue from 7 to 15 days after 3D heart tissue was constructed. Then we measured maturation related phenotype such as sarcomere gene expression, mitochondrial DNA content and cell size. Results Similar to hiPSCs-CM, the addition of T112 to the constructed 3D heart tissue significantly increased TNNI3 mRNA compared to that of DMSO. Furthermore, T112 treated 3D heart tissue showed increased cell size and oblong shape. Next, in order to promote more maturation of 3D heart tissue, we performed mechanical stretching with the addition of T112. The combination of T112 with mechanical stretching showed higher expression of mCherry, a reporter protein for TNNI3 expression, and higher isotropy of sarcomere alignment in 3D heart tissue than that with the static condition. Furthermore, 3D heart tissue in the treatment of T112 with or without mechanical stretching showed higher mitochondrial DNA content compared to the respective DMSO controls. Interestingly, we applied this combination method to hiPSCs carrying MYH7 R719Q mutation which is known to cause hypertrophic cardiomyopathy, and the 3D heart tissue composed of cardiomyocytes derived from mutant iPSCs demonstrated increased sarcomere disarray compared to isogenic wild-type 3D heart tissue. Conclusion These results suggest that the combination of T112 and mechanical stretching promotes metabolic and structural maturation of 3D heart tissue and would be useful for creating a HCM disease model. Funding Acknowledgement Type of funding source: Private company. Main funding source(s): T-CiRA project, Takeda Pharmaceutical Company Limited

Sign in / Sign up

Export Citation Format

Share Document