Is S100A1 involved in the programming effects of fetal hypoxia on cardiac function in chickens?
Independent thesis Basic level (degree of Bachelor), 20 credits / 30 HE creditsStudent thesis
Prolonged prenatal hypoxia has shown to cause fetal growth restriction inchickens due to restricted oxygen to the somatic tissue. The body goes through a critical periodof development. Insults during this critical period may have lifelong effects on the individual.Currently heart failure is treated either with symptomatic therapy using diuretics or by targetingthe renin-angiotensin-aldosterone system. Developing new successful treatments is importantwith the aging population and the increased rate of heart failure. Previous studies have shownsystolic contractile dysfunction in 5 week old broiler chicken hearts when the eggs have beenincubated in hypoxia until hatching. S100A1 in cardiomyocytes regulates the calcium-controllednetwork which plays a big role in cardiac contractility and in this study, using qPCR on S100A1(GOI), GADPH and β-actin to try and determine if the changes made to the heart while the fetusis developing is due to a lack of S100A1 expression resulting in a decreased handling of Ca2+uptake which causes contractile dysfunction A Roche Lightcycler 480 was used together with theRoche template running triplets of each sample at 15-15-15 seconds for 45 cycles No statisticalsignificance was observed between the control group and the experimental group. However inthis study only S100A1 gene is being considered but a better understanding of the whole S100family might give a better understanding of mechanisms causing the progressive deterioration ofcardiac function
Place, publisher, year, edition, pages
2014. , 11 p.
S100A1, gene expression, hypoxia, heart failure, gallus gallus
IdentifiersURN: urn:nbn:se:liu:diva-111556ISRN: LiTH-IFM- Ex--14/2906--SEOAI: oai:DiVA.org:liu-111556DiVA: diva2:757844
Subject / course