Abstract
Senescence in green turtle is an interesting process to study because until now no clear explanation has been established about senescence at cellular or molecular level in this species. One of common markers used for detecting senescence is telomere shortening. Reduced telomerase activity may also cause senescence. The aims of this research are to establish and identify dermal fibroblast cell culture from green turtle and also to compare telomere length and telomerase activity from the cells subculture 5 and 14. Cells were identified with Rabbit Anti-Vimentin Polyclonal Antibody and Goat Polyclonal Antibody using confocal microscope. Telomere length was obtained using TeloTAGGG Telomere Length Assay (Roche), while telomerase activity was obtained using TeloTAGGG Telomerase PCR ElisaPlus. Primary cell culture from green turtle skin showed fibroblastic morphology and immunocytochemistry results using vimentin antibody proved that the culture was fibroblast cell. Measurement of telomere length and telomerase activity showed that telomere length and telomerase activity of subculture 14 was greater than subculture 5. However, based on morphology, green turtle fibroblast skin cell culture showed senescent morphology. Therefore, possible aging mechanism that the green turtle fibroblast skin cell culture underwent did not go through both telomere shortening and reduced telomerase activity.
Highlights
Green turtle (Chelonia mydas) is one of the most popular long-lived animals whose age may exceed 100 years [1, 2]
Since C. mydas may not have a regular aging process such that is found in mammals, we hypothesize that telomere length and telomerase activity in dermal fibroblast cell culture at subculture 14 is higher than subculture 5
Cells cultured from C. mydas skin showed fibroblastic morphology which has spindle shaped-like structure with long cytoplasmic protruding
Summary
Green turtle (Chelonia mydas) is one of the most popular long-lived animals whose age may exceed 100 years [1, 2]. Once replication reaches the end of a chromosome, RNA primer at the 3’ end degraded and no DNA base can be added at this end This telomere shortening phenomenon is one of the main causes of replicative senescence which leads to an estimation of Hayflick limit, number of which cells can be passage until cells stop divide, and undergo apoptosis [5]. Cells will activate p53 protein to arrest the cell cycle in the late G1 phase before cells may show senescence phenotype such as decreased protein degradation, housekeeping enzyme expression, energy production, and increased ROS level (reactive oxygen species) [6] This phenotype may lead to a decrease in normal cell function, after which cell may undergo apoptosis. Since C. mydas may not have a regular aging process such that is found in mammals, we hypothesize that telomere length and telomerase activity in dermal fibroblast cell culture at subculture 14 is higher than subculture 5
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
