The uptake of [3H] leucine, [3H] thymidine, [14C] acetate, and [14C] mevalonic acid by aortic intima media from normal rabbits and from rabbits subjected to a single balloon de-endothelialization as measured 6 days, 2 months, and 4 months after treatment to determine how long the injury-induced stimulation of incorporation of these precursors into tissue components persisted beyond 6 days, the time of maximum proliferative response of the smooth muscle cells. We found that [3H] thymidine incorporation (indicative of DNA synthesis and the potential for cell proliferation) was about three times greater in the de-endothelialized tissue than in the control tissue 6 days after vessel injury, but that by 2 months it was normal. Labeled leucine incorporation into the de-endothelialized tissue (a measure of protein synthesis) was eight times higher than normal at the time of maximum proliferative response to injury (6 days), and showed no decrease under identical incubation conditions in ballooned tissue obtained 2 months after de-endothelialization; it continued high at 4 months. Both [14C] acetate and [14C] mevalonate uptake into lipids by the aortic tissue were enhanced by the injury; this increased incorporation was still evident at 4 months. Thus, de-endothelialization of the aorta triggers a vessel wall response characterized by augmented protein synthesis and lipogenesis, which persists at least 4 months after injury and at least 2 months after DNA synthesis has normalized.
Down syndrome (DS) is a genetic birth defect that results from Trisomy 21, which causes an overexpression of human chromosome 21 (HSA21) genes. Overexpressed HSA21 genes disturb development by altering morphogenesis and growth, resulting in cognitive impairment, characteristic facial morphology, and many other health problems for individuals with DS. The DYRK1A gene is found on chromosome 21 and is thought to play a significant role in cranial and neurological malformations associated with DS. Previous research has shown that EGCG, a compound that inhibits DYRK1A, has been used to improve cognition of individuals with DS as well as improve cranial vault morphology in Ts65Dn DS mouse models. Based on DYRK1A's strong role in brain and craniofacial development, and the fact that EGCG can reduce overexpression of this gene, we hypothesized that children with DS who have been supplemented with EGCG will exhibit improved facial morphology. We assessed children with DS who were supplemented with EGCG (n = 5), untreated children with DS (n = 72), siblings of individuals with DS (n = 49), and euploid controls (n = 40), aged from 0–3 years. Twenty‐one anatomical landmarks were identified on 3dMD facial images and the XYZ coordinates were saved for analysis. A Euclidean Distance Matrix Analysis (EDMA) based on a non‐parametric bootstrap was carried out (1,000 resamples) to assess statistically significant shape differences across samples. A total of 210 linear distance measurements were compared from each individual's facial image. The baseline comparison of DS faces with siblings and euploid controls revealed that 50% and 54% of linear distances were significantly different. However, when DS faces were compared to children with DS supplemented with EGCG, we found that only 26% of linear distances reached statistical significance. Overall, the results suggest that EGCG is producing positive changes in the faces of children with Down syndrome, however more research must be done for a more definitive answer.Support or Funding InformationFunding was received from the Burnett Research Scholars Grant, which was provided through the UCF Burnet Honers College. Funding was also received from the UCF Office of Undergraduate Research through the Summer Undergraduate Research Fellowship.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
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