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Thank you for visiting our website. We are a relatively small lab with big ideas. We are part of a much larger group of investigators known collectively as the LLUMC Molecular Radiation Biology Laboratories. It is our hope that this website will educate, communicate, and incite scientific debate. As the PI of our little group, I hope to post our data and discuss potential mechanisms, consequences, and countermeasures. With a bit of luck we'll all learn something. The links to the left include our merry band as well as collaborating investigators and laboratories. The links to the right include our archive and blogroll. The banner above will always bring you back to the main page page. Take a look around and please feel free to leave a comment on our blog (try to keep it civil and constructive) or shoot us an e-mail. - Michael " Ubertramp " Pecaut
Novemeber 2009 Lab Update
Posted by: Ubertramp on 2009.11.16
Categories & Tags: Props,Recognition
Comments: None
It’s been three months since my last update and I guess it’s about time. Believe it or not, we’ve had another publication show up in PubMed in the interim. It’s another manuscript about the STS-118 flight (our 4th from this flight, I think), but this time it’s geared more toward immunohistology than our usual cell count stuff. Jack Tian did all of the work. Here is the abstract.
Tian J, Pecaut MJ, Slater JM, Gridley DS.
NASA has reported pulmonary abnormalities in astronauts on space missions, but the molecular changes in lung tissue remain unknown. The goal of the present study was to explore the effects of spaceflight on expression of extracellular matrix (ECM), cell adhesion and pro-fibrotic molecules in lungs of mice flown on Space Shuttle Endeavour (STS-118). C57BL/6Ntac mice housed in animal enclosure modules during a 13-day mission in space (FLT) were euthanized within hours after return; ground controls were treated similarly for comparison (GRD). Analysis of genes associated with ECM and adhesion molecules was performed according to quantitative RT-PCR. The data revealed that FLT lung samples had statistically significant transcriptional changes, i.e., at least 1.5-fold, in 25 out of 84 examined genes (P < 0.05); 15 genes were up-regulated and 10 were down-regulated. The genes that were up-regulated by more than 2-fold were Ctgf, Mmp2, Ncam1, Sparc, Spock1, and Timp3, whereas the most down-regulated genes were Lama1, Mmp3, Mmp7, vcam-1, and Sele. Histology showed profibrosis-like changes occurred in FLT mice, more abundant collagen accumulation around blood vessels, and thicker walls compared with lung samples form GRD mice. Immunohistochemistry was used to compare expression of six selected proteins associated with fibrosis. Immunoreactivity of four proteins (MMP-2, CTGF, TGF-beta1, and NCAM) was enhanced by spaceflight, whereas, no difference was detected in expression of MMP-7 and MMP-9 proteins between the FLT and GRD groups. Taken together, the data demonstrate that significant changes can be readily detected shortly after return from spaceflight in the expression of factors that can adversely influence lung function. Key words: space shuttle, respiratory tract, gene expression, histopathology.
Jack’s been very productive this year. Believe it or not, he already has a third paper on the way and we’re about to send it out for review. We also have papers in review by Asma Rizvi (LLU), Ty Lebsack (ASU), and myself. Two of those have already been accepted with minor revisions, too, so we expect to see them in publication within the next couple of months.
Farnaz Baqai spent the summer studying for her MCATs, but she is back in the lab working hard on finishing up some of her immunohistochemistry. She has at least two papers worth of data from her dissertation and, hopefully, she’ll be able to write that data up in the next few months as well.
Erben Bayeta has been working on several in vitro studies using our macrophage cell lines. So far, we’ve repeated a number of dose response studies (testing the efficacy of ethyl pyruvate as a radioprotectant). Short version, we aren’t seeing much of a protective effect on oxidative burst capacity. In fact, it seems to be a bit toxic to our macrophages at higher concentrations. However, we’re not sure if it’s really killing the cells or slowing down replication. We’re working on teasing that out.
There have been a couple of conferences in the last month. In October, Farnaz and I went to the annual Radiation Research Society meeting in Savannah, Georgia. Farnaz had a poster and was invited to give a short talk describing her work (including a travel grant award). I was also invited out to give a short overview of spaceflight immune data for a seminar run by Ted Bateman and Greg Nelson.
More recently, I attended the annual meeting for the American Society for Gravitational and Space Biology. I wasn’t originally planning on attending this meeting even though it’s one of my favorites. I just didn’t have the money to go. However, Keith Chapes told me I needed to be there for a “round-table discussion about spaceflight.” So, Daila Gridley managed to scrounge up some funds and I was able to go. Turns out, there was no discussion. This was just a ruse (one which Daila was in on). Instead, they had nominated me to receive the “Thora W. Halstead Young Investigator Award.” Since I won, I kinda had to go. Haha. It’s an honor to win the award, but that was downright sneaky! Haha.
Last, but not least, I recently submitted another grant to NIH for the NIH/NASA ISS FOA. Here’s the abstract for that.
According to the National Institute of Health, “There are approximately 35 million Americans age 65 or older, and this number is expected to double in the next 25 years.” Consequently, there is a rapidly growing need to understand the mechanisms underlying age-associated illness. Evidence that suggests that many of the diseases associated with aging are also associated with dysregulation in immune responses and pro-inflammatory mediators. Age-associated deficits are likely linked to dynamic interactions between reactive oxygen species (ROS) and inflammatory cytokines. Prolonged exposure to the spaceflight environment results in many of the same deficits usually associated with aging, such as osteoporosis, muscle atrophy, and immune dysfunction. The International Space Station provides an ideal laboratory within which investigators can explore this unique environment. By characterizing these deficits in otherwise healthy human astronauts, we believe we will be able to establish a causal link between ROS metabolism and age-dependent immune dysfunction, clearing the way for the development of new treatments and techniques.
I guess that’s it!
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