Rheumatoid Arthritis and the Cell Cycle

This is a paper in which Sci has a certain amount of personal investment. You see, Sci has a family member who suffers from rheumatoid arthritis. And when I say suffer, I mean she suffers terribly. Rheumatoid arthritis is an autoimmune disease where you own body attacks the lining of the membranes between your joints. The result is painful swelling and stiffness (arthritis) which usually affects the smaller joints first (like your fingers) and which can severely impair your quality of life. Symptoms can wax and wane, but right now there is no cure, and treatments (which include things like aspirin or harder pain killers, steroids, and other immunosuppressants) are often not very effective and have a large number of side effects.
About 1% of the population is affected, and while the disease isn’t itself fatal, it does shorten your lifespan by about 5-10 years, and seriously affects quality of life. Sufferers of rheumatoid arthritis often can’t work and daily living is often impaired. So even though it’s not a large population of people, it’s still very important to find better treatments and attempt to find a cure to improve the lives of those who suffer from the disease.
And so this paper looks at two different proteins that might be able to help the disease…by controlling cell division. In fact, one of them is the SAME protein that Sci wrote about a few weeks ago when she looked at the incredible healing mouse. Interestingly, that mouse apparently is used for some autoimmune disease studies like lupus. Hmmmm.
ResearchBlogging.org Nasu et al. “Adenoviral transfer of cyclin-dependent kinase inhibitory genes suppresses collagen induced arthritis in mice” Journal of Immunology, 2000.
(Does anyone else always worry they are spelling “arthritis” wrong? It’s one of those words that look wrong if you look at it too long)
Anyway, let me introduce to you…the arthritic mouse:
(ok, they don’t really look like that, but it’s cute!)

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A Follow up: Depression, p21, CREB, and more

Everyone once in a while, someone sends Sci email. Often it’s silly. This one, however, was very good in that it asked for some clarification on a series of posts that I’ve been working on looking at clinical depression and possible causes and treatments, including neurogenesis in the hippocampus, cell cycle controls, and CREB.
And luckily, the guy who sent it gave Sci permission to repost, which is good, because it allows me to clarify some stuff. Here goes:

Hi Sci: I read your blog about how antidepressants stimulate neurogenesis in the hippocampus. Since the CREB deficient mice had robust neurogenesis and normal serotonin I wasn’t sure why they were anxious. Apparently they did benefit from antidepressants right away on the tail suspension and forced swim tests so the neurogenesis hypothesis took a bit of a whack. To add to the complexities I just read about MIF (macrophage migration inhibitory factor). Apparently reducing the amount of MIF in the rat hippocampus dramatically reduces neurogenesis and increases anxiety. Do you understand how CREB and MIF are related? I’m trying to get a handle on this whole complex area. Thanks.

All right, I’m going to try this before my first cup of coffee and we’ll see how it goes:

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Cell Cycle p21, Depression, and Neurogenesis and in the Hippocampus

This is somewhat of a followup post. What’s really cool about this paper (to Sci, anyway), is that it brings two different areas that she’s been interested in into one cool glob of SCIENCE. And it helps to explain many of the questions that Sci got in response to two of the papers she has blogged about recently.
They are these:
1) The Incredible Healing Mouse: Bedelbeava et al. “Lack of p21 expression links cell cycle control and appendage regeneration in mice” Proceeding of the National Academy of Sciences, 2010.
2) The neurogenesis theory of depression and a little guy called CREB: Gur et al. “cAMP Response Element-Binding Protein Deficiency Allows for Increased Neurogenesis and a Rapid Onset of Antidepressant Response” The Journal of Neuroscience, 2007.
And NOW, behold their MUTANT OFFSPRING:
ResearchBlogging.org Pechnick et al. “p21 restricts neuronal proliferation in the subgranular zone of the dentate gyrus of the hippocampus” PNAS, 2008.
Well ok, technically it isn’t a mutant offspring, because this paper was BEFORE the first paper and after the second. So I guess it’s a stepchild. Or a sibling. Or just the results of how Sci was searching PubMed that day.
Let’s start with some background.

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