Paola Campagnolo is half way on her PhD defense, that should take place at the end of 2009. Nonetheless, she is already thinking about her future, trying to widen professional collaborations and personal skills. Paola, who is a PhD fellow in the laboratory of Professor Paolo Madeddu (Chief of the Experimental Medicine and Gene Therapy Unit, at Bristol University), is one of the students who exploited the Exchange Programme available for EVGN members at an early phase of her PhD. This is the reason why...

Q. Paola, how come you chose to visit a foreign laboratory at a relatively early phase of your PhD course?
A. I always thought that some experiences should be done as soon as possible: they are highly educational and open your mind in advance. So, visiting a host laboratory and learning from foreign colleagues at the beginning or so of my training process helped a lot in terms of acquisition of self-reliance and confidence.

Q. Where did you go?
A. I followed Professor Madeddu and worked in the lab of François Alhenc-Gelas, at INSERM (Paris). I went there twice, to start a very dynamic collaboration. On my way to Paris I brought with me some reagents and tools from my home-lab, and when I came back I carried with me some preliminary results and semi-elaborated reagents that I used to finished the experiments here, in Bristol.

Q. What is your field of investigation?
A. I work on an enzyme called Tissue Kallikrein (TK), involved in angiogenic pathway. This protein has a peculiarity: it acts both as an enzyme and as molecule per se, and it is well-known because it speed up the recovery of a tissue where an ischemic event took place.

Q. Did you have any specific goal to achieve in visiting Professor Alhenc-Gelas’ laboratory?
A. Yes, of course. François had just published a paper describing his findings of a mutation in the kallikrein gene and established a mouse model so-called functional mutants that reproduce a situation akin to the one we find in human beings. A functional mutant is an organism where a given protein hosts a mutation at a specific point along its structure. This mutation can alter the properties of the protein, and our goal is to define how and to what extent.
On this particular model we tried a gene therapy approach using a two different plasmids (plasmids are circular molecules of DNA that can carry foreign genes into a host organism): the first one carries the information to produce a normal TK protein; the second one hosts a point mutation at a specific site of the gene, and this changes the resulting protein. We studied then on normal and mutant mice treated with either the normal or the mutant plasmid, to understand the outcome of the ischemic recovery.

Q. Did you obtain some basic results?
A. Not in Paris , because my stay was limited to four days each time. But I continued on that project in Bristol . Now we are investigating whether the mutation we are examining impairs the ability of TK to trigger post-ischemic recovery.

Q. Does this fit your every-day work in Bristol ?
A. Partially. It is a side path with respect to my daily work, which involves the extraction of stem cells from clinical specimens we receive from surgery rooms. The problem I am facing and trying to solve at present stems from the difficulty I encounter in the isolation of these cells, as they are poorly differentiated and difficult to spot from others. Besides, there are no established protocols so one of my tasks is to identify the proper extraction conditions to set up a well-defined protocol.

Q. Is there any specific aspect that you recall with pleasure?
A. The ease we could test our hypothesis on live models, especially in clinical experiments where this is of basic importance to understand the whole process.

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