Projects
Name
Neuron-microglia communication: role of carbon monoxide on modulation of neuroinflammation and neuroprotection
University
Portugal ( PorMSIC) - Nova University of Lisbon, Lisbon
Domain
Neurobiology
Departement
Cell Death and Disease Lab Lab, CEDOC
Head
Helena L. A. Vieira
Tutor
Nuno Soares and Helena Vieira
Languages
English
Duration
4 weeks
Availability
Cities/Months Jan Feb Mar Apr May Jun Jul Augt Sep Oct Nov Dec
No No No No No No No No Yes No No No
Type of Research Project
- Basic science
What is the background of the project?
Exacerbated neuroinflammation is a complex process leading to the progressive decline of neuronal activities associated with the development of neurodegenerative diseases, being also key features in the pathogenesis of ischemic stroke. The glia cells, particularly astrocytes and microglia, serve a critical role during brain injury and to maintain homeostasis, brain metabolism and neuronal functioning. Nevertheless, glia dysfunction contributes to neurodegenerative processes and the amplification of the inflammatory process. Low concentrations of carbon monoxide (CO) are known to present a cytoprotective and neuroprotective properties (inhibiting cell death), as well as CO is also an anti-inflammatory factor. How CO modulates communication between microglia and neurons is the main interest of the present project.
What is the aim of the project?
The final aim is to study the molecular mechanisms underlying CO axis modulation of neuron-microglia communication, under pathological and physiological conditions, using Carbon monoxide releasing molecules (CORM) for delivering CO. Two biological processes will be targeted: neuroinflammation and neuroprotection.
What techniques and methods are used?
Cell culture (neurons and/or microglia), using cell lines or primary cultures derived from mouse pups. Analysis of cell viability by flow cytometry and protein expression by western blots. Inflammation will be measured by protein expression and NO (nitric oxide) production.
What is the role of the student?
- The tasks will be done under supervision
What are the tasks expected to be accomplished by the student?
In the first week the student will follow one of the lab researchers in order to learn the different techniques of the project (cell culture, flow cytometry, western blot). If the student performs well, he/she will do western blot techniques and NO detection by colorimetry. The student is expected also to participate in our lab meetings, seminar and scientific discussions.
Will there be any theoretical teaching provided (preliminary readings, lectures, courses, seminars etc)
Seminars and preliminary reading
What is expected from the student at the end of the research exchange? What will be the general outcome of the student?
- The student will prepare a poster
- The student will prepare a presentation
What skills are required of the student? Is there any special knowledge or a certain level of studies needed?
None
Are there any legal limitations in the student’s involvement
No
Hours
6
Type of students accepted
This project accepts:
- Medical students
- Graduated students (less than 6 months)
- Pre-Medical students from the American-British system
- Students in biomedical fields
Articles
- 1) Queiroga C.S.F; Alves R.M.A; Conde S.V.; Alves P.M. and Vieira H.L.A. Paracrine effect of carbon monoxide: astrocytes promote neuroprotection via purinergic signaling Journal of Cell Science; 2016 Jul 6. 10.1242/jcs.187260
- 2) Queiroga C.S.F; Vercelli A. and Vieira H.L.A.; Carbon Monoxide and central Nervous System: Challenges and Achievements; British Journal of Pharmacology 2014 Apr 24. doi: 10.1111/bph.12729
- 3) Motterlini; R.; Otterbein; L.E.; 2010. The therapeutic potential of carbon monoxide. Nat Rev Drug Discov 9; 728?743. doi:10.1038/nrd3228
- 4) Motterlini; R.; Sawle; P.; Hammad; J.; Bains; S.; Alberto; R.; Foresti; R.; Green; C.J.; 2005. CORM-A1: a new pharmacologically active carbon monoxide-releasing molecule. Faseb J 19; 284?286.
- 5) Queiroga; C.S.; Tomasi; S.; Wideroe; M.; P.M.; A.; Vercelli; A.; H.L.A.; V.; 2012. Preconditioning triggered by carbon monoxide (CO) provides neuronal protection following perinatal hypoxia-ischemia. PLoS One 7; e42632.