PhD Scientific Days 2018

Budapest, April 19–20, 2018

Gal-1 Expression Profile in rat central nervous system derived cell cultures

Mir, Mohd Yaqub

Mohd Yaqub Mir, Department of Anatomy, Histology and Embryology, Semmelweis University, Budapest
Adam Legradi, Department of Cell Biology and Molecular Medicine, University of Szeged, Szeged

Language of the presentation


Text of the abstract

Aims: There is not much information about the role of Gal-1 in neuronal tissue, We would like to know how Gal-1 expression is changing in primary neuronal cell cultures, which type of neuronal or glial cells express Gal-1, is there any possibility to modify Gal-1 expression with immune or neuromodulatory agent.

Method: We examined the Gal-1 expression on rat derived primary neuronal cultures after different culturing time with Western-blot (WB). We analyzed, which type of cell is express the Gal-1 with double immunofluorescence method, labeling the cells with Gal-1 and specific neuronal and glial markers parallel. And also we treated the primary neuronal cells with different immune- (LPS, Rosuvastatin Aspirin) and neuromodulatory (Capsaicin, Triflouroprezine) drugs and examined the Gal-1 expression changing on primary neuronal cell cultures with WB.
Results: Gal-1 is expressed in all cell types located in the mixed neuronal cultures, but the signal intensity was higher in microglial cells. The Gal-1 expression is increased, depending on the culturing time and neither the immunomodulatory (LPS, Rosuvastatin Aspirin) nor the neuromodulatory (Capsaicin, Triflouroprezine) drugs affect the Gal-1 expression. The Gal-1 expression is mostly connected to the old, strongly activated, amoeboid microglial population, which derived from 14-day old mixed neuronal cultures after 3 hours shaking.
Conclusion: Galectin-1 expression is connected to the strongly attached amoeboid microglial population. The form of these cells can be quite similar to the “gitter” microglias. These fully ameboid microglial cells have an anti-inflammatory phenotype, and according to our results, one of the factors responsible for this inflammation inhibiting phenotype is possible to be Gal-1.

Data of the presenter

Doctoral School: János Szentágothai Doctoral School of Neurosciences
Program: Neuromorphology and Cell Biology
Supervisor: Adam Legradi