Related Experiment Videos
The p38 MAPK pathway mediates interleukin-1-induced Sertoli cell proliferation
Cecilia Petersen1, Konstantin Svechnikov, Berit Fröysa
1Department of Woman and Child Health, Paediatric Endocrinology Unit, Astrid Lindgren Children's Hospital, Karolinska Institutet, Stockholm, Sweden. cecilia.petersen@lbh.ki.se
Cytokine
|September 27, 2005
Summary
Interleukin-1 (IL-1) promotes immature Sertoli cell proliferation via the p38 MAPK pathway. This explains IL-1 and FSH synergy, but IL-1 may harm testicular development.
Area of Science:
- Reproductive biology
- Cell signaling
- Endocrinology
Background:
- Interleukin-1 (IL-1) is a known growth factor for immature Sertoli cells.
- Its mitogenic effect is synergistic with follicle-stimulating hormone (FSH).
Purpose of the Study:
- To investigate the role of MAPK pathways in mediating IL-1's mitogenic effect on Sertoli cells.
Main Methods:
- Western blotting to detect MAPK activation (p38 MAPK, JNK/SAPK, ERK).
- Inhibition of p38 MAPK using SB203580.
- Assessment of Sertoli cell proliferation via (3)H-thymidine incorporation, supravital staining, and cell counting.
Main Results:
- IL-1alpha activated p38 MAPK and JNK/SAPK, but not ERK, in immature rat Sertoli cells.
- SB203580 significantly attenuated IL-1alpha-induced Sertoli cell proliferation.
- The p38 MAPK pathway mediates IL-1alpha's proliferative effect in vitro.
Conclusions:
- The p38 MAPK pathway mediates IL-1alpha-induced proliferation of immature Sertoli cells.
- Synergistic action of IL-1alpha and FSH may result from their distinct intracellular signaling pathways (p38 MAPK vs. ERK).
- IL-1 induction by inflammation or injury could impair Sertoli cell development and spermatogenesis.