Andric 2019b MiP2019
Adaptability to stress is fundamental prerequisites for survival. Mitochondria are a key component of the stress response in all cells. For steroid-hormones-producing cells, including also Leydig cells of testes, the mitochondria are a key control point for the steroid biosynthesis and regulation. However, the mitochondrial biogenesis in steroidogenic cells has never been explored.
Here we show that increased mitochondrial biogenesis is the adaptive response of testosterone-producing Leydig cells from stressed rats. All markers of mitochondrial biogenesis together with transcription factors and related kinases are up-regulated in Leydig cells from rats exposed to repeated psychophysical stress. This is followed with increased mitochondrial mass. The expression of PGC1, master regulator of mitochondrial biogenesis and integrator of environmental signals, is stimulated by cAMP-PRKA, cGMP and β-adrenergic receptors. Accordingly, stress-triggered mitochondrial biogenesis represents an adaptive mechanism and does not only correlate-with but also is an essential for testosterone production, being both events depend on the same regulators.
Here we propose that all events induced by acute stress, the most common stress in human society, provoke adaptive response of testosterone-producing Leydig cells and activate PGC1, a protein required to make new mitochondria but also protector against the oxidative damage.
Giving the importance of mitochondria for steroid hormones production and stress response, as well as the role of steroid hormones in stress response and metabolic syndrome, we anticipate our result to be a starting point for more investigations since stress is a constant factor in life and has become one of the most significant health problems in modern societies.
Labels: MiParea: mt-Biogenesis;mt-density, Comparative MiP;environmental MiP
Organism: Rat Tissue;cell: Genital
Affiliations and support
- Gak IR*, Radovic SM*, Starovlah IM, Kostic TS, Andric SA
- *These authors contributed equally to this work.
- Lab Reproductive Endocrinology Signaling, Lab Chronobiology Aging, Centre Excellence CeRES, Fac Sciences, Univ Novi Sad, Novi Sad, Serbia. – firstname.lastname@example.org
- This work was supported by the grant no. 173057 and grant no. 451-0302807 Centre of Excellence CeRES from the Ministry of Education, Science and Technological Development, Republic of Serbia, as well as grant no. 2130 from the Autonomous Province of Vojvodina