Difference between revisions of "Andric 2019b MiP2019"

Revision as of 13:45, 26 September 2019

Mitochondrial morphology and mitochondrial biogenesis are altered in Leydig cells from stressed adult rats.

Link: MiP2019

Gak IR, Radovic SM, Starovlah IM, Kostic TS, Andric SA (2019)

Event: 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 -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.

• Bioblast editor: Plangger M, Tindle-Solomon L

Labels: MiParea: mt-Biogenesis;mt-density, mt-Structure;fission;fusion, mtDNA;mt-genetics Pathology: Other

Organism: Human Tissue;cell: Blood cells

PBMCs

Affiliations and support

Gak IR*, Radovic SM*, Starovlah IM, Kostic TS, Andric SA

These authors contributed equally to this work.

Laboratory for Reproductive Endocrinology and Signaling, Laboratory for Chronobiology and Aging, Centre of Excellence CeRES, Faculty of Sciences, University of Novi Sad, Novi Sad, Serbia – [email protected] 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

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 {{Abstract
-|title=[[Image:MiPsocietyLOGO.JPG|left|90px|Mitochondrial Physiology Society|MiPsociety]] Markers of mitochondrial biogenesis, fusion and architecture are disturbed in PBMC from war veterans with posttraumatic stress disorder (PTSD).
+|title=[[Image:MiPsocietyLOGO.JPG|left|90px|Mitochondrial Physiology Society|MiPsociety]] Mitochondrial morphology and mitochondrial biogenesis are altered in Leydig cells from stressed adult rats.
 |info=[[MiP2019]]
-|authors=Markovic AZ, Milosevic MM, Radovic SM, Starovlah IM, Brkljacic J, Vojnovic Milutinovic D, Matic G, Kostic TS, Andric SA
+|authors=Gak IR, Radovic SM, Starovlah IM, Kostic TS, Andric SA
 |year=2019
 |event=MiP2019
 |abstract=[[Image:MITOEAGLE-logo.jpg|left|100px|link=http://www.mitoglobal.org/index.php/MITOEAGLE|COST Action MitoEAGLE]]
-The aim of this study was to define the transcription profiles of the molecular markers of mitochondrial biogenesis and fusion/architecture, as well as the markers of mtDNA copy numbers in the peripheral blood mononuclear cells (PBMCs) from war veterans with/without post-traumatic stress disorder (PTSD). Also, in order to define signaling molecules involved in changes of transcription profiles immortalized human males monocytes were exposed ''in vitro'' to hormonal markers of PTSD.
+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.
-RQ-PCR-results showed that the transcription profiles of above mentioned markers were disturbed, with high individual variability within the groups. A significant increase in the expression of the PPARGC1A transcript was observed in a group of subjects who currently have PTSD, as well as in the subjects with “life-time" PTSD, compared to healthy controls. PPARGC1B, NRF2 and MFN2 transcripts increased only in PBMCs of “life-time"-PTSD, while the level of transcripts for other investigated genes and the ratio of markers of mtDNA copy numbers showed no significant difference between groups. The in vitro results showed parallelism in the transcription profile of molecular markers of mitochondrial biogenesis with results obtained using the PBMCs of the PTSD study.
+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 -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.
-It should be emphasized that all results should be considered as preliminary because the technical/time constraints did not allow the analysis of a larger number of PTSD subjects. However, the results are first findings in the field and can be used as a solid base for further extensive multidisciplinary research in order to clarify the molecular mechanisms for the prevention and treatment of trauma-induced pathological conditions.
+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.
 |editor=[[Plangger M]], [[Tindle-Solomon L]]
 }}
@@ Line 21: / Line 23: @@
 }}
 == Affiliations and support ==
-::::Markovic AZ(1)*, Milosevic MM(1)*, Radovic SM(1), Starovlah IM(1), Brkljacic J(2), Vojnovic Milutinovic D(2), Matic G(2), Kostic TS(1), Andric SA(1)
+Gak IR*, Radovic SM*, Starovlah IM, Kostic TS, Andric SA
-:::: *These authors contributed equally to this work.
+*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
+Laboratory for Reproductive Endocrinology and Signaling, Laboratory for Chronobiology and Aging, Centre of Excellence CeRES, Faculty of Sciences, University of Novi Sad, Novi Sad, Serbia – [email protected]
-::::#Dept Biochemistry, Inst Biological Research "Siniša Stankovic", Univ Belgrade, Belgrade, Serbia. -  – [email protected]
+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
-::::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.