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Consequently, testosterone may, by a direct AR–DNA interaction, stimulate parallel transcription in both nucleus and mitochondria. In conclusion, the identification of shared nucleotide sequences in both the nuclear and mitochondrial genomes capable of binding to the AR suggests the possibilities of a coordination of transcription between the two genomes. Consequently, this novel outcome suggests a plausible role for the AR as a mitochondrial transcription factor, potentially exerting a direct regulatory control over mitochondrial gene transcription. This experimental approach enabled us to determine the presence of certain sequences previously identified in silico, thereby confirming the existence of sequences within the mtDNA of C2C12 cells that are recognized and bound by the AR. The mouse mitochondrial DNA (mtDNA) consists of an inner light strand (L-strand) and an outer heavy strand (H-strand), each encoding distinct genes. The presence of transcription factor binding sites (TFBSs) beyond the D-loop region suggests the potential for AR-mediated effects not only during transcription initiation but also at subsequent stages of the mitochondrial transcription process, such as elongation, release and processing.
We therefore hypothesised that the mitochondrial damage status dictates motor binding to regulate this sorting. In contrast, silencing of the inward motor Myo6, which anchors mitochondria within the cytoplasm, enhanced mitochondrial export into EVs (Extended Data Fig. 4c–g). To elucidate the mechanism by which LCs selectively sort defective mitochondria into EVs, we investigated the role of motors that mediate mitochondrial translocation27,28,29. Autophagy is a well-known process by which cells dispose defective organelles26. Comparing the proteome of LC-EVs with the MitoCarta3.0 and Vesiclepedia databases24,25, we found 291 and 1,534 overlapping proteins (Fig. 2g), respectively. G, Venn diagrams of the LC-EV proteome with proteins reported in the MitoCarta3.0 and Vesiclepedia databases. B, Experimental strategy to label LC membranes by intratesticular injection of AAV-DIO-Lck–EGFP into the testes of Cyp17a1Cre; R26tdTomato mice.
However, compared to the latter group, CA1 samples from 24Mon-TP rats had much fewer pyknotic nuclei (Figure 4C). While HE-stained neurons in the pyramidal stratum of the HIPP/CA1 area of 6Mon rats displayed large and clear nuclei (Figure 4A), obvious nuclear pyknosis was observed in a fraction of CA1 neurons in 24Mon rats (Figure 4B). (A) Representative western blots of TH and DAT expression. In contrast, compared to 24Mon rats significant increments in climbing (56.92%), rearing (100%), and sniffing (40.76%) behaviors were noted in 24Mon-TP animals. Post hoc testing showed that walking, climbing, rearing, and sniffing activities were significantly reduced in 24Mon compared to 6Mon rats. The open field test was used to evaluate exploratory behavior in control and TP-supplemented rats. No significant changes in body weight were recorded during TP supplementation in 24Mon-TP compared to 24Mon rats (Figure 1B).
We only analyzed MDA, mitochondrial H2O2, and mitochondrial GSH/GSSG in GDX rats. Of the three mitochondrial respiratory chain complexes in the proton-extruding system, the activity of complex I was altered due to testosterone deficiency. Testosterone deficiency might interfere with the mitochondrial function by affecting the proton-extruding system of the mitochondrial respiratory chain. As an important indicator of mitochondrial function 10, 56, mitochondrial membrane potential is created by the proton gradient across the inner mitochondrial membrane through the proton-extruding system including complexes I, III, and IV of the respiratory chain .
A consequence of the action of these sex hormones is mitochondrial protection, although the specific mechanism of action has not yet been elucidated. In the nucleus, the dimer of the receptors binds to estrogen response elements (ERE) or androgen response elements (ARE) and affects the transcription of nuclear-encoded mitochondrial genes. Both steroids trigger complex molecular mechanisms involving crosstalk between mitochondria, the nucleus, and the plasma membrane, and the result of this action is mitochondrial protection (Figure 2). Age-related muscle degeneration is caused when mitochondria are defective or abnormal and cannot be cleared or degraded effectively. However, little is known about the role of AR in mitochondrial Localization, and further studies are needed to elucidate the underlying mechanisms. These studies suggest that androgens may maintain mitochondrial mass by inducing mitochondrial biogenesis and inhibiting autophagy. In the cell cytoplasm, testosterone is converted into its active form, dihydrotestosterone (DHT), by 5α-reductase.
Mitochondria are responsible for generating cellular energy, altering the reduction-oxidation potential of cells, and regulating cell viability 53, 54. Mitochondrial dysfunction induces free radical overproduction and increases lipid peroxidation 38, 51, 52. The increased H2O2 and decreased GSH/GSSG in SN mitochondria further revealed the existed oxidative stress in GDX rats. TP supplements to GDX rats at 1.0 mg/kg reversed them to the levels in sham rats.
Studies indicate that aging provokes certain alternations of several key mitophagy regulators, leading to mitophagy deficiency and subsequent accumulation of dysfunctional mitochondria in skeletal muscle (91, 92). Mitophagy is a particular type of macroautophagy (autophagy) and, as mentioned above, can selectively remove dysfunctional and damaged mitochondria to maintain mitochondrial homeostasis. Therefore, further investigation will be needed to clarify the precise molecular mechanisms of mitochondrial dynamics alteration in aging muscle and develop an efficient strategy to prevent or delay the onset of sarcopenia. Mitochondrial fission is necessary for subsequent mitophagy to dissipate dysfunctional parts from the mitochondrial network (90). These studies mentioned above indicated the essential role of mitochondrial dynamics in muscle aging and sarcopenia.
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