Analysis of gene expression of mice's thyroid glands according to the state of the Pink1 Knock-out
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE232119 | GEO | 2024/09/15
REPOSITORIES: GEO
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Project description:Analysis of gene expression of mice's thyroid glands according to the state of the Pink1 Knock-out
| PRJNA970913 | ENA
Project description:Thyroperoxidase (TPO) is a key enzyme in thyroid hormone (TH) synthesis in the thyroid gland. TPO inhibition can thus disrupt the TH system and cause deleterious effects associated with hypothyroidism. Many industrial chemicals can inhibit TPO activity in vitro, but it remains unclear how this manifest in the thyroid gland at the molecular level during development. Here, we characterized the transcriptome of rat thyroid glands developmentally exposed to either of three in vitro TPO-inhibitors including amitrole, 2-mercaptobenzimidazole (MBI) and cyanamide.
2025-08-19 | GSE242162 | GEO
Project description:Skeletal muscle-specific ablation of thyroid hormone receptor alpha (TRalpha) in young mice is sufficient to recapitulate key phenotypic hallmarks of age-related sarcopenia—including myofiber atrophy, exercise intolerance, and mitochondrial quality control failure—establishing receptor decline as a cell-autonomous driver of sarcopenia pathogenesis rather than a passive biomarker. The underlying mechanism reveals how systemic endocrine signals culminate in organelle-specific quality control defects: TRalpha transcriptionally drives the RNA-binding protein CLUH, which facilitates the perimitochondrial enrichment of Pink1 mRNA for localized synthesis of the mitophagy-initiating kinase. Consequently, TRalpha loss disrupts perimitochondrial Pink1 mRNA localization, impairing local PINK1 abundance and mitophagic priming, leading to accumulation of damaged mitochondria. Restoring CLUH expression rescues Pink1 mRNA spatial localization, mitophagy flux, and cellular senescence markers in both TRalpha-deficient myofibers and naturally aged muscle cells. These findings identify spatial transcriptome organization as an underappreciated regulatory layer in muscle wasting and provide a genetically defined framework linking endocrine decline to organelle-level post-transcriptional regulation.
2026-02-05 | GSE318551 | GEO
Project description:In this study, we aimed to explore the impact of PINK1 deficiency on MSC differentiation and bone health within the context of age-related bone loss, with a particular focus on the mechanisms regulating the balance between osteogenesis and adipogenesis. By examining how PINK1 influences bone health in both young and aged mice, we hope to gain a deeper understanding of the age-specific roles of PINK1 in skeletal bone maintenance and explore the possibility of targeting PINK1 to mitigate osteoporosis in the aging population.
2025-11-01 | GSE281254 | GEO
Project description:Global analysis of transcriptional changes in Drosophila pink1 mutants.
2013-12-02 | E-MEXP-3645 | biostudies-arrayexpress
Project description:Damaged mitochondria can be cleared from the cell by mitophagy, using a pathway formed by the recessive Parkinson’s disease genes PINK1 and Parkin. Whether the pathway senses diverse forms of mitochondrial damage by a common mechanism, however, remains uncertain. Here, using a novel Parkin reporter in genome-wide screens, we identified that diverse forms of mitochondrial damage converge on loss of mitochondrial membrane potential (MMP) to activate PINK1. Loss of MMP, but not the PAM import motor, blocked progression of PINK1 import through the translocase of the inner membrane (TIM23), causing it to remain bound to the translocase of the outer membrane (TOM). Ablation of TIM23 was sufficient to arrest PINK1 in TOM, irrespective of MMP. Meanwhile, TOM (including subunit TOMM5) was required for PINK1 retention on the mitochondrial surface. The energy-state outside of the mitochondria further modulated the pathway by controlling the rate of new PINK1 synthesis. Together, our findings point to a convergent mechanism of PINK1-Parkin activation by mitochondrial damage: loss of MMP stalls PINK1 import during its transfer from TOM to TIM23.
2025-08-06 | GSE298056 | GEO
Project description:PTEN-induced kinase 1 (PINK1) is a very short-lived protein that is required for the removal of damaged mitochondria through Parkin translocation and mitophagy. Because the short half-life of PINK1 limits its ability to be trafficked into neurites, local translation is required for this mitophagy pathway to be active far from the soma. The Pink1 transcript is associated with and cotransported with neuronal mitochondria. In concert with translation, the mitochondrial outer membrane protein Synaptojanin 2 Binding Protein (SYNJ2BP) and Synaptojanin 2 (SYNJ2) are required for tethering Pink1 mRNA to mitochondria via an RNA-binding domain in SYNJ2. This neuron-specific adaptation for local translation of PINK1 provides distal mitochondria with a continuous supply of PINK1 for activation of mitophagy.
2022-01-14 | GSE193443 | GEO
Project description:Loss of function in the PTEN-induced kinase 1 gene (Pink1) causes an early-onset, autosomal recessive form of PD. The translational Pink1-/- rat shows cranial sensorimotor deficits including: declines in ultrasonic vocalization, negative impacts on social vocal function, and alterations to thyroarytenoid muscle structure. The aim of this study was to identify differentially expressed genes using RNA-sequencing and bioinformatic analysis of the thyroarytenoid muscle of male Pink1-/- rats compared to wildtype controls. To construct gene co-expression networks and gene modules, a WGCNA was used to identify biological networks of interest including where Pink1 was a central node with interconnecting genes. Data are congruent with previous findings demonstrating changes to thyroarytenoid muscle structure. These data are consistent with the hypothesis that differences in peripheral biology may influence the early pathogenesis of vocalizations at the level of the thyroarytenoid muscle.
2020-05-27 | GSE151209 | GEO
Project description:Parkinson’s disease (PD) is a neurodegenerative disorder with a high variability of age at onset, disease severity, and progression. This suggests that other factors, including genetic, environ-mental, or biological factors, are at play in PD. Loss of PINK1 causes a recessive form of PD and is typically fully penetrant; however, it features a wide range in disease onset, further supporting the existence of protective factors, endogenous or exogenous, to play a role. Loss of Pink1 in Drosophila melanogaster results in locomotion deficits, also observed in PINK1-related PD in humans. In flies, Pink1 deficiency induces defects in the ability to fly; none-theless, around ten percent of the mutant flies are still capable of flying, indicating that advanta-geous factors affecting penetrance also exist in flies. Here, we aimed to identify the mechanisms underlying this reduced penetrance in Pink1-deficient flies. We performed genetic screening in pink1-mutant flies to identify RNA expression alterations affecting the flying ability. The most important biological processes involved were transcription-al and translational activities, endoplasmic reticulum (ER) regulation, and flagellated movement and microtubule organization. We validated 2 ER-related proteins, zonda, and windbeutel, to positively affect the flying ability of Pink1-deficient flies. Thus, our data suggest that these pro-cesses are involved in the reduced penetrance and that influencing them may be beneficial for Pink1 deficiency.
2025-01-31 | GSE287758 | GEO
Project description:To investigate the PINK1 regulates mitochondrial function, we performed the gene expression data for two independent libraries for Pink1-/- and Pink1+/+ mice, at two different time points, 4 and 24 months.
2023-05-16 | GSE217775 | GEO