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UCHL1 Maintains Microenvironmental Homeostasis of Male Germline Stem Cells by Antagonizing HSPA8

ABSTRACT: To illustrate the mechanism of UCHL1 and HSPA8 affects SSCs in the testis, mGSCs-I-SB cells were used to study in vitro, we down-regulated UCHL1 and HSPA8 using shRNA in mGSCs-I-SB cells. We then performed gene expression profiling analysis using data obtained from RNA-seq of 3 different cells

ORGANISM(S): Capra hircus

PROVIDER: GSE237083 | GEO | 2026/07/01

REPOSITORIES: GEO

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UCHL1 Maintains Microenvironmental Homeostasis of Male Germline Stem Cells by Antagonizing HSPA8

Project description:UCHL1 Maintains Microenvironmental Homeostasis of Male Germline Stem Cells by Antagonizing HSPA8

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Uchl1 maintains energy and metabolic homeostatic balance during spermatogenesis

Project description:In mammals, spermatogenesis plays a critical role in upholding the genetic stability of the male germline; however, disruptions such as viral and bacterial infections, toxic damage, genetic mutations, or deletions can disturb the delicate equilibrium of the testicular microenvironment, ultimately resulting in impaired spermatogenesis and male infertility. One key protein involved in this process is UCHL1, which possesses deubiquitinating enzyme, multiple ligases, and hydrolase activities. In addition to its roles in maintaining neuronal activity and memory function in the brain, UCHL1 is also implicated in spermatogenesis. Nevertheless, the precise mechanism by which it sustains metabolic homeostasis during spermatogenesis remains unclear. To investigate this, we generated Uchl1_KO mice and subjected their testes to snRNA-seq and metabolomics sequencing. Our analysis revealed that Uchl1_KO mice exhibited abnormal spermatogenesis, decreased testicular OXHPOS levels, and disrupted ADIPONECTIN signaling, concomitant with heightened inflammatory signaling and disturbances in lipid metabolism and energy homeostasis in the testes. These findings suggest that Uchl1 plays a crucial role in spermatogenesis by modulating energy and metabolic pathways within the testes to maintain orderly spermatogenesis. This study contributes to the understanding of the energy and metabolic balance required for successful male spermatogenesis.

2025-05-01 | GSE267378 | GEO

RNA-seq of HSPA8 knockdown in MDA-MB-468 cells

Project description:We used three siRNAs to silence HSPA8 in MDA-MB-468 cells, and then used RNA-seq to compare HSPA8 knockdown cells with the controls.

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Genes regulated by UCHL1 in ovarian cancer cells

Project description:UCHL1 is related to apoptosis and proliferation in cancers and we sought to identify genes regulated by UCHL1

2013-01-30 | GSE43884 | GEO

Genes regulated by UCHL1 in ovarian cancer cells

Project description:UCHL1 is related to apoptosis and proliferation in cancers and we sought to identify genes regulated by UCHL1 UCHL1 was knocked down in A2780 (A2780-shUCHL1). A2780-shUCHL1 and A2780-control were cultured in RPMI and total RNA was extracted and hybridizated on Affymetrix.GeneChip.HG-U133_Plus_2

2013-01-30 | E-GEOD-43884 | biostudies-arrayexpress

HSPA8 dampens SCAP/INSIG split and SREBP activation by reducing PKR-mediated INSIG phosphorylation

Project description:Lipid accumulation in the renal tubules is a major determinant of diabetic kidney disease (DKD), and activation of SREBPs plays a central role in this process. Our study aimed to explore whether HSPA8, a molecular chaperone, is the master regulator of INSIG/SREBPs function in DKD. Here, we showed that tubular epithelial cell (TEC)-specific knockout of HSPA8 upregulated the phosphorylation of INSIG1 and INSIG2, which disrupted the interaction between INSIG proteins and SCAP, leading to the translocation of the SCAP-SREBP complex to the Golgi apparatus, and the activation of SREBPs. TEC-specific overexpression of HSPA8 restrained these changes. INSIG1 and INSIG2 can be phosphorylated by protein kinase R (PKR), while HSPA8 can recognize PKR and recruit the E3 ubiquitin ligase (CHIP) to promote PKR ubiquitination and degradation. SREBP1 transcriptionally activated HSPA8 expression under temporary hyperglycemic stimulation. However, persistent hyperglycemia reduced HSPA8 levels by promoting nuclear factor (NF)-κB-mediated transcriptional inhibition and reducing USP43-mediated deubiquitination of HSPA8. Collectively, these findings indicate that the molecular chaperone HSPA8 serves as a negative feedback regulator of SREBPs, lipogenesis, and DKD development.

2024-12-12 | GSE283754 | GEO

Uchl1 maintains energy and metabolic homeostatic balance during spermatogenesis

Project description:Uchl1 maintains energy and metabolic homeostatic balance during spermatogenesis

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Ubiquitin C-terminal hydrolase isozyme L1 (UCHL1) is associated with shelterin complex at interstitial telomeric sites

Project description:Ubiquitin C-terminal hydrolase isozyme L1 (UCHL1) is primarily expressed in neuronal cells and neuroendocrine cells. It is a multifunctional protein involved in deubiquitination, ubiquitination, and ubiquitin homeostasis. UCHL1 has been associated with various diseases, including many cancers, but its specific roles are disputed and still generally undetermined. Herein, we demonstrate that UCHL1 is associated with genomic DNA in certain prostate cancer cell lines, including DU 145 cells derived from a brain metastatic site, and in HEK293T embryonic kidney cells with a neuronal lineage. Chromatin immunoprecipitation and sequencing revealed that UCHL1 localizes to TTAGGG repeats at telomeres and interstitial telomeric sequences, as do TRF1 and TRF2, components of the shelterin complex. A weak or transient interaction between UCHL1 and the shelterin complex was confirmed by immunoprecipitation and proximity ligation assays. UCHL1 and TERF2IP, also a component of the shelterin complex, were bound to the nuclear scaffold. UCHL1 may play a role in regulating gene expression by affecting the stabilization of the shelterin proteins or influencing nuclear targeting. As several shelterin proteins (TRF1, TRF2, POT1 and TERF2IP) are ubiquitinated, UCHL1 may have a role in regulating the stability of these proteins. UCHL1 may also regulate the nuclear location of shelterin-associated genomic regions.

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Differential gene expression in UCHL1 silenced ovarian cancer cells

Project description:We report dysregulated genes upon silencing UCHL1 in high-grade serous ovarian cancer cell line, Kuramochi.

2024-03-15 | GSE168935 | GEO

Metabolic reprogramming in astrocytes prevents neuronal death through a UCHL1/PFKFB3/H4K8la positive feedback loop

Project description:Astrocytic metabolic reprogramming is an adaptation of metabolic patterns to meet increased energy demands, although the role after spinal cord injury (SCI) remains unclear. Analysis of single-cell RNA sequencing (scRNA-seq) data identified an increase in astrocytic glycolysis, while PFKFB3, a key regulator of glycolytic flux, was significantly upregulated following SCI. Loss of PFKFB3 in astrocytes prohibited neuronal energy supply and enhanced neuronal ferroptosis in vitro and inhibited astrogliosis, expanded neuroinflammation, exacerbated neuronal loss, and hindered functional recovery in vivo after SCI. Mechanistically, deubiquitinase UCHL1 plays a crucial role in stabilizing and enhancing PFKFB3 expression by cleaving K48-linked ubiquitin chains. Genetic deletion of Uchl1 inhibited locomotor recovery after SCI by suppression of PFKFB3-induced glycolytic reprogramming in astrocytes. Furthermore, the UCHL1/PFKFB3 axis increased lactate production, leading to enhanced histone lactylation and subsequent transcription of Uchl1 and several genes related to glycolysis, suggesting a glycolysis/H4K8la/UCHL1 positive feedback loop. These findings help to clarify the role of the UCHL1/PFKFB3/H4K8la loop in modulation of astrocytic metabolic reprogramming and reveal a potential target for treatment of SCI.

2025-02-21 | GSE266984 | GEO

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