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Stem Leydig cells support macrophage immunological homeostasis through intercellular mitochondria transfer in a TRPM7-mediated manner in the testis

ABSTRACT: Stem Leydig cells support macrophage immunological homeostasis through intercellular mitochondria transfer in a TRPM7-mediated manner in the testis

PROVIDER: PRJNA1072138 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27840777_1.fastq.gz	Fastqsanger.gz
	SRR27840777_2.fastq.gz	Fastqsanger.gz
	SRR27840778_1.fastq.gz	Fastqsanger.gz
	SRR27840778_2.fastq.gz	Fastqsanger.gz
	SRR27840779_1.fastq.gz	Fastqsanger.gz

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Stem Leydig cells support macrophage immunological homeostasis through intercellular mitochondria transfer in a TRPM7-mediated manner in the testis

Project description:As a unique population of testicular mesenchymal stromal cells, stem Leydig cells (SLCs) have shown great promise in the treatment of male hypogonadism. The therapeutic functions of MSCs are largely determined by their reciprocal regulation by immune responses. However, the immunoregulatory properties of SLCs have not been fully studied. Here, we found that transplanted SLCs restored testicular immunological homeostasis via damage signal-triggered transient receptor potential cation channel subfamily member 7 (TRPM7)-mediated mitochondrial transfer to macrophages. Specifically, the results showed that SLCs transplantation restored male fertility and testosterone production in an ischemia‒reperfusion injury-induced acute inflammation model. This was achieved mainly via a mechanism involving the prevention of inflammatory cascades but not the differentiation to Leydig cells (LCs), the main testosterone-producing cells. Furthermore, we identified that ROS released from activated macrophages, which are the primary testicular immunocytes, induced nanotube-mediated mitochondrial transfer from SLCs to macrophages via TRPM7. Notably, TRPM7 knockdown by interfering RNA in transplanted SLCs compromised the therapeutic outcomes in both testicular ischemia‒reperfusion and testicular aging mouse models. Collectively, SLC rescued testicular damage in testicular ischemia‒reperfusion mouse models, and the damage signal activated TRPM7 signaling and induced mitochondrial transfer from SLCs to macrophages, playing important roles in the repair of SLCs. These findings provide insight into the clinical translation of SLCs and suggest that strategies targeting mitochondrial transfer may be effective treatments for patients with male hypogonadism related to immune disorders.

2024-02-01 | GSE254881 | GEO

Leydig cell transcripts from adult mouse stage synchronized testis array

Project description:Leydig cell gene expression across the different stages of the seminiferous epithelium of mice with Synchronized spermatogenesis by WIN18,446/RA treatment combined with the RiboTag methodology Microarray analysis was used to identified Leydig cell-specific transcripts across the different stages of the seminiferous epithelium.

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TRPM7 maintains progenitor-like features of neuroblastoma cells

Project description:Analysis of the effect of shRNA-mediated knockdown of TRPM7 on gene expression levels in SH-SY5Y and SH-EP2 human neuroblastoma cells. Results were used for the identification of neural-crest-associated transcription factors that were affected by TRPM7 knockdown. Total RNA isolated from SH-EP2 and SH-SY5Y human neuroblastoma cells transduced with a scrambled shRNA (control) or TRPM7 shRNA, experiment performed in duplicate.

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Expression profiles from HEK293 cells by overexpression of TRPM7 channel

Project description:The functional activity of TRPM7 is essential for cell viability and growth, and its expression is up-regulated in certain pathological conditions. In order to assess the effects of TRPM7 activity on cellular gene expression, inducible HEK293 cell-lines harboring the wild-type mouse TRPM7 and a mutant lacking the kinase domain were established. By using microarray analysis, we identified genetic profiles altered in transcription significantly and specifically by the expression of the functional TRPM7 channel. Overexpression of TRPM7 channel in HEK cells induce the cell damage and cell death. So we used tetracycline-inducible system for channel expression. However, since the treatment of inducer itself could also affect the transcription profile, we established another cell-line harboring a nonfunctional TRPM7 mutant (TRPM7DKD) as a control in which the entire kinase domain at the C-terminus was deleted. The wild-type and the non-functional TRPM7 channels were induced transiently, and the comparative changes in cellular transcription were investigated

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TRPM7 maintains mesenchymal phenotype of breast cancer cells by tensional regulation of SOX4 (TRPM7 shRNA)

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Expression profiles from HEK293 cells by overexpression of TRPM7 channel

2011-07-23 | GSE23102 | GEO

RNA-seq analysis of Trpm7-deficient muscle satellite cells

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TRPM7 maintains progenitor-like features of neuroblastoma cells

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Profiling of villi transcriptome in Trpm7 gene deficient mice and control littermates.

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Essential Role of Mg2+ for Mouse Preimplantation Embryo Development Revealed by TRPM7 Chanzyme Deficient Gametes

Project description:TRPM7 (transient receptor potential cation channel subfamily M member 7) is a chanzyme with channel and kinase domains essential for embryo development. Using gamete-specific Trpm7-null lines, we report that TRPM7-mediated Mg2+ influx is indispensable for reaching the blastocyst stage. TRPM7 was expressed dynamically from gametes to blastocysts, displaying stage-specific and distinct localizations on the plasma membrane, cytoplasm, and nucleus, and undergoes cleavage that produces C- terminal kinase fragments. TRPM7 underpinned Mg2+ homeostasis throughout this time, and excess Mg2+ but not Zn2+ or Ca2+ overcame the arrest of Trpm7-null embryos; expressing Trpm7 mRNA restored development, but mutant versions failed or were less effective. Transcriptomic analyses of embryos lacking Trpm7 revealed an abundance of oxidative stress-pathway genes, confirmed by mitochondrial dysfunction, and a reduction of transcription factor networks essential for proliferation; Mg2+ supplementation corrected these defects. Hence, TRPM7 underpins Mg2+ homeostasis in preimplantation embryos, prevents oxidative stress, and promotes gene expression patterns necessary for developmental progression and cell lineage specification.

2024-01-22 | GSE241487 | GEO

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