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Nynrin preserves hematopoietic stem cell function by inhibiting the mitochondrial permeability transition pore opening (RNA-Seq for Nynrin cko HSC)

ABSTRACT: Nynrin preserves hematopoietic stem cell function by inhibiting the mitochondrial permeability transition pore opening (RNA-Seq for Nynrin cko HSC)

PROVIDER: PRJNA1045292 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26949812_1.fastq.gz	Fastqsanger.gz
	SRR26949812_2.fastq.gz	Fastqsanger.gz
	SRR26949813_1.fastq.gz	Fastqsanger.gz
	SRR26949813_2.fastq.gz	Fastqsanger.gz
	SRR26949814_1.fastq.gz	Fastqsanger.gz

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Nynrin preserves hematopoietic stem cell function by inhibiting the mitochondrial permeability transition pore opening （human_HSC_RNA_Seq)

Project description:Mitochondria have recently been identified as a critical regulator for the homeostasis of hematopoietic stem cells (HSCs). However, the mechanism underlying HSC regulation still needs to be clarified. Here, we identify transcription factor Nynrin as a novel regulator of HSC maintenance through modulation of mitochondrial function. We demonstrate that Nynrin is highly expressed in HSC under steady and stress state. Nynrin knockout leads to significantly decreased long-term HSC frequency, markedly reduced HSC dormancy, and self-renewal capacity in steady-state and stress hematopoiesis. We observed abnormal mitochondrial metabolism and mitochondrial permeability transition pore (mPTP) opening in Nynrin-deficient HSCs. Notably, Nynrin-deficient HSCs are more compromised in tolerance of irradiation- and 5-fluorouracil-induced stresses and exhibit typical phenotypes of necrosis. In contrast, overexpression of Nynrin in HSC is resistant to the radiation. Mechanistically, Nynrin deletion induces transactivation of Ppif. Overexpression of cyclophilin D (CypD), the protein encoded by the Ppif gene, causes mPTP opening, mitochondrial swelling, ROS overinduction, and cell necrosis. Both blocking the function of CypD by using cyclosporin A (CsA) or reducing the expression of Ppif could inhibit Nynrin deficiency-induced mitochondrial metabolism enhancement and ROS overproduction, thereby evidently rescuing the impairment of HSCs in Nynrin mutant mice. Collectively, our data, for the first time, characterize Nynrin as a critical regulator of HSC function acting through the Ppif/mPTP mitochondria axis and highlight the importance of Nynrin in HSC maintenance. These data provide new insights into the mechanisms for controlling HSC fate.

2024-06-01 | GSE248636 | GEO

Nynrin preserves hematopoietic stem cell function by inhibiting the mitochondrial permeability transition pore opening (ChIP_Seq)

2024-06-01 | GSE248635 | GEO

Nynrin preserves hematopoietic stem cell function by inhibiting the mitochondrial permeability transition pore opening (RNA-Seq for Nynrin cko HSC)

2024-06-01 | GSE248637 | GEO

Nynrin preserves hematopoietic stem cell function by inhibiting the mitochondrial permeability transition pore opening (scRNA-Seq)

2024-06-01 | GSE248638 | GEO

Nynrin preserves hematopoietic stem cell function by inhibiting the mitochondrial permeability transition pore opening.

Project description:Nynrin preserves hematopoietic stem cell function by inhibiting the mitochondrial permeability transition pore opening.

| PRJNA1045290 | ENA

Nynrin preserves hematopoietic stem cell function by inhibiting the mitochondrial permeability transition pore opening (ChIP_Seq)

Project description:Nynrin preserves hematopoietic stem cell function by inhibiting the mitochondrial permeability transition pore opening (ChIP_Seq)

| PRJNA1045291 | ENA

Nynrin preserves hematopoietic stem cell function by inhibiting the mitochondrial permeability transition pore opening （human_HSC_RNA_Seq)

Project description:Nynrin preserves hematopoietic stem cell function by inhibiting the mitochondrial permeability transition pore opening （human_HSC_RNA_Seq)

| PRJNA1045293 | ENA

Nynrin preserves hematopoietic stem cell function by inhibiting the mitochondrial permeability transition pore opening (scRNA-Seq)

Project description:Nynrin preserves hematopoietic stem cell function by inhibiting the mitochondrial permeability transition pore opening (scRNA-Seq)

| PRJNA1045295 | ENA

CircBIRC6-2 inhibits transmissible gastroenteritis virus induced mitochondrial permeability transition pore opening by its encoding protein

Project description:Transmissible gastroenteritis virus (TGEV), a member of coronavirus, is the pathogen of TGE. We previously found 123 circular RNAs (circRNAs) were differential expression during activation of mitochondrial permeability transition in porcine intestinal epithelial cells-jejunum 2 cell line (IPEC-J2) in response to TGEV infection. Mitochondrial permeability transition pore (mPTP) is a transmembrane pore of mitochondria and plays a key role in MPT. mPTP abnormal opening causes MPT. Therefore, we postulated that circRNAs might be related to mPTP abnormal opening induced by TGEV. In this study, we found that circBIRC6-2 could inhibit the mPTP abnormal opening induced by TGEV. Interestingly, circBIRC6-2 encodes protein BIRC6-236aa. An open reading frame (ORF) and internal ribosomal entrance site (IRES) of circBIRC6-2 were identified. We also found that BIRC6-236aa rather than circBIRC6-2 inhibited the mPTP opening by overexpression of circBIRC6-2 related vectors. We obtained 91 proteins that interacted with BIRC6-236aa using immunoprecipitation-mass spectrometry (IP-MS). The interaction between voltage-dependent anion-selective channel protein 1 (VDAC1) and BIRC6-236aa was demonstrated through co-immunoprecipitation (Co-IP). Moreover, BIRC6-236aa could inhibit the formation of VDAC1 and Cyclophilin D (CypD) complexes. Overall, these results indicated that BIRC6-236aa antagonized mPTP opening by interacting with VDAC1 to weaken the extent of interaction between VDAC1 and CypD.

2022-10-13 | PXD029055 | Pride

Nynrin preserves hematopoietic stem cell function by inhibiting the mitochondrial permeability transition pore opening.

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-06-01 | GSE248639 | GEO