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The effect of PTP1B inhibitor (MSI-1436) on neutrophils.

ABSTRACT: The effect of PTP1B inhibitor (MSI-1436) on neutrophils.

PROVIDER: PRJNA763548 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15905028.fastq.gz	Fastqsanger.gz
	SRR15905029.fastq.gz	Fastqsanger.gz
	SRR15905030.fastq.gz	Fastqsanger.gz
	SRR15905031.fastq.gz	Fastqsanger.gz
	SRR15905032.fastq.gz	Fastqsanger.gz

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The effect of PTP1B inhibitor (MSI-1436) on neutrophils.

Project description:Acute Lung Injury (ALI) can cause Acute Respiratory Distress Syndrome (ARDS), a lethal condition with limited treatment options and currently a common global cause of death due to COVID-19-induced ALI. ARDS secondary to Transfusion-Related Acute Lung Injury (TRALI) has been recapitulated pre-clinically by anti-MHC-I antibody administration to LPS-primed mice. In this model, we demonstrated that inhibitors of PTP1B, a protein tyrosine phosphatase that regulates signaling pathways of fundamental importance to homeostasis and inflammation, prevented lung injury and increased survival. Treatment with PTP1B inhibitors attenuated the aberrant neutrophil function that drives ALI, and was associated with release of myeloperoxidase, suppression of Neutrophil Extracellular Trap (NET) formation, and inhibition of neutrophil migration. Mechanistically, reduced signaling through the CXCR4 chemokine receptor, particularly to the activation of mTOR, was essential for these effects, linking PTP1B in hibition to promoting an aged neutrophil phenotype. Considering dysregulated activation of neutrophils is implicated in sepsis and can cause collateral tissue damage, we demonstrated also that PTP1B inhibitors improved survival and ameliorated lung injury in the LPS-induced sepsis model. Our data highlight PTP1B inhibition for prevention of TRALI and ARDS from multiple etiologies.

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PTP1B deficiency effect on mammary gland development and differentiation

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Identification of the role of PTP1B in acute kidney injury and its regulation via siRNA delivery with milk-derived extracellular vesicles

Project description:Acute kidney injury (AKI) is a critical condition marked by a sudden decline in kidney function, often triggered by ischemia-reperfusion (IR) injury. Its pathophysiology involves inflammation, oxidative stress, and endoplasmic reticulum (ER) stress. Recently, protein tyrosine phosphatase 1B (PTP1B) has been highlighted as a therapeutic target for ischemic disease due to its potential implication in activating ER stress. In this study, we observed significant overexpression of PTP1B in human kidney tissues during AKI. Additionally, in mouse models of AKI, we confirmed that this overexpression is associated with the upregulation of ER stress and inflammatory pathways mediated by Src. To explore the effect of PTP1B inhibition in AKI, we employed PTP1B-targeting siRNA (PTPi) delivered via extracellular vesicles derived from commercial milk (mEVs). PTPi@mEVs effectively reduced PTP1B expression in proximal tubular cells, decreasing ER stress and Src kinase activation. In an IR-AKI mouse, PTPi@mEVs alleviated renal dysfunction, reduced cell death, and restored gene expression related to inflammation, ROS, and ER stress. Histological analysis confirmed that PTP1B knockdown mitigated tight junction disruption in renal tissue. These findings underscore the therapeutic potential of targeting PTP1B to mitigate AKI symptoms, highlighting the efficacy of mEVs-mediated PTPi delivery in reducing acute inflammatory responses and renal dysfunction.

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