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PTP1B deficiency effect on mammary gland development and differentiation

ABSTRACT: Analysis of protein tyrosine phosphatase 1B (PTP1B) deficient mammary glands from nulliparous mice at estrous and pregnancy day 3, 7, 10 and 15. We used a genetically ablated PTP1B mouse model to gain a deeper knowledge of the role PTP1B plays in mammary gland development and to define the mechanism regulated by this phosphatase. Results provide insight into the role of PTP1B in mammary gland development and differentiation.

ORGANISM(S): Mus musculus

PROVIDER: GSE41768 | GEO | 2012/10/23

SECONDARY ACCESSION(S): PRJNA178146

REPOSITORIES: GEO

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PTP1B deficiency effect on mammary gland development and differentiation

Project description:Analysis of protein tyrosine phosphatase 1B (PTP1B) deficient mammary glands from nulliparous mice at estrous and pregnancy day 3, 7, 10 and 15. We used a genetically ablated PTP1B mouse model to gain a deeper knowledge of the role PTP1B plays in mammary gland development and to define the mechanism regulated by this phosphatase. Results provide insight into the role of PTP1B in mammary gland development and differentiation. Mouse mammary glands were isolated from PTP1B -/- and PTP1B +/+ nulliparous mice at estrous and pregnancy day 3, 7, 10 and 15 for RNA extraction and hybridization on Affymetrix microarrays.

2012-10-23 | E-GEOD-41768 | biostudies-arrayexpress

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

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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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Quantitative Proteomics Identifies Protein Tyrosine Phosphatase 1B as Modulator of B Cell Antigen Receptor Signaling

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Quantitative Proteomics Identifies Protein Tyrosine Phosphatase 1B as Modulator of B Cell Antigen Receptor Signaling

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Transcriptomic Analysis of Pubertal and Adult Virgin Mouse Mammary Epithelial and Stromal Cell Populations

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