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Plasminogen activator inhibitor-2 regulates immune response in kidney injury and renal aging mpact of plasminogen activator inhibitor-2 in kidney injury and renal aging

ABSTRACT: Plasminogen activator inhibitor-2 regulates immune response in kidney injury and renal aging mpact of plasminogen activator inhibitor-2 in kidney injury and renal aging

PROVIDER: PRJNA578663 | ENA |

REPOSITORIES: ENA

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Plasminogen activator inhibitor-2 regulates immune response in kidney injury and renal aging mpact of plasminogen activator inhibitor-2 in kidney injury and renal aging

Project description:The plasminogen activator inhibitor-2 (PAI-2; encoded by the SerpinB2 gene) has been described in the context of macrophage activation and in cellular senescence. As both mechanisms are important in kidney disease we tested a possible role of PAI-2 in renal injury and repair. Methods:Aging, ischemia/reperfusion injury and unilateral ureteral obstruction were performed on the mice. Bone marrow was transplantefrom SerpinB2-/- to wild-type littermates and vice versa. Primary tubular cells and macrophages from SerpinB2-/- and wildtype mice were used for functional studies and transcriptional profiling. Results: PAI-2 expression was up-regulated in cultured senescent tubular cells and in kidneys of aged mice. In the lack of PAI-2 in SerpinB2-/- mice was associated with enhanced renal fibrosis and an inflammatory phenotype during aging and in kidney injury models. While acute injury was associated with fewer monocytes/macrophages in SerpinB2-/- kidneys the subsequent resolution of inflammation seen in wildtype kidneys was lacking in knockout mice. Conclusion: PAI-2 regulates renal aging, tubular damage, and resolution of inflammation. PAI-2 is crucial for kidney repair in mice .

2019-10-22 | GSE139156 | GEO

HDXMS of urokinase plasminogen activator

Project description:HDX-MS of urokinase plasminogen activator in single-chain vs two-chain forms

2022-10-28 | MSV000090611 | MassIVE

HDX-MS of murine urokinase plasminogen activator and variants

Project description:HDX-MS data revealing long-range allostery that affects the catalytic activity of the serine protease, murine urokinase plasminogen activator. The allostery is mediated by the disordered region connecting the N-terminal EGF and kringle domains to the protease domain.

2024-02-06 | MSV000094027 | MassIVE

AMPK activator O304 protects against kidney aging through promoting energy metabolism and autophagy

Project description:Energy homeostasis plays a key role in retarding aging, and mitochondria are responsible for energy production.AMPK plays a central role in maintaining energy homeostasis and mitochondrial homeostasis, and commands autophagy, a clearing and recycling process to maintain cellular homeostasis. However, the effect of AMPK activators on kidney aging has not been fully elucidated. We testified the effects of O304, a novel direct AMPK activator, in naturally aging mice model and D-galactose (D-gal)-treated renal tubular cell culture. We identified that O304 perfectly protects against cellular senescence and aged-related fibrosis in kidneys. Also, O304 restored energy metabolism, promoted autophagy, and preserved mitochondrial homeostasis. Transcriptomic sequencing also proved that O304 induced fatty acid metabolism, mitochondrial biogenesis and ATP process, and downregulated cell aging, DNA damage response and collagen organization. All these results suggest that O304 has a strong potential to retard aged kidney injury through regulating AMPK-induced multiple pathways.

2022-01-27 | GSE192512 | GEO

Yes-Associated Protein (YAP) Induces a Secretome Phenotype and Transcriptionally Regulates Plasminogen Activator Inhibitor-1 (PAI-1) Expression in Hepatocarcinogenesis

Project description:To investigate how tumour cell-derived YAP is changing the paracrine communication network between tumour cells and non-tumorous cells in hepatocarcinogenesis, the expression and secretion of cytokines, growth factors and chemokines were analysed in transgenic mice with liver-specific and inducible expression of constitutively active human YAP (YAPS127A). Transcriptome analysis of primary isolated hepatocytes revealed that YAP overexpression induced the expression and secretion of many paracrine-acting factors with potential impact on other tumorous or non-tumorous cells (e.g. plasminogen activator inhibitor-1 (PAI-1), C-X-C motif chemokine ligand 13 (CXCL13), CXCL16).

2020-09-15 | GSE128043 | GEO

Synergy between plasminogen activator inhibitor-1 and Snail in tumoral migration

2008-12-31 | GSE10395 | GEO

Plasminogen Activator Inhibitor-1 Regulates the Cytoskeleton and Intrinsic Stiffness of Vascular Smooth Muscle Cells

Project description:Plasminogen Activator Inhibitor-1 Regulates the Cytoskeleton and Intrinsic Stiffness of Vascular Smooth Muscle Cells

| PRJNA936874 | ENA

Synergy between plasminogen activator inhibitor-1 and Snail in tumoral migration

Project description:Snail, a family of transcriptional repressors implicated in cell movement, has been correlated with tumour invasivity. The Plasminogen Activation system (PAs), including urokinase (uPA), its receptor (uPAR), and its inhibitor (PAI-1), also plays a key role in cancer invasion and metastasis, either through proteolytic degradation or by non proteolytic modulation of cell adhesion and migration. Thus, Snail and PAs both influence those processes and are over-expressed in cancers. In this study we aimed to determine first whether Snail activity is correlated with PAs components expression and second how this correlation can influence tumoral cell migration. Keywords: Tumoral migration Comparison the invasive breast cancer cell-line MDA-MB-231 expressing Snail (MDA-Neo) with its derived clone expressing a dominant negative form of Snail (Snail-DN). Expression of PAs mRNAs was performed by cDNA microarrays and real time quantitative RT-PCR. Wound healing assay was used to determine cell migration. PAI-1â??s distribution was assessed by immunostaining.

2010-06-24 | E-GEOD-10395 | biostudies-arrayexpress

Transcriptomic analysis of Urokinase plasminogen activator receptor silenced MDA-MB-231 breast cancer cells, stimulated with radiation.

Project description:Urokinase plasminogen activator receptor (PLAUR) is a GPI anchored extracellular surface receptor, playing a major role in remodeling of the extracellular matrix. It has the ability to interact with a variety of co-receptors for intracellular signaling. Over-expression of PLAUR is observed in many pathological conditions such as cancer, cardiovascular and chronic kidney diseases. We have recently demonstrated a novel role for PLAUR in DNA damage and repair processes. Here, we performed a two color microarray to understand the transcriptomic changes occuring in PLAUR silenced cells on treatment with DNA damaging radiation. Further, we would like to use this data to predict affected pathways and discover targets of therapeutic value.

2019-01-31 | E-MTAB-5298 | biostudies-arrayexpress

Plasminogen proteoform profiling

Project description:Plasminogen, the zymogen of plasmin, is a glycoprotein involved in fibrinolysis and a wide variety of other physiological processes. Plasminogen dysregulation has been implicated in a range of diseases. Classically, human plasminogen is categorized into two types based on the presence (type I) or absence (type II) of a single N-linked glycan, supposedly having different functional features. Using high-resolution native mass spectrometry (native MS), we uncover that the proteoform profiles of plasminogen (and plasmin) are substantially more extensive than this simple binary classification. In samples derived from human plasma, we identified up to 14 distinct proteoforms of human plasminogen, including a novel, highly abundant phosphorylation site at Ser339. To elucidate potential functional effects of these post-translational modifications, we performed proteoform-resolved kinetic analyses of the plasminogen-to-plasmin conversion using a canonical activator. This conversion is thought to involve at least two independent cleavage events: one to remove the N-terminal peptide, and another to form the active catalytic site. Our analyses reveal that these processes are not independent but are instead tightly regulated and occur in a step-wise order. Notably, N-terminal cleavage at the canonical site (Lys77) does not occur directly from intact plasminogen. Instead, an activation intermediate corresponding to cleavage at Arg68 is initially produced, which only then is further processed to the canonical Lys77 product. Based on our results, we propose a new categorization system for human plasminogen isoforms. This work highlights the capacity of high-resolution native MS to reveal new aspects of structure, even in frequently-studied serum glycoproteins.

2024-05-24 | PXD042225 | Pride

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