Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Lactate facilitates pancreatic repair following acute pancreatitis by promoting reparative macrophage polarization

ABSTRACT: Lactate facilitates pancreatic repair following acute pancreatitis by promoting reparative macrophage polarization

PROVIDER: PRJNA1264967 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR33618923_1.fastq.gz	Fastqsanger.gz
	SRR33618923_2.fastq.gz	Fastqsanger.gz
	SRR33618924_1.fastq.gz	Fastqsanger.gz
	SRR33618924_2.fastq.gz	Fastqsanger.gz
	SRR33618925_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 56

Similar Datasets

Lactate facilitates pancreatic repair following acute pancreatitis by promoting reparative macrophage polarization

Project description:Based on the role of lactate in mitigating inflammation during acute pancreatitis (AP) repair, we focused on macrophages, as previous studies have highlighted their essential role in pancreatic tissue repair following AP. To investigate the relationship between lactate and the phenotype and function of macrophages during the recovery phase after AP, we performed high-throughput mRNA sequencing on macrophages isolated from the pancreatic tissues of C57BL/6J wild-type mice, which were administered lactate or PBS following induction of a recovery AP model.

2025-05-22 | GSE297476 | GEO

Effect of kinsenoside on bone marrow-derived macrophages during acute pancreatitis

Project description:Studies have shown that the small molecular compound kinsenoside (KD) can inhibit the M1 polarization of macrophages and inhibit the expression of proinflammatory genes. However, the role of kinsenoside in acute pancreatitis is unclear. Our study showed that intraperitoneal injection of kinsenoside can alleviate acute pancreatitis in mice. In order to find out the main mechanism by which kinsenoside affects the polarization of macrophages in acute pancreatitis, we further performed transcriptomic analysis of bone marrow-derived macrophages (BMDMs) stimulated by injured pancreatic acinar cell conditioned media (PAC-CM) treated with or without kinsenoside. This work provides a potential therapeutic approach for acute pancreatitis.

2025-01-27 | GSE285782 | GEO

Lactate regulates cell cycle and proliferation by remodeling the anaphase promoting complex

Project description:Lactate is abundant in rapidly dividing cells, due to the requirement for elevated glucose catabolism to support proliferation. However, it is not known whether accumulated lactate affects the proliferative state. Here, we deploy a systematic approach to determine lactate-dependent regulation of proteins across the human proteome. From this data, we elucidate a mechanism of cell cycle regulation whereby accumulated lactate activates the anaphase promoting complex (APC/C). Remodeling of APC/C in this way is caused by direct inhibition of the SUMO protease SENP1 by lactate. We discover that accumulated lactate binds and inhibits SENP1 by forming a complex with zinc in the SENP1 active site. SENP1 inhibition by lactate stabilizes SUMOylation of two residues on APC4, which are required to reorient APC/C to allow UBE2C binding and thus increase APC/C activity. This direct regulation of APC/C by lactate is required to stimulate timed degradation of cell cycle proteins, and efficient mitotic exit in proliferative mammalian cells. The above mechanism is initiated upon mitotic entry when lactate abundance reaches its apex. In this way, accumulation of lactate communicates the consequences of a nutrient replete growth phase to stimulate timed opening of APC/C, cell division, and proliferation. Conversely, we show that aberrant remodeling of APC/C by lactate occurs when lactate concentrations are chronically elevated, which is a hallmark of numerous cancers. Moreover, persistent lactate accumulation overcomes anti-mitotic pharmacology to drive mitotic slippage via the newfound mode of APC/C activation. Taken together, we define a biochemical mechanism through which lactate directly regulates protein function to control cell cycle and proliferation.

2023-02-07 | PXD036641 | Pride

Proteomic Identification of Interferon-induced Proteins with Tetratricopeptide Repeats (IFITs) as Markers of M1 Macrophage Polarization

Project description:Proteomic studies of macrophage polarization to pro-inflammatory (M1) or tissue reparative (M2) phenotypes has identified interferon-induced proteins with tetratricopeptide repeats (IFIT1, IFIT2 and IFIT3) as potential biomarkers of inflammatory diseases such as atherosclerosis.

2018-03-15 | PXD008204 | Pride

TNF promotes SREBP activity to regulate macrophage polarization and tissue repair [RNA-seq]

Project description:TNF-mediated macrophage polarization is important for inflammatory disease pathogenesis, but mechanisms that regulate polarization are not well understood. Transcriptomic and epigenomic analysis of the TNF response in primary human macrophages revealed late phase activation of SREBP2, the master regulator of cholesterol biosynthesis genes. TNF stimulation extended the genomic profile of SREBP2 occupancy to include binding to and activation of inflammatory and interferon response genes independently of its functions in sterol metabolism. Genetic ablation of SREBP function shifted the balance of macrophage polarization from M1 to an M2-like reparative phenotype in peritonitis and skin wound healing models. Genetic ablation of SREBP activity in myeloid cells or topical pharmacological inhibition of SREBP improved skin wound healing under homeostatic and chronic inflammatory conditions. Our results identify a new function and mechanism of action for SREBP2 in augmenting TNF-induced M1 macrophage polarization and inflammation, and open therapeutic avenues for promoting wound repair.

2019-04-03 | GSE129210 | GEO

TNF promotes SREBP activity to regulate macrophage polarization and tissue repair [ATAC-seq]

2019-04-03 | GSE129167 | GEO

TNF promotes SREBP activity to regulate macrophage polarization and tissue repair [ChIP-seq]

2019-04-03 | GSE129202 | GEO

TNF promotes SREBP activity to regulate macrophage polarization and tissue repair [scRNA-seq]

2019-04-03 | GSE129225 | GEO

Transcription profiling of human pancreas from patients with autoimmune pancreatitis and alcohol-induced chronic pancreatitis

Project description:Autoimmune pancreatitis (AIP) is a recently identified disease of the pancreas with unknown etiology and antigens. The aim of this study was to determine new target antigens and differentially regulated genes and proteins by means of transcriptomics and proteomics and to validate them in patients with autoimmune pancreatitis. Here we report a distinct downregulation at the RNA and protein level of pancreatic proteases (anionic trypsinogen, cationic trypsinogen, mesotrypsinogen, elastase IIIB) and pancreatic stone protein in autoimmune pancreatitis in comparison to alcohol-induced chronic pancreatitis.

2008-12-31 | E-MEXP-804 | biostudies-arrayexpress

RNA-Seq of isolated pancreatic stellate cells from mice with autoimmune pancreatitis and chronic pancreatitis

Project description:Autoimmune pancreatitis (AIP) is a disease with unclear immunologic triggers. This study shows that the pancreatic stellate cells(PSCs) are involved in the regulation of the immune response and can cause autoimmunity when the NF-κB signalling in these cells is disrupted. The PSCs were isolated from animals which show autoimmune pancreatitis (NEMO knockout group) or chronic pancreatitis (NEMO wildtype group).

2023-06-30 | E-MTAB-7337 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data