Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Mesenchymal stromal cells ameliorate epithelial damage after extended partial hepatectomy in the pig by modulation of thrombospondin-1/TGF-β [liver]

ABSTRACT: By using high-density DNA microarrays, we analyzed the gene-expression profile of liver biopsies from pigs Brückner et al. 2021 published

ORGANISM(S): Sus scrofa

PROVIDER: GSE134968 | GEO | 2021/07/01

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Mesenchymal stromal cells ameliorate epithelial damage after extended partial hepatectomy in the pig by modulation of thrombospondin-1/TGF-β [lung]

Project description:By using high-density DNA microarrays, we analyzed the gene-expression profile of lung biopsies from pigs.

2021-07-01 | GSE134969 | GEO

Mesenchymal stromal cells ameliorate epithelial damage after extended partial hepatectomy in the pig by modulation of thrombospondin-1/TGF-β

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

2021-07-01 | GSE134970 | GEO

Mesenchymal stromal cells ameliorate epithelial damage after extended partial hepatectomy in the pig by modulation of thrombospondin-1/TGF-β

Project description:Mesenchymal stromal cells ameliorate epithelial damage after extended partial hepatectomy in the pig by modulation of thrombospondin-1/TGF-β

| PRJNA556892 | ENA

Mesenchymal stromal cells ameliorate epithelial damage after extended partial hepatectomy in the pig by modulation of thrombospondin-1/TGF-β [lung]

Project description:Mesenchymal stromal cells ameliorate epithelial damage after extended partial hepatectomy in the pig by modulation of thrombospondin-1/TGF-β [lung]

| PRJNA556893 | ENA

Mesenchymal stromal cells ameliorate epithelial damage after extended partial hepatectomy in the pig by modulation of thrombospondin-1/TGF-β [liver]

Project description:Mesenchymal stromal cells ameliorate epithelial damage after extended partial hepatectomy in the pig by modulation of thrombospondin-1/TGF-β [liver]

| PRJNA556894 | ENA

Mesenchymal stromal cells mitigate liver damage after extended resection in the pig by modulating thrombospondin-1/TGF-β.

Project description:Post-surgery liver failure is a serious complication for patients after extended partial hepatectomies (ePHx). Previously, we demonstrated in the pig model that transplantation of mesenchymal stromal cells (MSC) improved circulatory maintenance and supported multi-organ functions after 70% liver resection. Mechanisms behind the beneficial MSC effects remained unknown. Here we performed 70% liver resection in pigs with and without MSC treatment, and animals were monitored for 24 h post surgery. Gene expression profiles were determined in the lung and liver. Bioinformatics analysis predicted organ-independent MSC targets, importantly a role for thrombospondin-1 linked to transforming growth factor-β (TGF-β) and downstream signaling towards providing epithelial plasticity and epithelial-mesenchymal transition (EMT). This prediction was supported histologically and mechanistically, the latter with primary hepatocyte cell cultures. MSC attenuated the surgery-induced increase of tissue damage, of thrombospondin-1 and TGF-β, as well as of epithelial plasticity in both the liver and lung. This suggests that MSC ameliorated surgery-induced hepatocellular stress and EMT, thus supporting epithelial integrity and facilitating regeneration. MSC-derived soluble factor(s) did not directly interfere with intracellular TGF-β signaling, but inhibited thrombospondin-1 secretion from thrombocytes and non-parenchymal liver cells, therewith obviously reducing the availability of active TGF-β.

| S-EPMC8642541 | biostudies-literature

Transcriptome sequencing and metabolome analysis reveal the metabolic reprogramming of partial hepatectomy and extended hepatectomy.

Project description:Surgical resection remains a critical treatment option for many patients with primary and secondary hepatic neoplasms. Extended hepatectomy (eHx) may be required for some patients with large tumors, which may cause liver failure and death. Partial hepatectomy (pHx) and eHx mouse models were constructed, liver tissues were sampled at 18, 36, and 72 h posthepatectomy. Transcriptome and metabolome analyses were employed to explore the different potential mechanisms in regeneration and injury between pHx and eHx. The results showed that eHx was associated with more severe liver injury and lower survival rates than pHx. Transcriptomics data showed there were 1842, 2129, and 1277 differentially expressed genes (DEGs) in eHx and 962, 1305, and 732 DEGs in pHx at 18, 36, and 72 h posthepatectomy, respectively, compared with the those in the sham groups. Compared with pHx, the number of DEGs in the eHx group reached a maximum of 230 at 18 h after surgery and decreased sequentially to 87 and 43 at 36 and 72 h. Metabolomics analysis identified a total of 1399 metabolites, and 48 significant differentially produced metabolites (DPMs) were screened between eHx and pHx. Combined analysis of DEGs and DPMs indicated that cholesterol metabolism and insulin resistance may be two important pathways for liver regeneration and mouse survival postextended hepatectomy. Our results showed the global influence of pHx and eHx on the transcriptome and metabolome in mouse liver, and revealed cholesterol metabolism and insulin resistance pathways might be involved in regeneration post-pHx and -eHx.

| S-EPMC10486020 | biostudies-literature

Haploinsufficiency of Def activates p53-dependent TGF? signalling and causes scar formation after partial hepatectomy.

Project description:The metazoan liver exhibits a remarkable capacity to regenerate lost liver mass without leaving a scar following partial hepatectomy (PH). Whilst previous studies have identified components of several different signaling pathways that are essential for activation of hepatocyte proliferation during liver regeneration, the mechanisms that enable such regeneration to occur without accompanying scar formation remain poorly understood. Here we use the adult zebrafish liver, which can regenerate within two weeks following PH, as a new genetic model to address this important question. We focus on the role of Digestive-organ-expansion-factor (Def), a nucleolar protein which has recently been shown to complex with calpain3 (Capn3) to mediate p53 degradation specifically in the nucleolus, in liver regeneration. Firstly, we show that Def expression is up-regulated in the wild-type liver following amputation, and that the defhi429/+ heteroozygous mutant (def+/-) suffers from haploinsufficiency of Def in the liver. We then show that the expression of pro-inflammatory cytokines is up-regulated in the def+/- liver, which leads to distortion of the migration and the clearance of leukocytes after PH. Transforming growth factor ? (TGF?) signalling is thus activated in the wound epidermis in def+/- due to a prolonged inflammatory response, which leads to fibrosis at the amputation site. Fibrotic scar formation in def+/- is blocked by the over-expression of Def, by the loss-of-function of p53, and by treatment with anti-inflammation drug dexamethasone or TGF?-signalling inhibitor SB431542. We finally show that the Def- p53 pathway suppresses fibrotic scar formation, at least in part, through the regulation of the expression of the pro-inflammatory factor, high-mobility group box 1. We conclude that the novel Def- p53 nucleolar pathway functions specifically to prevent a scar formation at the amputation site in a normal amputated liver.

| S-EPMC4011785 | biostudies-literature

Is Increased Sinusoidal Flow in the Liver Remnant the primary Stimulus to Regeneration after partial Hepatectomy

Project description:The impact of portal arterialization on the liver parenchyma was studied in a series of six pigs with aortoportal shunting of liver segments II, III and IV (and 6 sham animals). Gene expression in the arterialized segments was compared to expression in sham animals. Primary endpoints were gene expression profiles in the hyperperfused segments at sampling time points 1, 5, 10, 30, 60, 90 minutes and 2, 3, 4 and 6 hours after shunt opening. Keywords: time course, treatment comparison Six pigs were treated with aortoportal shunting of segments II, III and IV and six animals were subject to sham surgery. Expression profiling was conducted by hybridizing each sample against a common reference, consisting of liver RNA from an unrelated animal..

2010-05-07 | E-GEOD-13683 | biostudies-arrayexpress

Thrombospondin-1 is a novel negative regulator of liver regeneration after partial hepatectomy through transforming growth factor-beta1 activation in mice.

Project description:The matricellular protein, thrombospondin-1 (TSP-1), is prominently expressed during tissue repair. TSP-1 binds to matrix components, proteases, cytokines, and growth factors and activates intracellular signals through its multiple domains. TSP-1 converts latent transforming growth factor-beta1 (TGF-?1) complexes into their biologically active form. TGF-? plays significant roles in cell-cycle regulation, modulation of differentiation, and induction of apoptosis. Although TGF-?1 is a major inhibitor of proliferation in cultured hepatocytes, the functional requirement of TGF-?1 during liver regeneration remains to be defined in vivo. We generated a TSP-1-deficient mouse model of a partial hepatectomy (PH) and explored TSP-1 induction, progression of liver regeneration, and TGF-?-mediated signaling during the repair process after hepatectomy. We show here that TSP-1-mediated TGF-?1 activation plays an important role in suppressing hepatocyte proliferation. TSP-1 expression was induced in endothelial cells (ECs) as an immediate early gene in response to PH. TSP-1 deficiency resulted in significantly reduced TGF-?/Smad signaling and accelerated hepatocyte proliferation through down-regulation of p21 protein expression. TSP-1 induced in ECs by reactive oxygen species (ROS) modulated TGF-?/Smad signaling and proliferation in hepatocytes in vitro, suggesting that the immediately and transiently produced ROS in the regenerating liver were the responsible factor for TSP-1 induction.We have identified TSP-1 as an inhibitory element in regulating liver regeneration by TGF-?1 activation. Our work defines TSP-1 as a novel immediate early gene that could be a potential therapeutic target to accelerate liver regeneration.

| S-EPMC3295913 | biostudies-literature

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