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Transcriptional changes in Wnt antagonism- and TGFβ agonism-induced MSC chondrogenesis.

ABSTRACT: Transcriptional changes in Wnt antagonism- and TGFβ agonism-induced MSC chondrogenesis.

PROVIDER: PRJNA870902 | ENA |

REPOSITORIES: ENA

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Transcriptional changes in Wnt antagonism- and TGFβ agonism-induced MSC chondrogenesis.

Project description:Wnt/β-catenin signaling is important in skeletal related-tissue development. We have found that Wnt/β-catenin antagonist XAV could replace traditionally used TGFβ3 as chondrogenic inducer. Here we applied gene expression array to characterize transcriptomic changes between XAV- and TGFβ-induced chondrogenic differentiation in human bone marrow (BM) and induced pluripotent stem cell (iPSC) derived MSCs.

2023-01-04 | GSE211559 | GEO

GIPR agonism and antagonism decrease body weight and food intake via different mechanisms of action.

Project description:Agonists and antagonists of the glucose-dependent insulinotropic polypeptide receptor (GIPR) enhance body weight loss induced by glucagon-like peptide-1 receptor (GLP-1R) agonism. But while GIPR agonism decreases body weight and food intake in a GLP-1R-independent manner via GABAergic GIPR+ neurons, it remains unclear whether GIPR antagonism affects energy metabolism via a similar mechanism. Here we show that the body weight and food intake reducing effects of GIPR antagonism vanish in mice with global loss of either Gipr or Glp-1r but are preserved in mice with loss of Gipr in either GABAergic or peripheral neurons. RNA-sequencing shows opposing effects of GIPR agonism and antagonism in the hindbrain, with antagonism, but not agonism, mimicking GLP-1R signaling, and with GIPR antagonism and GLP-1R agonism both regulating gene programs implicated in synaptic plasticity. Collectively, we show that GIPR agonism and antagonism decrease body weight via different mechanisms, with GIPR antagonism, unlike agonism, depending on functional GLP-1R signaling.

2025-03-12 | GSE288514 | GEO

Effects of dynamic compressive loading on MSC chondrogenesis

Project description:Long-term dynamic compression enhanced the mechanical properties of MSC-seeded constructs only when loading was initiated after 21 days of chondrogenic differentiation. This study examined the molecular differences of chondrogenic MSCs compared to undifferentiated MSCs (TGF-beta vs no TGF-beta) and the effects of dynamic loading on MSC chondrogenesis (loading vs free-swelling). Free-swelling MSC-seeded constructs were cultured for 21 days in chemically defined media. Chondrogenesis was induced with TGF-beta3. Undifferentiated controls were maintained in parallel. After 21 days of chondrogenic differentiation, a subset of constructs were subjected to 21 days of dynamic compressive loading. On days 21 and 42, construct mechanical properties and biochemical content were assessed. Microarray analysis was carried out on day 3, day 21 and day 42 constructs. 6 arrays.

2010-11-01 | E-GEOD-18879 | biostudies-arrayexpress

Estrogen receptor agonism/antagonism in T47D cells

Project description:Estrogen receptor agonism/antagonism in T47D cells

| PRJNA1055455 | ENA

LILRB3 agonism and antagonism using monocolonal antibodies

Project description:LILRB3 agonism and antagonism using monocolonal antibodies

| PRJNA819481 | ENA

Effects of dynamic compressive loading on MSC chondrogenesis

2010-11-01 | GSE18879 | GEO

Wnt antagonism without TGFβ induces rapid MSC chondrogenesis via increasing AJ interactions and restricting lineage commitment.

Project description:Human mesenchymal stem cells (MSCs) remain one of the best cell sources for cartilage, a tissue without regenerative capacity. However, MSC chondrogenesis is commonly induced through TGFβ, a pleomorphic growth factor without specificity for this lineage. Using tissue- and induced pluripotent stem cell-derived MSCs, we demonstrate an efficient and precise approach to induce chondrogenesis through Wnt/β-catenin antagonism alone without TGFβ. Compared to TGFβ, Wnt/β-catenin antagonism more rapidly induced MSC chondrogenesis without eliciting off-target lineage specification toward smooth muscle or hypertrophy; this was mediated through increasing N-cadherin levels and β-catenin interactions-key components of the adherens junctions (AJ)-and increasing cytoskeleton-mediated condensation. Validation with transcriptomic analysis of human chondrocytes compared to MSCs and osteoblasts showed significant downregulation of Wnt/β-catenin and TGFβ signaling along with upregulation of α-catenin as an upstream regulator. Our findings underscore the importance of understanding developmental pathways and structural modifications in achieving efficient MSC chondrogenesis for translational application.

| S-EPMC9792887 | biostudies-literature

GLP-1 directed NMDA receptor antagonism for obesity treatment

Project description:The N-methyl-D-aspartate (NMDA) receptor is a glutamate-activated cation channel critical to many processes in the brain. Genome-wide association studies (GWAS) suggest that glutamatergic neurotransmission and NMDA receptor-mediated synaptic plasticity is important for body weight homeostasis1. Here, we report the engineering and preclinical development of a first-in-class bimodal molecule that integrates NMDA receptor antagonism with glucagon-like peptide-1 (GLP-1) receptor agonism to effectively reverse obesity, hyperglycemia, and dyslipidemia in rodent models of metabolic disease. We demonstrate that GLP-1-directed delivery of the NMDA receptor antagonist MK-801 affects NMDA receptor-mediated synaptic plasticity in the hypothalamus. Importantly, peptide-targeting of MK-801 specifically to GLP-1 receptor-expressing brain regions circumvent adverse physiological and behavioral effects associated with MK-801 monotherapy. In sum, our approach demonstrates the feasibility of cell specific ionotropic receptor-modulation via peptide targeting and highlights the therapeutic potential of unimolecular mixed GLP-1 receptor agonism and NMDA receptor antagonism for obesity treatment.

2024-04-26 | PXD045816 | Pride

Gene expression by AR agonism and AR antagonism in isotope-labeled PCa cells

Project description:Gene expression by AR agonism and AR antagonism in isotope-labeled PCa cells

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Genomic agonism and phenotypic antagonism between estrogen and progesterone receptors in breast cancer.

Project description:Genomic agonism and phenotypic antagonism between estrogen and progesterone receptors in breast cancer.

| PRJNA317919 | ENA