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Activity of the GHRH Antagonist MIA-602 and its Underlying Mechanisms of Action in sarcoidosis

ABSTRACT: Growth hormone releasing hormone (GHRH) is a potent stimulator of growth hormone secretion from pituitary gland. Although GHRH is essential for growth of immune cells, the regulatory effects of its antagonist in granulomatous disease remains unknown. The goal is to evaluate the expression of GHRH receptor in human tissue with sarcoidosis granuloma and demonstrate the anti-inflammatory effects of MIA-602 (a GHRH antagonist) in in vitro and in vivo studies. Granulomatous reaction in the mouse lung was developed as previously described (PMID: 31921151). Mice were treated with 5 micrograms of MIA-602 (an GHRH antagonist) daily subcutanously. RNA from mouse lungs were extracted and RNASeq was perfomed.

ORGANISM(S): Mus musculus

PROVIDER: GSE156397 | GEO | 2023/08/16

REPOSITORIES: GEO

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Gene expression in liver tissue from Ghrh-KO and normal (wild-type) mice

Project description:The hypothalamus has recently emerged as a key regulator of metabolism and aging in mammals. We have examined the impact of targeted disruption of hypothalamic hypophysiotropic peptide: Growth Hormone-releasing Hormone (GHRH) in mice on longevity, and the putative mechanisms of delayed aging. GHRH knockout (KO) mice are remarkably long-lived and in comparison to genetically normal (wild type) animals exhibiting major shifts in the expression of genes related to xenobiotic detoxification, stress resistance, and insulin signaling. These mutant mice also have increased adiponectin levels and alterations in glucose homeostasis consistent with the removal of the counter-insulin effects of GH. While these effects overlap with those of caloric restriction (CR), we show that effects of CR and the GHRH mutation are additive, with lifespan of GHRH-KO mutants further increased by CR. We conclude that GHRH-KO mice feature perturbations in a network of signaling pathways related to stress resistance, metabolic control and inflammation, and therefore provide a new model that can be used to explore links between GHRH repression, downregulation of the somatotropic axis, and extended longevity. Hepatic tissue was obtained from 3 Ghrh-KO mice and 3 control (wild-type) mice (males). Expression in each sample was profiled using Affymetrix Mouse Genome 430 2.0 arrays.

2013-11-18 | E-GEOD-51108 | biostudies-arrayexpress

Transcriptomic and metabolomic profiling of long-lived growth hormone releasing hormone knock-out mice: Evidence for altered mitochondrial function and amino acid metabolism

Project description:Numerous genetic manipulations that extend lifespan in mice have been discovered over the past two decades, the most robust of which has arguably been the down regulation of growth hormone (GH) signaling. However, while decreased GH signaling has been associated with improved health and lifespan, many of the underlying physiological changes and molecular mechanisms have yet to be elucidated. To this end, we have completed the first transcriptomic and metabolomic study on long-lived growth hormone releasing hormone knockout (GHRH-KO) and wild-type mice in brown adipose tissue (transcriptomics) and blood serum (metabolomics). We find that GHRH-KO mice have increased transcript levels of mitochondrial and amino acid genes with decreased levels of extracellular matrix genes. Concurrently, mitochondrial metabolites are differentially regulated in GHRH-KO. Furthermore, we find a strong signal of genotype-by-sex interactions, suggesting the sexes have differing physiological responses to GH deficiency. Overall, our results point towards a strong influence of mitochondrial metabolism in GHRH-KO mice which potentially is tightly intertwined with their extended lifespan phenotype.

2020-03-30 | GSE143672 | GEO

Spleen vs GHRH Treated B cell

Project description:total RNA from mouse (male c57BL/6) spleen labeled with Cy3 vs total RNA from mouse (male c57BL/6) B cells treated with Growth Hormone Release Hormone (GHRH) labeled with Cy5- time course with repeats Keywords: ordered

2003-04-14 | GSE382 | GEO

Gene expression in liver tissue from Ghrh-KO and normal (wild-type) mice

2013-11-18 | GSE51108 | GEO

The histone H3-lysine 4-methyltransferase Mll4 governs the development of growth hormone-releasing hormone-producing neurons

Project description:In humans, inactivating mutations in MLL4, which encodes a histone H3-lysine 4-methyltrasferase, lead to Kabuki syndrome (KS). While dwarfism is a cardinal feature of KS, the underlying etiology remains unclear. Here we report that Mll4 is a critical regulator of the development of growth hormone-releasing hormone (GHRH)-producing neurons in the hypothalamus. The two distinct Mll4 mutant mouse models exhibited dwarfism, accompanied by impairment of developmental programs for GHRH-neurons. Our genome-wide studies revealed that, in the developing hypothalamus, Mll4 collaborates mainly with the transcription factor Nrf1 to trigger the expression of GHRH-neuronal genes. Interestingly, the deficiency of Mll4 resulted in a marked reduction of transcriptionally active histone marks in the embryonic hypothalamus, which was rescued by treatment with the histone deacetylase inhibitor AR-42. Further, AR-42 treatment restored GHRH-neuronal production in Mll4 mutant mice. Together, our results suggest that the dysregulation of MLL4-directed epigenetic control of GHRH-neuronal genes is a substantial contributing factor to dwarfism in human KS.

2020-11-07 | GSE149439 | GEO

MIA gene family-related signaling in oral squamous cell carcinoma cells

2016-07-01 | GSE80347 | GEO

MIA-PaCa2 cells transfected with silencer RNA against HuR and YAP1

Project description:Purpose: To determine biological impact between silencing HuR and YAP1, in MIA-PaCa2. Methods: Expression profiling of MIA-PaCa2 cells knocked-down for HuR and YAP1 and control cells transfected with scramble siRNA.

2022-06-07 | GSE167525 | GEO

MIA gene family-related signaling in oral squamous cell carcinoma cells

Project description:Melanoma inhibitory activity (MIA) gene family is novel tumor-associated molecules. Although MIA gene family has several tumor progressive and/or suppressive functions, the detailed relevant signaling partners are unclear and investigated. In this study, we investigated the detailed MIA gene family-associated signaling using human oral squamous cell carcinoma cells. Human oral squamous cell carcinoma-derived HSC3 cells were transfected withãcontrol, MIA, MIA2, TANGO, MATE2, or LEMD1 siRNA. The effect on geneãknockdown was evaluated by cDNA microarray.

2016-07-01 | E-GEOD-80347 | biostudies-arrayexpress

CRISPR deletion of ELAVL1 (HuR) in MIA PaCa-2 in vitro cells and in vivo tumors

Project description:To investigate the impact of the mRNA stabilty factor HuR on the pancreatic cancer transcriptome in MIA PaCa-2 in vitro cell line and in vivo tumors at multiple time points of tumor growth

2023-01-01 | GSE221250 | GEO

MIA overexpression

Project description:In experiments using tissue recombinants and mesenchyme-free culture, we have demonstrated that the entire embryonic respiratory tract epithelium, from the trachea to the distal lung tips, exhibits substantial plasticity in its eventual phenotype that is dependent on the inductive cues it receives from its associated mesenchyme. This observation led us to speculate that the differences between embryonic trachea and lung are defined by limited subset of genes, and that the molecular comparison of these two tissues might provide new information on genes that are important for both lung and trachea development. Microarray experiments designed to identify genes differentially expressed in the E11.5 lung and trachea showed that melanoma inhibitory activity (Mia1) was expressed only in the lung. Mia1 was abundantly expressed during early lung development, but was virtually absent by the end of gestation. Bitransgenic mice expressing MIA under the control of the SFTPC promoter after E16.5, the age when Mia1 is normally silenced, died from respiratory failure at birth with morphologically immature lungs associated with reduced levels of saturated phosphatidylcholine and mature SP-B. Microarray analysis showed significant reductions expression of Sftpa, Sftpb, Abca3, Aqp5, Lzp-s, Scd2, and Aytl2 in lungs misexpressing MIA. Keywords: genotype comparison

2008-04-12 | GSE9312 | GEO

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