scholarly journals Study of gene expression alteration in male androgenetic alopecia: evidence of predominant molecular signalling pathways

2017 ◽  
Vol 177 (5) ◽  
pp. 1322-1336 ◽  
Author(s):  
L. Michel ◽  
P. Reygagne ◽  
P. Benech ◽  
F. Jean‐Louis ◽  
S. Scalvino ◽  
...  
Keyword(s):  
Gene Expression ◽  
Androgenetic Alopecia ◽  
Signalling Pathways ◽  
Gene Expression Alteration ◽  
Molecular Signalling Pathways

Nutrient-regulated gene expression in eukaryotes

2006 ◽  
Vol 73 ◽  
pp. 85-96 ◽  
Author(s):  
Richard J. Reece ◽  
Laila Beynon ◽  
Stacey Holden ◽  
Amanda D. Hughes ◽  
Karine Rébora ◽  
...  
Keyword(s):  
Gene Expression ◽  
Rna Polymerase ◽  
Rna Polymerase Ii ◽  
Transcriptional Control ◽  
Direct Interaction ◽  
Signalling Pathways ◽  
A Cell ◽  
One Step ◽  
Higher Eukaryotes ◽  
Regulated Gene Expression

The recognition of changes in environmental conditions, and the ability to adapt to these changes, is essential for the viability of cells. There are numerous well characterized systems by which the presence or absence of an individual metabolite may be recognized by a cell. However, the recognition of a metabolite is just one step in a process that often results in changes in the expression of whole sets of genes required to respond to that metabolite. In higher eukaryotes, the signalling pathway between metabolite recognition and transcriptional control can be complex. Recent evidence from the relatively simple eukaryote yeast suggests that complex signalling pathways may be circumvented through the direct interaction between individual metabolites and regulators of RNA polymerase II-mediated transcription. Biochemical and structural analyses are beginning to unravel these elegant genetic control elements.

PBF is a component of the molecular signalling pathways that drive hyperplastic and neoplastic thyroid growth

2014 ◽  
Author(s):  
Vicki Smith ◽  
Martin Read ◽  
Rachel Watkins ◽  
Vikki Poole ◽  
Bhavika Modasia ◽  
...  
Keyword(s):  
Signalling Pathways ◽  
Molecular Signalling Pathways

MOLECULAR CONTROL OF ARTICULAR CARTILAGE DEGENERATION BY TRANSFORMING GROWTH FACTOR ALPHA

2008 ◽  
Vol 31 (4) ◽  
pp. 2
Author(s):  
Tom Appleton ◽  
Shirine Usmani ◽  
John Mort ◽  
Frank Beier
Keyword(s):  
Gene Expression ◽  
Articular Cartilage ◽  
Growth Factor ◽  
P38 Mapk ◽  
Transforming Growth Factor ◽  
Cartilage Degeneration ◽  
Signalling Pathways ◽  
Transforming Growth Factor Alpha ◽  
Factor Alpha ◽  
Articular Cartilage Degeneration

Background: Articular cartilage degeneration is a hallmark of osteoarthritis (OA). We previously identified increased expression of transforming growth factor alpha (TGF?) and chemokine (C-C motif) ligand 2 (CCL2) in articular cartilage from a rat modelof OA (1,2). We subsequently reported that TGF? signalling modified chondrocyte cytoskeletal organization, increased catabolic and decreased anabolic gene expression and suppressed Sox9. Due to other roles in chondrocytes, we hypothesized that the effects ofTGF? on chondrocytes are mediated by Rho/ROCK and MEK/ERK signaling pathways. Methods: Primary cultures of chondrocytes and articularosteochondral explants were treated with pharmacological inhibitors of MEK1/2(U0126), ROCK (Y27632), Rho (C3), p38 MAPK (SB202190) and PI3K (LY294002) to elucidate pathway involvement. Results: Using G-LISA we determined that stimulation of primary chondrocytes with TGF? activates RhoA. Reciprocally, inhibition of RhoA/ROCK but not other signalling pathways prevents modification of the actin cytoskeleton in responseto TGF?. Inhibition of MEK/ERKsignaling rescued suppression of anabolic gene expression by TGF? including SOX9 mRNA and protein levels. Inhibition of MEK/ERK, Rho/ROCK, p38 MAPK and PI3K signalling pathways differentially controlled the induction of MMP13 and TNF? gene expression. TGF? also induced expression of CCL2 specifically through MEK/ERK activation. In turn, CCL2 treatment induced the expression of MMP3 and TNF?. Finally, we assessed cartilage degradation by immunohistochemical detection of type II collagen cleavage fragments generated by MMPs. Blockade of RhoA/ROCK and MEK/ERK signalling pathways reduced the generation of type IIcollagen cleavage fragments in response to TGF? stimulation. Conclusions: Rho/ROCK signalling mediates TGF?-induced changes inchondrocyte morphology, while MEK/ERK signalling mediates the suppression ofSox9 and its target genes, and CCL2 expression. CCL2, in turn, induces the expression of MMP3 and TNF?, two potent catabolic factors known to be involved in OA. These pathways may represent strategic targets for interventional approaches to treating cartilage degeneration in osteoarthritis. References: 1. Appleton CTG et al. Arthritis Rheum 2007;56:1854-68. 2. Appleton CTG et al. Arthritis Rheum 2007; 56:3693-705.

Enrichment of IGF-1R and PPARγ signalling pathways in orbital inflammatory diseases: steps toward understanding pathogenesis

2021 ◽  
pp. bjophthalmol-2020-318330
Author(s):  
Rohan Verma ◽  
Dongseok Choi ◽  
Allison J Chen ◽  
Christina A Harrington ◽  
David J Wilson ◽  
...  
Keyword(s):  
Gene Expression ◽  
Inflammatory Diseases ◽  
Target Therapy ◽  
Signalling Pathways ◽  
Peroxisome Proliferator ◽  
Healthy Controls ◽  
Gene Expressions ◽  
Peroxisome Proliferator Activated Receptor ◽  
Orbital Inflammation ◽  
Wide Range

BackgroundOrbital inflammatory disease (OID) encompasses a wide range of pathology including thyroid-associated orbitopathy (TAO), granulomatosis with polyangiitis (GPA), sarcoidosis and non-specific orbital inflammation (NSOI), accounting for up to 6% of orbital diseases. Understanding the underlying pathophysiology of OID can improve diagnosis and help target therapy.AimsTo test the hypothesis that shared signalling pathways are activated in different forms of OID.MethodsIn this secondary analysis, pathway analysis was performed on the previously reported differentially expressed genes from orbital adipose tissue using patients with OID and healthy controls who were characterised by microarray. For the original publications, tissue specimens were collected from oculoplastic surgeons at 10 international centres representing four countries (USA, Canada, Australia and Saudi Arabia). Diagnoses were independently confirmed by two masked ocular pathologists (DJW, HEG). Gene expression profiling analysis was performed at the Oregon Health & Science University. Eighty-three participants were included: 25 with TAO, 6 with orbital GPA, 7 with orbital sarcoidosis, 25 with NSOI and 20 healthy controls.ResultsAmong the 83 subjects (mean (SD) age, 52.8 (18.3) years; 70% (n=58) female), those with OID demonstrated perturbation of the downstream gene expressions of the IGF-1R (MAPK/RAS/RAF/MEK/ERK and PI3K/Akt/mTOR pathways), peroxisome proliferator-activated receptor-γ (PPARγ), adipocytokine and AMPK signalling pathways compared with healthy controls. Specifically, GPA samples differed from controls in gene expression within the insulin-like growth factor-1 receptor (IGF-1R, PI3K-Akt (p=0.001), RAS (p=0.005)), PPARγ (p=0.002), adipocytokine (p=0.004) or AMPK (p=<0.001) pathways. TAO, sarcoidosis and NSOI samples were also found to have statistically significant differential gene expression in these pathways.ConclusionsAlthough OID includes a heterogenous group of pathologies, TAO, GPA, sarcoidosis and NSOI share enrichment of common gene signalling pathways, namely IGF-1R, PPARγ, adipocytokine and AMPK. Pathway analyses of gene expression suggest that other forms of orbital inflammation in addition to TAO may benefit from blockade of IGF-1R signalling pathways.

Inducible NO synthase: role in cellular signalling

1999 ◽  
Vol 202 (6) ◽  
pp. 645-653 ◽  
Author(s):  
K.F. Beck ◽  
W. Eberhardt ◽  
S. Frank ◽  
A. Huwiler ◽  
U.K. Messmer ◽  
...  
Keyword(s):  
Gene Expression ◽  
No Synthase ◽  
Signalling Pathways ◽  
Target Cells ◽  
Activated Macrophages ◽  
The Past ◽  
Relaxing Factor ◽  
Endothelium Derived Relaxing Factor ◽  
Intercellular Messenger

The discovery of endothelium-derived relaxing factor and its identification as nitric oxide (NO) was one of the most exciting discoveries of biomedical research in the 1980s. Besides its potent vasodilatory effects, NO was found under certain circumstances to be responsible for the killing of microorganisms and tumour cells by activated macrophages and to act as a novel, unconventional type of neurotransmitter. In 1992, Science picked NO as the ‘Molecule of the Year’, and over the past years NO has become established as a universal intercellular messenger that acutely affects important signalling pathways and, on a more long-term scale, modulates gene expression in target cells. These actions will form the focus of the present review.

Principles of hormone action

2020 ◽  
pp. 2245-2257
Author(s):  
Rob Fowkes ◽  
V. Krishna Chatterjee ◽  
Mark Gurnell
Keyword(s):  
Gene Expression ◽  
Growth Hormone ◽  
Vitamin D ◽  
Nuclear Receptors ◽  
Physiological Response ◽  
Membrane Receptors ◽  
Signalling Pathways ◽  
Hormone Action ◽  
Biochemical Pathways ◽  
Releasing Factors

Hormones, produced by glands or cells, are messengers which act locally or at a distance to coordinate the function of cells and organs. Types of hormone include: peptides (e.g. hypothalamic releasing factors) and proteins (e.g. insulin, growth hormone)—these generally interact with membrane receptors located on the cell surface, causing activation of downstream signalling pathways leading to alteration in gene transcription or modulation of biochemical pathways to effect a physiological response; steroids (e.g. cortisol, progesterone, testosterone, oestradiol) and other lipophilic substances (e.g. vitamin D, retinoic acid, thyroid hormone)—these act by crossing the plasma membrane to interact with intracellular receptors, with hormone action via nuclear receptors altering cellular gene expression directly.

scholarly journals UV and blue light signalling: pathways regulating chalcone synthase gene expression in Arabidopsis

2001 ◽  
Vol 151 (1) ◽  
pp. 121-131 ◽  
Author(s):  
Gareth I. Jenkins ◽  
Joanne C. Long ◽  
Helena K. Wade ◽  
Matthew R. Shenton ◽  
Tatiana N. Bibikova
Keyword(s):  
Gene Expression ◽  
Blue Light ◽  
Chalcone Synthase ◽  
Signalling Pathways ◽  
Chalcone Synthase Gene ◽  
Light Signalling

110 Temporal Changes in Endometrial Gene Expression Between Ipsi- and Contralateral Uterine Horns in Cattle

2018 ◽  
Vol 30 (1) ◽  
pp. 194
Author(s):  
J. M. Sánchez ◽  
C. Passaro ◽  
N. Forde ◽  
S. Behura ◽  
J. A. Browne ◽  
...  
Keyword(s):  
Gene Expression ◽  
Stem Cells ◽  
Luteal Phase ◽  
Expression Patterns ◽  
Uterine Horn ◽  
Oestrous Cycle ◽  
Signalling Pathway ◽  
Signalling Pathways ◽  
Robust Analysis ◽  
The Impact

The transfer of an embryo into the uterine horn contralateral to the ovary bearing the corpus luteum has been associated with a decreased pregnancy rate in cattle compared with transfer into the ipsilateral horn. These findings suggest that the environment in the contralateral horn is less conducive to supporting conceptus development than that of the ipsilateral horn. Therefore, this study compared the endometrial transcriptome of the ipsi- and contralateral uterine horns during the luteal phase. Endometrial samples from the ipsi- (IPSI) and contralateral (CONTRA) horns were collected from synchronized nonpregnant beef heifers on Days 5, 7, 13 or 16 post-oestrus (n = 5 heifers per time point). Total RNA was isolated and sequenced. Differences in the transcriptome were determined by edgeR-robust analysis. Principal component analysis found that IPSI and CONTRA have distinct patterns of gene expression on each day, with Day 5 exhibiting the most variation and Day 16 being least variable. Further, the 2 uterine horns had distinct expression patterns on Day 5, with IPSI exhibiting significantly higher variation in gene expression compared twitho CONTRA. EdgeR-robust analysis found 217 (201 up- and 16 down-regulated), 54 (44 up- and 10 down-regulated), 14 (13 up- and 1 down-regulated), and 18 (14 up- and 4 down-regulated) differentially expressed genes (DEG; >2-fold change, false discovery rate P < 0.05) between IPSI and CONTRA endometria on Days 5, 7, 13, and 16 of the oestrous cycle, respectively. The top 5 canonical pathways associated with DEG between IPSI and CONTRA during the luteal phase of the oestrous cycle were involved in signalling pathways regulating pluripotency of stem cells (73/138), progesterone-mediated oocyte maturation (55/89), endometrial cancer (31/51), ErbB signalling pathway (50/87), and mTOR signalling pathway (36/61). The impact of DEG on signalling pathways was assessed using a pathway perturbation algorithm called Signalling Pathway Impact Analysis (SPIA). This topology-based pathway analysis was conducted using the Bioconductor ToPAseq package (https://bioconductor.org/packages/release/bioc/html/ToPASeq.html) and revealed that signalling pathways regulating pluripotency of stem cells showed the highest perturbation score when IPSI was compared with CONTRA irrespective of day. Discovering and cataloguing which pathways are perturbed in each uterine horn throughout the oestrous cycle may contribute to our understanding of the mechanisms underlying early embryonic loss. Ths study was supported by Science Foundation Ireland (13/IA/1983) and the Irish Department of Agriculture, Food and The Marine (13S528).

Genetics

2016 ◽  
Author(s):  
Ana M. Valdes
Keyword(s):  
Risk Factors ◽  
Genetic Risk ◽  
Complex Trait ◽  
Genetic Risk Factors ◽  
Underlying Disease ◽  
Epidemiological Studies ◽  
Signalling Pathways ◽  
Treatment Regimens ◽  
Tailored Treatment ◽  
Molecular Signalling Pathways

Epidemiological studies have demonstrated that osteoarthritis (OA) is a complex trait with numerous environmental and genetic risk factors. A great deal of effort has been spent elucidating these risk factors and progress has been made. It is clear however that the causes behind OA development and progression continue to remain largely elusive. Identification of those genes that, in conjunction with environmental factors, predispose to OA severity will lead to a better understanding of the mechanisms underlying disease development and thus promote improved health strategies for prevention. An understanding of the molecular signalling pathways involved in the initiation and progression of the disease will improve clinical diagnosis and help identify improved, tailored treatment regimens. This chapter focuses on these issues, exploring the heritability of OA, known genetic risk factors, and specific traits and outcomes studied in the genetics of OA.

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