scholarly journals Carbon monoxide -- a "new" gaseous modulator of gene expression.

2003 ◽  
Vol 50 (1) ◽  
pp. 31-47 ◽  
Author(s):  
Józef Dulak ◽  
Alicja Józkowicz
Keyword(s):  
Gene Expression ◽  
Nitric Oxide ◽  
Cell Proliferation ◽  
Carbon Monoxide ◽  
Heme Proteins ◽  
Regulation Of Gene Expression ◽  
Inflammatory Reactions ◽  
Inhibition Of Platelet Aggregation ◽  
Neural Transmission ◽  
Underlying Processes

Carbon monoxide (CO) is an odorless, tasteless and colorless gas which is generated by heme oxygenase enzymes (HOs). HOs degrade heme releasing equimolar amounts of CO, iron and biliverdin, which is subsequently reduced to bilirubin. CO shares many properties with nitric oxide (NO), an established cellular messenger. Both CO and NO are involved in neural transmission and modulation of blood vessel function, including their relaxation and inhibition of platelet aggregation. CO, like NO, binds to heme proteins, although CO binds only ferrous (FeII) heme, whereas NO binds both ferrous and ferric (FeIII). CO enhances the activity of guanylate cyclase although it is less potent than NO. In contrast, CO inhibits other heme proteins, such as catalase or cytochrome p450. The effects of CO on gene expression can be thus varied, depending on the cellular microenvironment and the metabolic pathway being influenced. In this review the regulation of gene expression by HO/CO in the cardiovascular system is discussed. Recent data, derived also from our studies, indicate that HO/CO are significant modulators of inflammatory reactions, influencing the underlying processes such as cell proliferation and production of cytokines and growth factors.

Nitric Oxide Prevents Mouse Embryonic Stem Cell Differentiation Through Regulation of Gene Expression, Cell Signaling, and Control of Cell Proliferation

2016 ◽  
Vol 117 (9) ◽  
pp. 2078-2088 ◽  
Author(s):  
Rafael Tapia-Limonchi ◽  
Gladys M. Cahuana ◽  
Estefania Caballano-Infantes ◽  
Carmen Salguero-Aranda ◽  
Amparo Beltran-Povea ◽  
...  
Keyword(s):  
Gene Expression ◽  
Nitric Oxide ◽  
Cell Proliferation ◽  
Stem Cell ◽  
Regulation Of Gene Expression ◽  
Embryonic Stem ◽  
Mouse Embryonic Stem Cell ◽  
Stem Cell Differentiation ◽  
Embryonic Stem Cell Differentiation ◽  
And Control

scholarly journals STAU2 protein level is controlled by caspases and the CHK1 pathway and regulates cell cycle progression in the non-transformed hTERT-RPE1 cells

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Lionel Condé ◽  
Yulemi Gonzalez Quesada ◽  
Florence Bonnet-Magnaval ◽  
Rémy Beaujois ◽  
Luc DesGroseillers
Keyword(s):  
Gene Expression ◽  
Cell Cycle ◽  
Cell Proliferation ◽  
Dna Damage ◽  
Steady State ◽  
Posttranscriptional Regulation ◽  
Cell Cycle Progression ◽  
Rna Binding ◽  
Regulation Of Gene Expression ◽  
Cycle Progression

AbstractBackgroundStaufen2 (STAU2) is an RNA binding protein involved in the posttranscriptional regulation of gene expression. In neurons, STAU2 is required to maintain the balance between differentiation and proliferation of neural stem cells through asymmetric cell division. However, the importance of controlling STAU2 expression for cell cycle progression is not clear in non-neuronal dividing cells. We recently showed that STAU2 transcription is inhibited in response to DNA-damage due to E2F1 displacement from theSTAU2gene promoter. We now study the regulation of STAU2 steady-state levels in unstressed cells and its consequence for cell proliferation.ResultsCRISPR/Cas9-mediated and RNAi-dependent STAU2 depletion in the non-transformed hTERT-RPE1 cells both facilitate cell proliferation suggesting that STAU2 expression influences pathway(s) linked to cell cycle controls. Such effects are not observed in the CRISPR STAU2-KO cancer HCT116 cells nor in the STAU2-RNAi-depleted HeLa cells. Interestingly, a physiological decrease in the steady-state level of STAU2 is controlled by caspases. This effect of peptidases is counterbalanced by the activity of the CHK1 pathway suggesting that STAU2 partial degradation/stabilization fines tune cell cycle progression in unstressed cells. A large-scale proteomic analysis using STAU2/biotinylase fusion protein identifies known STAU2 interactors involved in RNA translation, localization, splicing, or decay confirming the role of STAU2 in the posttranscriptional regulation of gene expression. In addition, several proteins found in the nucleolus, including proteins of the ribosome biogenesis pathway and of the DNA damage response, are found in close proximity to STAU2. Strikingly, many of these proteins are linked to the kinase CHK1 pathway, reinforcing the link between STAU2 functions and the CHK1 pathway. Indeed, inhibition of the CHK1 pathway for 4 h dissociates STAU2 from proteins involved in translation and RNA metabolism.ConclusionsThese results indicate that STAU2 is involved in pathway(s) that control(s) cell proliferation, likely via mechanisms of posttranscriptional regulation, ribonucleoprotein complex assembly, genome integrity and/or checkpoint controls. The mechanism by which STAU2 regulates cell growth likely involves caspases and the kinase CHK1 pathway.

The control of gene expression and cell proliferation by the epithelial apical junctional complex

2012 ◽  
Vol 53 ◽  
pp. 83-93 ◽  
Author(s):  
Domenica Spadaro ◽  
Rocio Tapia ◽  
Pamela Pulimeno ◽  
Sandra Citi
Keyword(s):  
Gene Expression ◽  
Cell Proliferation ◽  
Transcription Factors ◽  
Protein Complexes ◽  
Regulation Of Gene Expression ◽  
Small Gtpases ◽  
Junctional Complex ◽  
Nucleotide Exchange ◽  
Control Of Gene Expression ◽  
Apical Junctional Complex

The AJC (apical junctional complex) of vertebrate epithelial cells orchestrates cell–cell adhesion and tissue barrier function. In addition, it plays a pivotal role in signalling. Several protein components of the AJC, e.g. the cytoplasmic proteins β-catenin, p120-catenin and ZO (Zonula Occludens)-2, can shuttle to the nucleus, where they interact with transcription factors to regulate gene expression and cell proliferation. Other junctional proteins, e.g. angiomotin, α-catenin and cingulin, are believed to act by sequestering either transcription factors, such as YAP (Yes-associated protein), or regulators of small GTPases, such as GEF (guanine-nucleotide-exchange factor)-H1, at junctions. The signalling activities of AJC proteins are triggered by different extracellular and intracellular cues, including cell density, and physiological or pathological activation of developmentally regulated pathways, such as the Wnt pathway. The interplay between junctional protein complexes, the actin cytoskeleton and signalling pathways is of crucial importance in the regulation of gene expression and cell proliferation.

scholarly journals The Effects of Cobalt Protoporphyrin IX and Tricarbonyldichlororuthenium (II) Dimer Treatments and Its Interaction with Nitric Oxide in the Locus Coeruleus of Mice with Peripheral Inflammation

2019 ◽  
Vol 20 (9) ◽  
pp. 2211 ◽  
Author(s):  
Patricia Moreno ◽  
Rafael Alves Cazuza ◽  
Joyce Mendes-Gomes ◽  
Andrés Felipe Díaz ◽  
Sara Polo ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Carbon Monoxide ◽  
Locus Coeruleus ◽  
Inflammatory Pain ◽  
Protoporphyrin Ix ◽  
Heme Oxygenase 1 ◽  
Peripheral Inflammation ◽  
Inflammatory Reactions ◽  
Cobalt Protoporphyrin ◽  
Cobalt Protoporphyrin Ix

Heme oxygenase 1 (HO-1) and carbon monoxide were shown to normalize oxidative stress and inflammatory reactions induced by neuropathic pain in the central nervous system, but their effects in the locus coeruleus (LC) of animals with peripheral inflammation and their interaction with nitric oxide are unknown. In wild-type (WT) and knockout mice for neuronal (NOS1-KO) or inducible (NOS2-KO) nitric oxide synthases with inflammatory pain induced by complete Freund’s adjuvant (CFA), we assessed: (1) antinociceptive actions of cobalt protoporphyrin IX (CoPP), an HO-1 inducer; (2) effects of CoPP and tricarbonyldichlororuthenium(II) dimer (CORM-2), a carbon monoxide-liberating compound, on the expression of HO-1, NOS1, NOS2, CD11b/c, GFAP, and mitogen-activated protein kinases (MAPK) in the LC. CoPP reduced inflammatory pain in different time-dependent manners in WT and KO mice. Peripheral inflammation activated astroglia in the LC of all genotypes and increased the levels of NOS1 and phosphorylated extracellular signal-regulated kinase 1/2 (p-ERK 1/2) in WT mice. CoPP and CORM-2 enhanced HO-1 and inhibited astroglial activation in all genotypes. Both treatments blocked NOS1 overexpression, and CoPP normalized ERK 1/2 activation. This study reveals an interaction between HO-1 and NOS1/NOS2 during peripheral inflammation and shows that CoPP and CORM-2 improved HO-1 expression and modulated the inflammatory and/or plasticity changes caused by peripheral inflammation in the LC.

scholarly journals Epigenetic Regulation of Gene Expression Induced by Butyrate in Colorectal Cancer: Involvement of MicroRNA

2017 ◽  
Vol 9 ◽  
pp. 1179237X1772990 ◽  
Author(s):  
Karen S Bishop ◽  
Huawen Xu ◽  
Gareth Marlow
Keyword(s):  
Gene Expression ◽  
Colorectal Cancer ◽  
Cell Proliferation ◽  
Mirna Expression ◽  
Regulation Of Gene Expression ◽  
High Intake ◽  
Common Cause ◽  
The Third ◽  
Plant Fibre ◽  
Non Coding Rnas

Colorectal cancer (CRC) is the third most common cause of cancer mortality globally. Development of CRC is closely associated with lifestyle, and diet may modulate risk. A Western-style diet is characterised by a high intake of red meat but low consumption of fruit, vegetables, and whole cereals. Such a diet is associated with CRC risks. It has been demonstrated that butyrate, produced by the fermentation of dietary plant fibre, can alter both genetic and epigenetic expressions. MicroRNAs (miRNAs) are small non-coding RNAs that are commonly present in both normal and tumour cells. Aberrant miRNA expression is associated with CRC initiation, progression, and metastasis. In addition, butyrate can modulate cell proliferation, differentiation, apoptosis, and miRNA expression in CRC. In this review, the effects of butyrate on modulating miRNA expression in CRC will be discussed. Furthermore, evidence on the effect of butyrate on CRC risk through reducing oncogenic miRNA expression will be presented.

Regulation of gene expression by nitric oxide

2001 ◽  
Vol 442 (4) ◽  
pp. 479-486 ◽  
Author(s):  
Josef Pfeilschifter ◽  
Wolfgang Eberhardt ◽  
Karl-Friedrich Beck
Keyword(s):  
Gene Expression ◽  
Nitric Oxide ◽  
Regulation Of Gene Expression
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