High Glucose–Induced Oxidative Stress Increases Transient Receptor Potential Channel Expression in Human Monocytes

Wuensch, Tilo; Thilo, Florian; Krueger, Katharina; Scholze, Alexandra; Ristow, Michael; Tepel, Martín

doi:10.2337/db09-1100

Cited by 96 publications

(78 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It has been reported that high glucose modulates the expression of TRPC such as TRPC6 (29,73). Therefore, we investigated the effects of high glucose (20 and 30 mM) on TRPA1 expression.…”

Section: Expression Of Trpa1 Protein In Human Cardiac Fibroblasts (Immentioning

confidence: 98%

Effects of methylglyoxal on human cardiac fibroblast: roles of transient receptor potential ankyrin 1 (TRPA1) channels

Oguri

Nakajima

Yamamoto

et al. 2014

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

Effects of methylglyoxal on human cardiac fibroblast: roles of transient receptor potential ankyrin 1 (TRPA1) channels. Am J Physiol Heart Circ Physiol 307: H1339 -H1352, 2014. First published August 29, 2014; doi:10.1152/ajpheart.01021.2013.-Cardiac fibroblasts contribute to the pathogenesis of cardiac remodeling. Methylglyoxal (MG) is an endogenous carbonyl compound produced under hyperglycemic conditions, which may play a role in the development of pathophysiological conditions including diabetic cardiomyopathy. However, the mechanism by which this occurs and the molecular targets of MG are unclear. We investigated the effects of MG on Ca 2ϩ signals, its underlying mechanism, and cell cycle progression/cell differentiation in human cardiac fibroblasts. The conventional and quantitative real-time RT-PCR, Western blot, immunocytochemical analysis, and intracellular Ca 2ϩ concentration [Ca 2ϩ ]i measurement were applied. Cell cycle progression was assessed using the fluorescence activated cell sorting. MG induced Ca 2ϩ entry concentration dependently. Ruthenium red (RR), a general cation channel blocker, and HC030031, a selective transient receptor potential ankyrin 1 (TRPA1) antagonist, inhibited MG-induced Ca 2ϩ entry. Treatment with aminoguanidine, a MG scavenger, also inhibited it. Allyl isothiocyanate, a selective TRPA1 agonist, increased Ca 2ϩ entry. The use of small interfering RNA to knock down TRPA1 reduced the MGinduced Ca 2ϩ entry as well as TRPA1 mRNA expression. The quantitative real-time RT-PCR analysis showed the prominent existence of TRPA1 mRNA. Expression of TRPA1 protein was confirmed by Western blotting and immunocytochemical analyses. MG promoted cell cycle progression from G0/G1 to S/G2/M, which was suppressed by HC030031 or RR. MG also enhanced ␣-smooth muscle actin expression. The present results suggest that methylglyoxal activates TRPA1 and promotes cell cycle progression and differentiation in human cardiac fibroblasts. MG might participate the development of pathophysiological conditions including diabetic cardiomyopathy via activation of TRPA1.human cardiac fibroblast; transient receptor potential ankyrin 1 channels; methylglyoxal CARDIAC FIBROBLASTS ARE THE predominant secretary cell types located within the extracellular matrix (ECM) (18), which account for 60ϳ70% of the cells in human hearts and play a key role in regulating normal myocardial function and in the adverse myocardial remodeling that occurs with hypertension, heart failure, and myocardial infarction (12, 71). Many of the functional effects of cardiac fibroblasts are mediated through differentiation of cardiac fibroblasts to myofibroblasts phenotype that expresses contractile proteins such as ␣-smooth muscle actin (␣-SMA), and they consequently exhibit increased migratory and proliferative properties. Cardiac fibroblasts also take a part in the maintenance of myocardial function by producing the type I and type III collagens and by secreting growth factors (48), and a key source of components of the ECM that regulat...

show abstract

“…It has been reported that high glucose modulates the expression of TRPC such as TRPC6 (29,73). Therefore, we investigated the effects of high glucose (20 and 30 mM) on TRPA1 expression.…”

Section: Expression Of Trpa1 Protein In Human Cardiac Fibroblasts (Immentioning

confidence: 98%

Effects of methylglyoxal on human cardiac fibroblast: roles of transient receptor potential ankyrin 1 (TRPA1) channels

Oguri

Nakajima

Yamamoto

et al. 2014

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

show abstract

“…30,31 In addition, it has been shown recently by our group that increased TRPC6 expression is a hallmark of atherosclerosis. 10 Analysis of the TRPC6 promoter revealed possible binding sites for GATA transcription factors, which are known to be regulated by shear stress, 18 which are acknowledged to regulate TRPC6 as part of a signaling circuit during pathological cardiac remodeling, 17 and which play a significant role in endothelial cells, for example, in vessel formation, endothelial cell migration, and apoptosis. 19 Both, the significant association of GATA1 and GATA4 mRNA expression with TRPC6 mRNA expression and the determination of GATA1 binding sites in the promoter region of TRPC6 point to these transcription factors as the underlying mechanisms, by which TRPC6 expression is enhanced by atheroprone shear stress.…”

Section: Thilo Et Al Trp Channels In Shear Stressmentioning

confidence: 99%

“…6 Moreover, several subtypes of transient receptor potential (TRP) channels, including transient receptor potential cation channel, subfamily C, member 3 (TRPC3) TRPC6, TRPM7, and TRPV1, have been linked to cardiovascular disease, hypertension, and atherosclerosis. [7][8][9][10][11][12][13] TRP channels are activated by a variety of factors, including chemical stimuli and mechanical stimuli, like shear stress. TRP channels are known to be mechanosensitive, although the specific mechanisms still need to be elucidated.…”

mentioning

confidence: 99%

Pulsatile Atheroprone Shear Stress Affects the Expression of Transient Receptor Potential Channels in Human Endothelial Cells

et al. 2012

Self Cite

View full text Add to dashboard Cite

Abstract-The goal of the study was to assess whether pulsatile atheroprone shear stress modulates the expression of transient receptor potential (TRP) channels, TRPC3, TRPC6, TRPM7, and TRPV1 mRNA, in human umbilical vascular endothelial cells. Exposure of cultured vascular endothelial cells to defined shear stress, producing a constant laminar flow (generating a shear stress of 6 dyne/cm 2 ), laminar pulsatile atheroprotective flow (with a mean shear stress of 20 dyne/cm 2 ), or laminar atheroprone bidirectional flow (with a mean shear stress of 0 dyne/cm 2 ) differentially induced TRPC6 and TRPV1 mRNA as measured by quantitative real-time RT-PCR and normalized to GAPDH expression. Thereby, TRPC6 and TRPV1 mRNA expressions were significantly increased after 24 hours of exposure to an atheroprone flow profile compared with an atheroprotective flow profile. Furthermore, the expression of transcription factors GATA1 and GATA4 was significantly correlated with the expression of TRPC6 mRNA. In contrast, after 24 hours of constant laminar flow, the expression of TRPC6 and TRPV1 mRNA was unchanged, whereas the expression of TRPC3 and TRPM7 was significantly higher in endothelial cells exposed to shear stress in comparison with endothelial cells grown under static conditions. There was a significant association between the expression of TRPC6 and tumor necrosis factor-␣ mRNA in human vascular tissue. No-flow and atheroprone flow conditions are equally characterized by an increase in the expression of tumor necrosis factor-␣; however, inflammation-associated endothelial cell reactions may be further aggravated at atheroprone flow conditions by the increase of TRPV1 and TRPC6, as observed in our study. (Hypertension. 2012;59:1232-1240.)

show abstract

“…Oxidative stress increases inward divalent ion permeation through TRPM7 (5, 9), whereas acute and chronic oxidative stress in culture (24)(25)(26) or during ischemia-reperfusion in vivo (27,28) induces TRPM7 expression. The resulting increase in cytosolic Zn 2+ could result in toxic cytosolic concentrations (9).…”

mentioning

confidence: 99%

TRPM7 senses oxidative stress to release Zn ²⁺ from unique intracellular vesicles

Abiria

Krapivinsky

Sah

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

TRPM7 (transient receptor potential cation channel subfamily M member 7) regulates gene expression and stress-induced cytotoxicity and is required in early embryogenesis through organ development. Here, we show that the majority of TRPM7 is localized in abundant intracellular vesicles. These vesicles (M7Vs) are distinct from endosomes, lysosomes, and other familiar vesicles or organelles. , an ion channel and cytoplasmic kinase, is ubiquitously expressed and essential in early embryonic development (1-4) but also may mediate oxidative stress-induced anoxic neuronal death in adults (5, 6). As an ion channel, TRPM7 conducts Zn 2+ >Mg 2+ ∼ Ca 2+ and monovalent cations (7-10) and contributes to labile cytosolic and nuclear Zn 2+ concentrations (8). TRPM7's C-terminal kinase can phosphorylate multiple substrates (11-13) and is cleaved to release a proapoptotic, chromatin-modifying enzyme (8,14). Zn 2+ regulates TRPM7's kinase activity (11) and binding to transcription factors (8). It is a potent signal for many cellular processes previously related to TRPM7 function, including gene expression, mitosis, and cell survival, but is also proapoptotic at extreme concentrations (15)(16)(17)(18) Oxidative stress increases inward divalent ion permeation through TRPM7 (5, 9), whereas acute and chronic oxidative stress in culture (24-26) or during ischemia-reperfusion in vivo (27, 28) induces TRPM7 expression. The resulting increase in cytosolic Zn 2+ could result in toxic cytosolic concentrations (9). Conversely, reduction of TRPM7 expression protects animals from postischemia reperfusion (5), a condition typically accompanied by increased reactive oxygen species (ROS) and Zn 2+ release from intracellular stores (29). Physiological redox transitions required for stem cell differentiation and gene expression during embryonic development (30, 31) may also be sensed by TRPM7 and transduced via Zn -dependent signals (32). Because TRPM7 patch-clamp recording is limited to the plasma membrane, the assumption has been that TRPM7's main function is on the plasma membrane. However, we have previously shown that TRPM7 is also on intracellular membranes (33-35). Indeed, ROS activation of divalent ion influx through TRPM7 (5, 9) is reminiscent of ROS activation of TRPM2, which releases Ca 2+ and Zn 2+ from lysosomes (36,37 ] and ROS during development and injury.

show abstract

High Glucose–Induced Oxidative Stress Increases Transient Receptor Potential Channel Expression in Human Monocytes

Cited by 96 publications

References 33 publications

Effects of methylglyoxal on human cardiac fibroblast: roles of transient receptor potential ankyrin 1 (TRPA1) channels

Effects of methylglyoxal on human cardiac fibroblast: roles of transient receptor potential ankyrin 1 (TRPA1) channels

Pulsatile Atheroprone Shear Stress Affects the Expression of Transient Receptor Potential Channels in Human Endothelial Cells

TRPM7 senses oxidative stress to release Zn ²⁺ from unique intracellular vesicles

Contact Info

Product

Resources

About

High Glucose–Induced Oxidative Stress Increases Transient Receptor Potential Channel Expression in Human Monocytes

Cited by 96 publications

References 33 publications

Effects of methylglyoxal on human cardiac fibroblast: roles of transient receptor potential ankyrin 1 (TRPA1) channels

Effects of methylglyoxal on human cardiac fibroblast: roles of transient receptor potential ankyrin 1 (TRPA1) channels

Pulsatile Atheroprone Shear Stress Affects the Expression of Transient Receptor Potential Channels in Human Endothelial Cells

TRPM7 senses oxidative stress to release Zn 2+ from unique intracellular vesicles

Contact Info

Product

Resources

About

TRPM7 senses oxidative stress to release Zn ²⁺ from unique intracellular vesicles