TGF-β1 acts as mediator in fluoride-induced autophagy in the mouse osteoblast cells

Zhao, Yangfei; Li, Yanyan; Gao, Yufeng; Yuan, Mengke; Manthari, Ram Kumar; Wang, Jinming

doi:10.1016/j.fct.2018.02.065

Cited by 26 publications

(16 citation statements)

References 49 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A previous study demonstrated that inhibition of autophagy reduced TGF-beta2-stimulated RPE cell migration and invasion 53 . In another study, overexpression of TGF-beta1 significantly increased protein expression levels of Beclin1 and LC3-II/I, with a concomitant decrease in p62, while TGF-β silencing had the opposite effect 54 . This evidence suggests that autophagy signaling acts as a downstream signaling pathway of TGF-β.…”

Section: Discussionmentioning

confidence: 92%

“…These findings suggest that the miR-181a-enhanced autophagic flux may be one of the molecular mechanisms underlying nicotine-mediated heart infraction and dysfunction in rat offspring. In addition, previous studies have suggested that TGF-β could also trigger autophagic flux 53 , 54 . A previous study demonstrated that inhibition of autophagy reduced TGF-beta2-stimulated RPE cell migration and invasion 53 .…”

Section: Discussionmentioning

confidence: 97%

See 1 more Smart Citation

Reprogramming of miR-181a/DNA methylation patterns contribute to the maternal nicotine exposure-induced fetal programming of cardiac ischemia-sensitive phenotype in postnatal life

Jian¹,

Zhang²,

Li³

et al. 2020

Theranostics

View full text Add to dashboard Cite

Background: E-cigarette and other novel electronic nicotine delivery systems (ENDS) have recently entered the market at a rapid pace. The community desperately needs answers about the health effects of ENDS. The present study tested the hypothesis that perinatal nicotine exposure (PNE) causes a gender-dependent increase in vulnerability of the heart to ischemia-reperfusion (I/R) injury and cardiac dysfunction in male rat offspring via reprogramming of the miRNA-181a (miR-181a)-mediated signaling pathway and that miR-181a antisense could rescue this phenotype. Methods: Nicotine or saline was administered to pregnant rats via subcutaneous osmotic minipumps from gestational day 4 until postnatal day 10. Cardiac function and molecular biological experiments were conducted in ~3- month-old offspring. Results: PNE enhanced I/R-induced cardiac dysfunction and infarction in adult male but not in female offspring, which was associated with miR-181a over-expression in left ventricle tissues. In addition, PNE enhanced offspring cardiac angiotensin receptor (ATR) expressions via specific CpG hypomethylation of AT 1 R/AT 2 R promoter. Furthermore, PNE attenuated cardiac lncRNA H19 levels, but up-regulated cardiac TGF-β/Smads family proteins and consequently up-regulated autophagy-related protein (Atg-5, beclin-1, LC3 II, p62) expression in the male offspring. Of importance, treatment with miR-181a antisense eliminated the PNE's effect on miR-181a expression/H19 levels and reversed PNE-mediated I/R-induced cardiac infarction and dysfunction in male offspring. Furthermore, miR-181a antisense also attenuated the effect of PNE on AT 1 R/AT 2 R/TGF-β/Smads/autophagy-related biomarkers in the male offspring. Conclusion: Our data suggest that PNE could induce a reprogramming of cardiac miR-181a expression/DNA methylation pattern, which epigenetically modulates ATR/TGF-β/autophagy signaling pathways, leading to gender-dependent development of ischemia-sensitive phenotype in postnatal life. Furthermore, miR-181a could severe as a potential therapeutic target for rescuing this phenotype.

show abstract

Section: Discussionmentioning

confidence: 92%

Section: Discussionmentioning

confidence: 97%

Reprogramming of miR-181a/DNA methylation patterns contribute to the maternal nicotine exposure-induced fetal programming of cardiac ischemia-sensitive phenotype in postnatal life

Jian¹,

Zhang²,

Li³

et al. 2020

Theranostics

View full text Add to dashboard Cite

show abstract

“…Notably, Lv et al observed that F induced IFNγ signalling activates osteoclasts and aggravates oestrogen deficiency inducing osteoporosis [145]. It has also been reported that TGF-β1 plays an important role in fluorosis and increased levels of TGF-β1 have been suggested as an important marker in the evaluation of the pathological action of F in bone tissue [146,147]. In vivo and in vitro experimental studies of fluorosis have shown that F upregulates TGF-β1 protein and mRNA expression in bone cells [146,148,149,150].…”

Section: Molecular Mechanisms Of Fluoride Inhibition Of Iodine Hommentioning

confidence: 99%

Fluoride Exposure Induces Inhibition of Sodium/Iodide Symporter (NIS) Contributing to Impaired Iodine Absorption and Iodine Deficiency: Molecular Mechanisms of Inhibition and Implications for Public Health

Waugh¹

2019

IJERPH

View full text Add to dashboard Cite

The sodium iodide symporter (NIS) is the plasma membrane glycoprotein that mediates active iodide transport in the thyroid and other tissues, such as the salivary, gastric mucosa, rectal mucosa, bronchial mucosa, placenta and mammary glands. In the thyroid, NIS mediates the uptake and accumulation of iodine and its activity is crucial for the development of the central nervous system and disease prevention. Since the discovery of NIS in 1996, research has further shown that NIS functionality and iodine transport is dependent on the activity of the sodium potassium activated adenosine 5′-triphosphatase pump (Na+, K+-ATPase). In this article, I review the molecular mechanisms by which F inhibits NIS expression and functionality which in turn contributes to impaired iodide absorption, diminished iodide-concentrating ability and iodine deficiency disorders. I discuss how NIS expression and activity is inhibited by thyroglobulin (Tg), tumour necrosis factor alpha (TNF-α), transforming growth factor beta 1 (TGF-β1), interleukin 6 (IL-6) and Interleukin 1 beta (IL-1β), interferon-γ (IFN-γ), insulin like growth factor 1 (IGF-1) and phosphoinositide 3-kinase (PI3K) and how fluoride upregulates expression and activity of these biomarkers. I further describe the crucial role of prolactin and megalin in regulation of NIS expression and iodine homeostasis and the effect of fluoride in down regulating prolactin and megalin expression. Among many other issues, I discuss the potential conflict between public health policies such as water fluoridation and its contribution to iodine deficiency, neurodevelopmental and pathological disorders. Further studies are warranted to examine these associations.

show abstract

“…However, when the inhibitor 3methyladenineis used to inhibit autophagy, the P62 substrate accumulates [24]. P62 can be used as a marker of autophagy [25]. Microtubule-associated protein light chain 3 (LC3) is a mammalian homolog of yeast Atg8.…”

Section: Introductionmentioning

confidence: 99%

Deletion of the transcriptional regulator GntR affects apoptosis and autophagy in Brucella abortus-infected RAW 264.7 cells

Wei

Wang

et al. 2020

Preprint

View full text Add to dashboard Cite

Background: Brucellosis is an important zoonotic disease caused by the pathogen Brucella. Regulating apoptosis and autophagy is the prerequisite for the intracellular survival of Brucella. GntR is an important transcriptional regulator of Brucella that can regulate the expression of many target genes, and then play a regulatory role in many cell processes, including regulation apoptosis and autophagy. Therefore, understanding the relationship between GntR and apoptosis and autophagy is crucial to comprehending the pathogenic mechanism of Brucella. Methods: In the present study, we described the influence of GntR on apoptosis and autophagy after the infection of RAW 264.7 cells with Brucella. We constructed the GntR mutant strain (2308ΔGntR) of Brucella abortus 2308 (S2308). Following the infection of the RAW 264.7 cells with S2308 and 2308ΔGntR, apoptosis and autophagy were detected. Results: Western blot analysis and flow cytometry analysis indicated that the apoptosis rate of the 2308ΔGntR-infected group was remarkably higher than that of the S2308-infected group. Confocal laser microscopy experiments indicated the presence of the P62 protein as punctate aggregates in the 2308ΔGntR group. Conclusion: These results showed that 2308ΔGntR promoted apoptosis and inhibited autophagy in the RAW 264.7 cells during Brucella infection.

show abstract

TGF-β1 acts as mediator in fluoride-induced autophagy in the mouse osteoblast cells

Cited by 26 publications

References 49 publications

Reprogramming of miR-181a/DNA methylation patterns contribute to the maternal nicotine exposure-induced fetal programming of cardiac ischemia-sensitive phenotype in postnatal life

Reprogramming of miR-181a/DNA methylation patterns contribute to the maternal nicotine exposure-induced fetal programming of cardiac ischemia-sensitive phenotype in postnatal life

Fluoride Exposure Induces Inhibition of Sodium/Iodide Symporter (NIS) Contributing to Impaired Iodine Absorption and Iodine Deficiency: Molecular Mechanisms of Inhibition and Implications for Public Health

Deletion of the transcriptional regulator GntR affects apoptosis and autophagy in Brucella abortus-infected RAW 264.7 cells

Contact Info

Product

Resources

About