CD147-induced cell proliferation is associated with Smad4 signal inhibition

Hui, Qin; Rasul, Azhar; Li, Xin; Masood, Muqaddas; Yang, Guang; Wang, Na; Wei, Wei; He, Xiaofeng; Watanabe, Nobumoto; Jiang, Li; Li, Yongming

doi:10.1016/j.yexcr.2017.07.003

Cited by 10 publications

(9 citation statements)

References 42 publications

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“…Natural products persist as a promising source of immense chemical diversity, biochemical specificity and various molecular characteristics which make them suitable for the modulation of multiple signaling pathways/cascades in various pathological conditions such as cancer and neurodegnerative diseases [ 16 , 17 , 18 , 19 , 20 , 21 , 22 ]. Currently, phytochemicals including flavonoids, alkaloids, terpenoids, and phenols are of considerable interest for the treatment of such diseases [ 12 ].…”

Section: Introductionmentioning

confidence: 99%

Role of Plant-Derived Flavonoids and Their Mechanism in Attenuation of Alzheimer’s and Parkinson’s Diseases: An Update of Recent Data

et al. 2018

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Neurodegeneration is a progressive loss of neuronal cells in certain regions of the brain. Most of the neurodegenerative disorders (NDDs) share the communal characteristic such as damage or reduction of various cell types typically including astrocytes and microglial activity. Several compounds are being trialed to treat NDDs but they possess solitary symptomatic advantages along with copious side effects. The finding of more enthralling and captivating compounds to suspend and standstill the pathology of NDDs will be considered as a hallmark of present times. Phytochemicals possess the potential to alternate the synthetic line of therapy against NDDs. The present review explores the potential efficacy of plant-derived flavonoids against most common NDDs including Alzheimer’s disease (AD) and Parkinson’s disease (PD). Flavonoids are biologically active phytochemicals which possess potential pharmacological effects, including antiviral, anti-allergic, antiplatelet, anti-inflammatory, anti-tumor, anti-apoptotic and anti-oxidant effects and are able to attenuate the pathology of various NDDs through down-regulating the nitric oxide (NO) production, by reducing the tumor necrosis factor-α (TNF-α), by reducing the excitotoxicity of superoxide as well as acting as tyrosine kinase (TK) and monoamine oxidase (MAO) inhibiting enzyme.

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Section: Introductionmentioning

confidence: 99%

Role of Plant-Derived Flavonoids and Their Mechanism in Attenuation of Alzheimer’s and Parkinson’s Diseases: An Update of Recent Data

et al. 2018

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“…Furthermore, we detected the change in intracellular Smad4 localization using immunofluorescence staining. Studies have shown that CD147 plays a key role in the translocation of Smad4 from the cytoplasm to the nucleus, and silencing CD147 gene expression promoted Smad4 nuclear translocation [ 29 , 30 ]. However, whether CD147 is related to the functions of ClC-3 chloride channels requires further exploration.…”

Section: Discussionmentioning

confidence: 99%

The role of the Smad2/3/4 signaling pathway in osteogenic differentiation regulation by ClC-3 chloride channels in MC3T3-E1 cells

Wang

et al. 2022

J Orthop Surg Res

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Background ClC-3 chloride channels promote osteogenic differentiation. Transforming growth factor-β1 (TGF-β1) and its receptors are closely related to ClC-3 chloride channels, and canonical TGF-β1 signaling is largely mediated by Smad proteins. The current study aimed to explore the role of the Smad2/3/4 signaling pathway in the mechanism by which ClC-3 chloride channels regulate osteogenic differentiation in osteoblasts. Methods First, real-time PCR and western blotting were used to detect the expression of Smad and mitogen-activated protein kinase (MAPK) proteins in response to ClC-3 chloride channels. Second, immunocytochemistry, coimmunoprecipitation (Co-IP) and immunofluorescence analyses were conducted to assess formation of the Smad2/3/4 complex and its translocation to the nucleus. Finally, markers of osteogenic differentiation were determined by real-time PCR, western blotting, ALP assays and Alizarin Red S staining. Results ClC-3 chloride channels knockdown led to increased expression of Smad2/3 but no significant change in p38 or Erk1/2. Furthermore, ClC-3 chloride channels knockdown resulted in increases in the formation of the Smad2/3/4 complex and its translocation to the nucleus. In contrast, the inhibition of TGF-β1 receptors decreased the expression of Smad2, Smad3, p38, and Erk1/2 and the formation of the Smad2/3/4 complex. Finally, the expression of osteogenesis-related markers were decreased upon ClC-3 and Smad2/3/4 knockdown, but the degree to which these parameters were altered was decreased upon the knockdown of ClC-3 and Smad2/3/4 together compared to independent knockdown of ClC-3 or Smad2/3/4. Conclusions The Smad2/3 proteins respond to changes in ClC-3 chloride channels. The Smad2/3/4 signaling pathway inhibits osteogenic differentiation regulation by ClC-3 chloride channels in MC3T3-E1 cells.

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“…The cells were collected for experiments during the exponential growth phase. Cells (2 × 10 5 ) were seeded into 6-well plates and cultured 12 h, then a mixture 300 μM oleic acid/palmitic acid (OA/PA, 2∶1, M/M) was added and the cells were incubated for an additional 12 h, following a previously reported modified method 22 . At 2 h prior to the addition of adenovirus, 0.25 μM BVT2733 (dissolved in DMSO) was added to inhibit the activity of 11β-HSD1 and the inhibitor was present in the medium during the following time.…”

Section: Methodsmentioning

confidence: 99%

The GR-gp78 Pathway is involved in Hepatic Lipid Accumulation Induced by Overexpression of 11β-HSD1

Hu¹,

Han²,

Pan³

et al. 2022

Int. J. Biol. Sci.

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Glucocorticoids are essential participants in the regulation of lipid metabolism. On a tissue-specific level, glucocorticoid signal is controlled by 11β-Hydroxysteroid dehydrogenase 1 (11β-HSD1). Up-regulation of 11β-HSD1 expression during non-alcoholic fatty liver disease (NAFLD) has been previously shown, while 11β-HSD1 inhibition has been shown to reduce hepatic lipids in NAFLD, but the underlying mechanisms remain unclear. Here, in this study, we created in vitro cell culture and in vivo transgenic hepatocyte-specific 11β-HSD1 mouse models of NAFLD to determine the regulatory mechanisms of 11β-HSD1 during lipid metabolism dysfunction. We found that 11β-HSD1 overexpression activated glucocorticoid receptors and promoted their nuclear translocation, and then stimulating gp78. The induction of gp78 sharply reduced expression of Insig2, but not Insig1, which led to up-regulation of lipogenesis regulatory proteins including SREBP1, FAS, SCD1, and ACC1. Our results suggested that overexpression of 11β-HSD1 induced lipid accumulation, at least partially through the GR/gp78/Insig2/SREBP1 pathway, which may serve as a potential diagnostic and therapeutic target for treatment of NAFLD.

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CD147-induced cell proliferation is associated with Smad4 signal inhibition

Cited by 10 publications

References 42 publications

Role of Plant-Derived Flavonoids and Their Mechanism in Attenuation of Alzheimer’s and Parkinson’s Diseases: An Update of Recent Data

Role of Plant-Derived Flavonoids and Their Mechanism in Attenuation of Alzheimer’s and Parkinson’s Diseases: An Update of Recent Data

The role of the Smad2/3/4 signaling pathway in osteogenic differentiation regulation by ClC-3 chloride channels in MC3T3-E1 cells

The GR-gp78 Pathway is involved in Hepatic Lipid Accumulation Induced by Overexpression of 11β-HSD1

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