Transcriptional regulation of increased CCL2 expression in pulmonary fibrosis involves nuclear factor-κB and activator protein-1

Deng, Xiaoling; Xu, Mingyan; Yuan, Chao; Yin, Liqin; Chen, Xihe; Zhou, Xiaoqiong; Li, Guanwu; Fu, Yucai; Feghali‐Bostwick, Carol; Pang, Linhua

doi:10.1016/j.biocel.2013.04.003

Cited by 54 publications

(53 citation statements)

References 46 publications

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“…The activation of TLRs and NF-κB is one of the hallmarks of PF 22 . Previous studies have shown that PC treatment reduced the expression of NF-κB in lung tissues 15 .…”

Section: Resultsmentioning

confidence: 99%

Phycocyanin attenuates pulmonary fibrosis via the TLR2-MyD88-NF-κB signaling pathway

et al. 2017

Sci Rep

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Our aim was to investigate the effects of phycocyanin (PC) on bleomycin (BLM)-induced pulmonary fibrosis (PF). In this study, C57 BL/6 wild-type (WT) mice and toll-like receptor (TLR) 2 deficient mice were treated with PC for 28 days following BLM exposure. Serum and lung tissues were collected on days 3, 7 and 28. Data shows PC significantly decreased the levels of hydroxyproline (HYP), vimentin, surfactant-associated protein C (SP-C), fibroblast specific protein-1 (S100A4) and α-smooth muscle actin (α-SMA) but dramatically increased E-cadherin and podoplanin (PDPN) expression on day 28. Moreover, PC greatly decreased the levels of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) and myeloperoxidase (MPO) at the earlier time. Reduced expression of key genes in the TLR2 pathway was also detected. Compared with WT mice, TLR2-deficient mice exhibited less injury, and the protective effect of PC was partly diminished in this background. These data indicate the anti-fibrotic effects of PC may be mediated by reducing W/D ratio, MPO, IL-6, TNF-α, protecting type I alveolar epithelial cells, inhibiting fibroblast proliferation, attenuating epithelial-mesenchymal transitions (EMT) and reducing oxidative stress. The TLR2-MyD88-NF-κB pathway plays an important role in PC-mediated reduction in pulmonary fibrosis.

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“…The activation of TLRs and NF-κB is one of the hallmarks of PF 22 . Previous studies have shown that PC treatment reduced the expression of NF-κB in lung tissues 15 .…”

Section: Resultsmentioning

confidence: 99%

Phycocyanin attenuates pulmonary fibrosis via the TLR2-MyD88-NF-κB signaling pathway

et al. 2017

Sci Rep

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“…Ctdsp1 was targeted by 4 lncRNAs (AK089579, AV310809, uc007dlv.1 and AK142426) and 2 miRNAs (miR-182 and miR-488) simultaneously. Many targets mentioned here have been reported to be linked to cell proliferation or tissue fibrosis (Wang et al, 2006;Rajasekaran et al, 2012;Xiao et al, 2012;Deng et al, 2013;Ponticos et al, 2015).…”

Section: Establishment Of Gene Co-expression Networkmentioning

confidence: 95%

The expression profiling and ontology analysis of noncoding RNAs in peritoneal fibrosis induced by peritoneal dialysis fluid

Guo

Hao

et al. 2015

Gene

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“…Moreover, Ccl2 mRNA expression varied in a time-dependent manner in wild-type 5/6Nx mice and was regulated by p65. The expression of Ccl2 is activated by binding of transcription factors to NF-κB elements in the Ccl2 promoter (Deng et al, 2013). Although the CLOCK protein enhances transcription mediated by NF-κB, CLOCKΔ19 protein does not affect NF-κB-dependent transcription (Spengler et al, 2012), and the mechanism by which NF-κB regulates transcription in Clk / Clk mice remains unclear.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of G0/G1 Switch 2 Ameliorates Renal Inflammation in Chronic Kidney Disease

et al. 2016

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Chronic kidney disease (CKD) is a global health problem, and novel therapies to treat CKD are urgently needed. Here, we show that inhibition of G0/G1 switch 2 (G0s2) ameliorates renal inflammation in a mouse model of CKD. Renal expression of chemokine (C-C motif) ligand 2 (Ccl2) was increased in response to p65 activation in the kidneys of wild-type 5/6 nephrectomy (5/6Nx) mice. Moreover, 5/6Nx Clk/Clk mice, which carry homozygous mutations in the gene encoding circadian locomotor output cycles kaput (CLOCK), did not exhibit aggravation of apoptosis or induction of F4/80-positive cells. The renal expression of G0s2 in wild-type 5/6Nx mice was important for the transactivation of Ccl2 by p65. These pathologies were ameliorated by G0s2 knockdown. Furthermore, a novel small-molecule inhibitor of G0s2 expression was identified by high-throughput chemical screening, and the inhibitor suppressed renal inflammation in 5/6Nx mice. These findings indicated that G0s2 inhibitors may have applications in the treatment of CKD.

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Transcriptional regulation of increased CCL2 expression in pulmonary fibrosis involves nuclear factor-κB and activator protein-1

Cited by 54 publications

References 46 publications

Phycocyanin attenuates pulmonary fibrosis via the TLR2-MyD88-NF-κB signaling pathway

Phycocyanin attenuates pulmonary fibrosis via the TLR2-MyD88-NF-κB signaling pathway

The expression profiling and ontology analysis of noncoding RNAs in peritoneal fibrosis induced by peritoneal dialysis fluid

Inhibition of G0/G1 Switch 2 Ameliorates Renal Inflammation in Chronic Kidney Disease

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