Vacuolar protein sorting 4B regulates apoptosis of intestinal epithelial cells via p38 MAPK in Crohn's disease

Zhang, Dongmei; Wang, Liang; Yan, Lijun; Miao, Xianjing; Chen, Gong; Xiao, Min; Ni, Runzhou; Tang, Qiyun

doi:10.1016/j.yexmp.2014.12.007

Cited by 18 publications

(19 citation statements)

References 45 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Moreover, we found that the protein levels of VPS4B, PCNA, and cyclin A concomitantly increased after serum starvation and refeeding ( Figure 4C). Of note, other studies have also shown that VPS4B depletion is associated with a marked reduction in the proliferation rate of various cell types including multiple myeloma cells, hepatocellular carcinoma cells, HT-29 colon carcinoma cells, and A549 lung carcinoma cells [5,6,8,23]. Our results are consistent with these findings and show that an impairment of VPS4B function can influence the proliferation of hDPSCs.…”

Section: Discussionsupporting

confidence: 92%

“…VPS4B is an essential component of the endosomal sorting complexes required for the transport (ESCRT) machinery that mediates the final abscission step of cytokinesis in eukaryotes and many archaeal species [4]. Some studies have shown that VPS4B can regulate the progression of non-small cell lung cancer [5] and is involved in hepatocellular carcinoma [6] and in the apoptosis of chondrocytes and intestinal epithelial cells during osteoarthritis and Crohn's disease, respectively [7,8]. Furthermore, VPS4B has been identified as a putative tumour suppressor in breast cancer because VPS4B promotes degradation of epidermal growth factor receptor, EGFR [9].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Vacuolar protein sorting 4B regulates the proliferation and odontoblastic differentiation of human dental pulp stem cells through the Wnt-β-catenin signalling pathway

Pan

Lü

Peng

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

View full text Add to dashboard Cite

Our previous studies have revealed that a dominant mutation in vacuolar protein sorting 4B (VPS4B), a member of the AAA ATPase family, causes dentin dysplasia type I. The purpose of the present study was to investigate the roles of VPS4B in human dental pulp stem cells (hDPSCs) and to elucidate the underlying molecular mechanisms. In this study, we found that VPS4B was highly expressed in the dental pulp cells of the mouse molar tooth germ, and the expression of VPS4B increased significantly during the odontoblastic differentiation of hDPSCs. VPS4B downregulation inhibited the proliferation, migration, and odontoblastic differentiation of hDPSCs. Moreover, treatment with lithium chloride, an agonist of the Wnt-b-catenin signalling pathway, partially reversed the VPS4B knockdown-driven suppression of proliferation and of odontoblastic differentiation of hDPSCs. Collectively, our findings indicate that VPS4B, via Wnt-b-catenin signalling, acts as a regulator of the proliferation and differentiation of hDPSCs. Our results suggest potential therapeutic avenues for dentin formation and regenerative endodontics in patients with dentin dysplasia type I. ARTICLE HISTORY

show abstract

Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Vacuolar protein sorting 4B regulates the proliferation and odontoblastic differentiation of human dental pulp stem cells through the Wnt-β-catenin signalling pathway

Pan

Lü

Peng

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

View full text Add to dashboard Cite

show abstract

“…Similarly, a previous study detected elevated levels of active caspase3 and phosphorylated p38MAPK in mice with TNBS-induced colitis (31). In an in vitro TNF-α-induced HT29 intestinal epithelial cell apoptosis model, p38MAPK phosphorylation was increased (31). It was also reported that the JNK inhibitor XG-102 protects against TNBS-induced mouse colitis, where the production of TNF-α, expression of Bim, B-cell lymphoma 2-associated X protein and p53 as well as activation of caspase3 and JNK substrate c-Jun were significantly reduced (32).…”

Section: Discussionsupporting

confidence: 61%

“…In addition, dexamethasone may protect the colon against damage through inhibition of the p38MAPK/JNK/c-Jun pathway depending on the local levels of TGF-β1. Similarly, a previous study detected elevated levels of active caspase3 and phosphorylated p38MAPK in mice with TNBS-induced colitis (31). In an in vitro TNF-α-induced HT29 intestinal epithelial cell apoptosis model, p38MAPK phosphorylation was increased (31).…”

Section: Discussionsupporting

confidence: 57%

Local level of TGF-β1 determines the effectiveness of dexamethasone through regulating the balance of Treg/Th17 cells in TNBS-induced mouse colitis

Peng

Chen

et al. 2018

Exp Ther Med

View full text Add to dashboard Cite

Transforming growth factor β1 (TGF-β1) has a crucial role in regulating the balance of type 17 T-helper cells (Th17) and T regulatory cells (Tregs) that are involved in the pathogenesis of inflammatory bowel disease, while the function of local TGF-β1 in this process has remained to be fully elucidated. The present study investigated the effects of different local TGF-β1 levels on the Treg/Th17 balance and on the dexamethasone efficacy in mice with 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced colitis. Various TGF-β1 levels in colon tissue were achieved by enema delivery of a high, medium or low amount of adenovirus expressing TGF-β1 (10, 10 or 10 pfu, denoted as AdTGF-1, AdTGF-2 and AdTGF-3, respectively). Dexamethasone further decreased colon damage and myeloperoxidase activity in TNBS mice receiving AdTGF-1 and AdTGF-2. When AdTGF-1 was administered, dexamethasone enhanced its effect by reducing interferon (IFN)-γ and increasing interleukin (IL)-10 production. In TNBS mice receiving AdTGF-2, the increase in IFN-γ, tumor necrosis factor-α, IL-6, IL-17 and IL-23 was significantly prevented by dexamethasone treatment. In comparison with the lower doses, AdTGF-3 exerted the opposite effect on regulating the cytokine production in TNBS mice, which was not affected by dexamethasone treatment. In mesenteric lymph nodes, AdTGF-1 prevented the TNBS-induced reduction of Tregs and IL-10, and potentially increased the efficacy of dexamethasone. In addition, dexamethasone further decreased the levels of activated caspase3 in TNBS mice receiving adenoviral TGF-β1, particularly in the AdTGF-1 group. The activation of the p38 mitogen-activated protein kinase/c-Jun N-terminal kinase/c-Jun pathway was significantly inhibited by a low amount of TGF-β1 administered to TNBS-treated mice, which was further decreased by dexamethasone. The present study provided evidence that the therapeutic effect of dexamethasone may depend on the local levels of TGF-β1 in TNBS-induced colitis and may be mediated, at least partially, through promoting the differentiation of Tregs and thus altering the balance of pro- and anti-inflammatory cytokines.

show abstract

“…Equal amounts of protein from colonic tissues were loaded onto SDS‐PAGE gels (Zhang et al, ). After electrophoresis and transference, membranes were blocked with 5% non‐fat dry milk in TBS‐T or BSA (for phosphorylated antibodies) and incubated overnight at 4°C with different primary antibodies (Table ).…”

Section: Methodsmentioning

confidence: 99%

Stimulation of autophagy prevents intestinal mucosal inflammation and ameliorates murine colitis

Macias-Ceja

Cosín-Roger

Ortiz-Masiá

et al. 2017

British J Pharmacology

View full text Add to dashboard Cite

show abstract

Vacuolar protein sorting 4B regulates apoptosis of intestinal epithelial cells via p38 MAPK in Crohn's disease

Cited by 18 publications

References 45 publications

Vacuolar protein sorting 4B regulates the proliferation and odontoblastic differentiation of human dental pulp stem cells through the Wnt-β-catenin signalling pathway

Vacuolar protein sorting 4B regulates the proliferation and odontoblastic differentiation of human dental pulp stem cells through the Wnt-β-catenin signalling pathway

Local level of TGF-β1 determines the effectiveness of dexamethasone through regulating the balance of Treg/Th17 cells in TNBS-induced mouse colitis

Stimulation of autophagy prevents intestinal mucosal inflammation and ameliorates murine colitis

Contact Info

Product

Resources

About