TNF-α induces vascular endothelial cells apoptosis through overexpressing pregnancy induced noncoding RNA in Kawasaki disease model

Jiang, Chunming; Fang, Xiang; Jiang, Yanqiu; Shen, Fang; Hu, Zhaoyang; Li, Xiaoli; Huang, Xu

doi:10.1016/j.biocel.2016.01.011

Cited by 40 publications

(22 citation statements)

References 18 publications

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“…Since AQP-1, MMP9, and JAM-C all play key roles in regulating capillary permeability in SAP [9-11], we also observed changes in the expression of endothelial barrier function-related proteins such as AQP-1, MMP-9, and JAM-C proteins and mRNA. We found that after adding TNF-α (10 ng/mL), the TEER permeability measurements and apoptosis rates of the endothelial cells increased at 6 h, 12 h, and 24 h. These results are consistent with the results of our previous study [22]. The most significant rise in the rate of apoptosis took place at 12 h, so we chose 12 h as a check point.…”

Section: Discussionsupporting

confidence: 81%

Dachengqi Decoction Attenuates Intestinal Vascular Endothelial Injury in Severe Acute Pancreatitis in Vitro and in Vivo

Pan

Chen

et al. 2017

Cell Physiol Biochem

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Background/Aims: Dachengqi decoction (DCQD) is a well-known traditional Chinese herbal drug with strong anti-inflammatory effects. Angiopoietin-1 (Ang-1) plays a vital role in maintaining the stability and integrity of the vascular wall and prevents vascular leakage due to inflammatory mediators. Our previous work found that DCQD protects against pancreatic injury in rats with severe acute pancreatitis (SAP). This study aims to investigate the effects of DCQD on intestinal endothelial damage in both damaged human umbilical vein endothelial cells (HUVECs) and SAP rats. Methods: HUVECs were randomly divided into four groups: control group, TNF-α group, TNF-α plus Ang-1 group (Ang-1 group), and TNF-α plus DCQD group (DCQD group). Cells were incubated for 6 h, 12 h, and 24 h, before collection. The treatment concentration of DCQD was decided based on a Cell Counting Kit-8 (CCK-8) assay. The monolayer permeability of the HUVECs was assessed by measuring the transendothelial electrical resistance (TEER). Apoptosis was analyzed by flow cytometry. mRNA and protein expression of aquaporin 1 (AQP-1), matrix metalloproteinase 9 (MMP9), and junctional adhesion molecule-C (JAM-C) was evaluated by RT-PCR, immunocytofluorescence, and western blot. Forty male Sprague-Dawley rats were randomized into a control group, SAP group, SAP plus Ang-1 group (Ang-1 group), and SAP plus DCQD group (DCQD group). SAP was induced by intraperitoneal injection of cerulein and lipopolysaccharide (LPS), while the control group received 0.9% saline solution. Evans blue was injected through the penile vein and the rats were then sacrificed 12 h after modeling. Levels of serum amylase, TNF-α, IL-1β, IL-2, and IL-6 were determined by using ELISA. Intestinal tissue was analysed by histology, and capillary permeability in the tissues was evaluated by Evans blue extravasation assay. Protein and mRNA expression of AQP-1, MMP9, and JAM-C were assessed by immunohistofluorescence, western blot, and RT-PCR. Results: DCQD reduced the permeability of HUVEC induced by TNF-α in vitro. Furthermore, DCQD altered the mRNA and protein levels of JAM-C, MMP9, and AQP-1 in HUVECs after TNF-α induction. SAP intestinal injury induced by cerulein combined with lipopolysaccharides was concomitant with increased expression of JAM-C and MMP9, and reduced expression of AQP-1 in intestinal tissue. Pretreatment with DCQD attenuated SAP intestinal injury and lowered the levels of serum amylase, TNF–α, IL-1β, IL-2, and IL-6 effectively. Our study demonstrated that DCQD decreased the expression of JAM-C and MMP9 and increased the expression of AQP-1 both in vitro and in vivo. Conclusion: DCQD can reduce capillary endothelial damage in acute pancreatitis-associated intestinal injury and the mechanism may be associated with the regulation of endothelial barrier function-associated proteins AQP-1, MMP9, and JAM-C.

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Section: Discussionsupporting

confidence: 81%

Dachengqi Decoction Attenuates Intestinal Vascular Endothelial Injury in Severe Acute Pancreatitis in Vitro and in Vivo

Pan

Chen

et al. 2017

Cell Physiol Biochem

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“…For example, in Kawasaki disease, TNF-α induces vascular endothelial cell apoptosis by causing the overexpression of pregnancy-induced non-coding RNA49. Here, E. coli -induced cytokines, such as TNF-α, IL-1β, IL-6, IL-8, GRO-α and MIP-2, were selected to stimulate the primary hBMECs.…”

Section: Discussionmentioning

confidence: 99%

Differential transcription profiles of long non-coding RNAs in primary human brain microvascular endothelial cells in response to meningitic Escherichia coli

Yang

Huang²,

et al. 2016

Sci Rep

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Accumulating studies have indicated the influence of long non-coding RNAs (lncRNAs) on various biological processes as well as disease development and progression. However, the lncRNAs involved in bacterial meningitis and their regulatory effects are largely unknown. By RNA-sequencing, the transcriptional profiles of host lncRNAs in primary human brain microvascular endothelial cells (hBMECs) in response to meningitic Escherichia coli were demonstrated. Here, 25,257 lncRNAs were identified, including 24,645 annotated lncRNAs and 612 newly found ones. A total of 895 lncRNAs exhibited significant differences upon infection, among which 382 were upregulated and 513 were downregulated (≥2-fold, p < 0.05). Via bioinformatic analysis, the features of these lncRNAs, their possible functions, and the potential regulatory relationships between lncRNAs and mRNAs were predicted. Moreover, we compared the transcriptional specificity of these differential lncRNAs among hBMECs, human astrocyte cell U251, and human umbilical vein endothelial cells, and demonstrated the novel regulatory effects of proinflammatory cytokines on these differential lncRNAs. To our knowledge, this is the first time the transcriptional profiles of host lncRNAs involved in E. coli-induced meningitis have been reported, which shall provide novel insight into the regulatory mechanisms behind bacterial meningitis involving lncRNAs, and contribute to better prevention and therapy of CNS infection.

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“…Therefore, low-intensity exercise was not enough to decrease the systemic expression level of inflammatory cytokines. However, increased TNF-a could promote vascular endothelial cell apoptosis (40). Therefore, capillary regression was induced rapidly and drastically by increased TNF-a through promoted vascular endothelial cell apoptosis in cancer cachexia.…”

Section: Discussionmentioning

confidence: 99%

Preventive effects of low‐intensity exercise on cancer cachexia–induced muscle atrophy

et al. 2019

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We hypothesized that low‐intensity endurance exercise might be more effective in preventing cancer cachexia–induced muscle atrophy through both an increase in protein synthesis and a decrease in protein degradation. The purpose of present study was to evaluate the effects and to clarify the mechanism of low‐intensity endurance exercise on cancer cachexia–induced muscle atrophy. Twenty‐four male Wistar rats were randomly divided into 4 groups: control (Cont), Cont plus exercise (Ex), AH130‐induced cancer cachexia (AH130), and AH130 plus Ex. Cancer cachexia was induced by intraperitoneal injections with AH130 Yoshida ascites hepatoma cells; we analyzed the changes in muscle mass and the gene and protein expression levels of major regulators or indicators of skeletal muscle protein degradation and synthesis pathway in the soleus muscles. Low‐intensity exercise inhibited the muscle mass loss through a suppression of the ubiquitin‐proteasome pathway, increased hypoxia‐inducible factor‐1α and phosphorylated AMPK, and inhibited the deactivation of mammalian target of rapamycin pathway in the soleus muscle, which contributed to the prevention of cancer cachexia–induced muscle atrophy. These results suggest that low‐intensity exercise has the potential to become an effective therapeutic intervention for the prevention of cancer cachexia–induced muscle atrophy.—Tanaka, M., Sugimoto, K., Fujimoto, T., Xie, K., Takahashi, T., Akasaka, H., Kurinami, H., Yasunobe, Y., Matsumoto, T., Fujino, H., Rakugi, H. Preventive effects of low‐intensity exercise on cancer cachexia–induced muscle atrophy. FASEB J. 33, 7852–7862 (2019). http://www.fasebj.org

show abstract

TNF-α induces vascular endothelial cells apoptosis through overexpressing pregnancy induced noncoding RNA in Kawasaki disease model

Cited by 40 publications

References 18 publications

Dachengqi Decoction Attenuates Intestinal Vascular Endothelial Injury in Severe Acute Pancreatitis in Vitro and in Vivo

Dachengqi Decoction Attenuates Intestinal Vascular Endothelial Injury in Severe Acute Pancreatitis in Vitro and in Vivo

Differential transcription profiles of long non-coding RNAs in primary human brain microvascular endothelial cells in response to meningitic Escherichia coli

Preventive effects of low‐intensity exercise on cancer cachexia–induced muscle atrophy

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