4.7 Article

Impact of oxygen concentration on growth of mesenchymal stromal cells from the marrow of patients with chronic lymphocytic leukemia

期刊

BLOOD
卷 121, 期 6, 页码 971-974

出版社

AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2012-08-447813

关键词

-

资金

  1. National Institutes of Health grant for the CLL Research Consortium [P01-CA081534]
  2. Blood Cancer Research Fund
  3. Le Fond de la Recherche en Sante du Quebec

向作者/读者索取更多资源

Chronic lymphocytic leukemia (CLL) cells interact in the marrow with mesenchymal stromal cells (MSCs), which can enhance CLL-cells' resistance to spontaneous or drug-induced apoptosis. Here we examined the effect of oxygen on the growth and function of MSCs from marrow aspirates of CLL patients. Cultures in ambient oxygen provided for poor recovery and growth of MSCs, which developed features of cell-senescence. However, MSCs were propagated readily from the same cells when they were cultured at a physiologic oxygen concentration of 5%. Such MSCs promoted short-term CLL-cell survival in either 5% or ambient O-2. However, longer-term CLL-cell survival was enhanced when the cocultures were maintained in 5% O-2 versus 21% O-2 because of increased MSC proliferation and production of soluble prosurvival factors, such as CXCL12. This study establishes the importance of physiologic oxygen concentration in the propagation and function of MSCs derived from marrow aspirates of CLL patients in vitro. (Blood. 2013;121(6):971-974)

作者

我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。

评论

主要评分

4.7
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

Article Oncology

Disruption of the EGFR-SQSTM1 interaction by a stapled peptide suppresses lung cancer via activating autophagy and inhibiting EGFR signaling

Jiao-jiao Yu, Dan-dan Zhou, Bing Cui, Cheng Zhang, Feng-wei Tan, Shan Chang, Ke Li, Xiao-xi Lv, Xiao-wei Zhang, Shuang Shang, Yu-Jin Xiang, Fei Chen, Jin-mei Yu, Shan-shan Liu, Feng Wang, Zhuo-Wei Hu, Fang Hua

CANCER LETTERS (2020)

Article Multidisciplinary Sciences

TRIB3-EGFR interaction promotes lung cancer progression and defines a therapeutic target

Jiao-jiao Yu, Dan-dan Zhou, Xiao-xiao Yang, Bing Cui, Feng-wei Tan, Junjian Wang, Ke Li, Shuang Shang, Cheng Zhang, Xiao-xi Lv, Xiao-wei Zhang, Shan-shan Liu, Jin-mei Yu, Feng Wang, Bo Huang, Fang Hua, Zhuo-Wei Hu

NATURE COMMUNICATIONS (2020)

Article Multidisciplinary Sciences

TRIB3 promotes MYC-associated lymphoma development through suppression of UBE3B-mediated MYC degradation

Ke Li, Feng Wang, Zhao-na Yang, Ting-ting Zhang, Yu-fen Yuan, Chen-xi Zhao, Zaiwuli Yeerjiang, Bing Cui, Fang Hua, Xiao-xi Lv, Xiao-wei Zhang, Jiao-jiao Yu, Shan-shan Liu, Jin-mei Yu, Shuang Shang, Yang Xiao, Zhuo-wei Hu

NATURE COMMUNICATIONS (2020)

Article Cell Biology

Faciogenital Dysplasia 5 supports cancer stem cell traits in basal-like breast cancer by enhancing EGFR stability

Ke Li, Ting-ting Zhang, Chen-xi Zhao, Feng Wang, Bing Cui, Zhao-na Yang, Xiao-xi Lv, Zaiwuli Yeerjiang, Yu-fen Yuan, Jin-mei Yu, Zhen-he Wang, Xiao-wei Zhang, Jiao-jiao Yu, Shan-shan Liu, Shuang Shang, Bo Huang, Fang Hua, Zhuo-wei Hu

Summary: The study showed that FGD5 is associated with poor prognosis in BLBCs and interacts with EGFR in BLBC cells, affecting cell proliferation, invasion, and tumorsphere formation, providing a potential therapeutic option for BLBC.

SCIENCE TRANSLATIONAL MEDICINE (2021)

Article Immunology

The chemokine CCL1 triggers an AMFR-SPRY1 pathway that promotes differentiation of lung fibroblasts into myofibroblasts and drives pulmonary fibrosis

Shan-Shan Liu, Chang Liu, Xiao-Xi Lv, Bing Cui, Jun Yan, Yun-Xuan Li, Ke Li, Fang Hua, Xiao-Wei Zhang, Jiao-Jiao Yu, Jin-Mei Yu, Feng Wang, Shuang Shang, Ping-Ping Li, Zhi-Guang Zhou, Yang Xiao, Zhuo-Wei Hu

Summary: Recruitment of immune cells to the site of inflammation by CCL1 is crucial in inflammatory diseases, including pulmonary fibrosis. The study found that alveolar macrophages and CD4(+) T cells are major producers of CCL1, and targeting CCL1 expression can attenuate the pathology of PF.

IMMUNITY (2021)

Article Pharmacology & Pharmacy

TRIB3-GSK-3β interaction promotes lung fibrosis and serves as a potential therapeutic target

Shanshan Liu, Xiaoxi Lv, Xupeng Wei, Chang Liu, Qiao Li, Jiali Min, Fang Hua, Xiaowei Zhang, Ke Li, Pingping Li, Yang Xiao, Zhuowei Hu, Bing Cui

Summary: This study reveals an intact profibrotic axis of TRIB3-GSK-3 beta-A20-C/EBP beta in alveolar macrophages, which represents a target that may provide a promising treatment strategy for pulmonary fibrosis.

ACTA PHARMACEUTICA SINICA B (2021)

Correction Immunology

The chemokine CCL1 triggers an AMFR-SPRY1 pathway that promotes differentiation of lung fibroblasts into myofibroblasts and drives pulmonary fibrosis (vol 54, pg 2042, 2021)

Shan-shan Liu, Chang Liu, Xiao-xi Lv, Bing Cui, Jun Yan, Yun-xuan Li, Ke Li, Fang Hua, Xiao-wei Zhang, Jiao-jiao Yu, Jin-mei Yu, Feng Wang, Shuang Shang, Ping-ping Li, Zhi-guang Zhou, Yang Xiao, Zhuo-wei Hu

IMMUNITY (2021)

Article Cell Biology

TRIB3 reduces CD8+ T cell infiltration and induces immune evasion by repressing the STAT1-CXCL10 axis in colorectal cancer

Shuang Shang, Yu-wei Yang, Fei Chen, Liang Yu, Shuo-hao Shen, Ke Li, Bing Cui, Xiao-Xi Lv, Cheng Zhang, Chen Yang, Jing Liu, Jiao-jiao Yu, Xiao-wei Zhang, Ping-ping Li, Sheng-tao Zhu, Hai-zeng Zhang, Fang Hua

Summary: TRIB3 inhibits CD8(+) T cell infiltration in colorectal cancer by inhibiting STAT1 activation and reducing tumor-infiltrating T cells. Acetyltransferase P300 acetylates TRIB3 and prevents its ubiquitination and degradation. Genetic ablation of TRIB3 or pharmacological acceleration of TRIB3 degradation with a P300 inhibitor increases T cell recruitment and sensitizes colorectal cancers to immune checkpoint blockade therapy.

SCIENCE TRANSLATIONAL MEDICINE (2022)

Article Pharmacology & Pharmacy

TRAF6 Suppresses the Development of Pulmonary Fibrosis by Attenuating the Activation of Fibroblasts

Jiali Min, Qiao Li, Suosi Liu, Qianrong Wang, Min Yin, Yan Zhang, Jun Yan, Bing Cui, Shanshan Liu

Summary: This study explores the role of TNF receptor-associated factor 6 (TRAF6) in the pathogenesis of pulmonary fibrosis (PF). It demonstrates that decreased expression of TRAF6 in lung fibroblasts is essential for the progression of PF. Moreover, overexpression of TRAF6 can reverse the activation of myofibroblasts in PF mice by suppressing Wnt/beta-catenin signaling. The study also reveals a negative correlation between the abundance of TRIB3 and TRAF6 in lung fibroblasts, suggesting that disruption of the TRIB3-TRAF6 interaction could be a potential therapeutic strategy for fibroproliferative lung diseases.

FRONTIERS IN PHARMACOLOGY (2022)

Article Gastroenterology & Hepatology

Hepatocyte leukotriene B4 receptor 1 promotes NAFLD development in obesity

Xingfeng Liu, Kai Wang, Luhai Wang, Lijuan Kong, Shaocong Hou, Yanjun Wan, Chunxiao Ma, Jingwen Chen, Xiaowei Xing, Caiyi Xing, Qian Jiang, Qijin Zhao, Bing Cui, Zhifeng Huang, Pingping Li

Summary: This study found that Ltb4r1 plays a role in promoting hepatic lipogenesis in the development of NAFLD. It activates the PKA-IRE1α-XBP1s pathway to promote the expression of lipogenic genes. Inhibition of Ltb4r1 can improve hepatic steatosis and insulin resistance. The results suggest that Ltb4r1 may be a potential therapeutic target for NAFLD.

HEPATOLOGY (2023)

Article Pharmacology & Pharmacy

TRIB3 promotes pulmonary fibrosis through inhibiting SLUG degradation by physically interacting with MDM2

Xiaoxi Lv, Shanshan Liu, Chang Liu, Yunxuan Li, Tingting Zhang, Jie Qi, Ke Li, Fang Hua, Bing Cui, Xiaowei Zhang, Yuxin Liu, Jiaojiao Yu, Jinmei Yu, Li Li, Xia Li, Zhigang Yao, Bo Huang

Summary: This study reveals that repetitive lung damage leads to the accumulation of the transcriptional repressor SLUG, inhibiting lung alveolar regeneration and causing the failure of pulmonary fibrosis. The elevated SLUG represses the expression of phosphate transporter SLC34A2, reducing intracellular phosphate and inhibiting key kinases JNK and P38 MAPK, resulting in LAR failure. Targeting the TRIB3/MDM2 interaction can restore LAR capacity and provide potential therapeutic efficacy against fibroproliferative lung diseases.

ACTA PHARMACEUTICA SINICA B (2023)

Article Pharmacology & Pharmacy

Mesaconine alleviates doxorubicin-triggered cardiotoxicity and heart failure by activating PINK1-dependent cardiac mitophagy

Ji-Chao Zhou, Cai-Cai Jin, Xiao-Li Wei, Rui-Bing Xu, Ruo-Yu Wang, Zhi-Meng Zhang, Bo Tang, Jin-Mei Yu, Jiao-Jiao Yu, Shuang Shang, Xiao-Xi Lv, Fang Hua, Ping-Ping Li, Zhuo-Wei Hu, Yong-Mei Shen, Feng-Peng Wang, Xiu-Ying Ma, Bing Cui, Fu-Neng Geng, Xiao-Wei Zhang

Summary: Aberrant mitophagy has been identified as a driver for energy metabolism disorder in most cardiac pathological processes. Fuzi, a traditional Chinese medicine, contains a compound called mesaconine, which has been proven effective in various cardiomyopathy models. In this study, it was found that mesaconine could reverse cardiac dysfunction, energy disorder, and impaired mitophagy in mice models of heart failure induced by doxorubicin. This cardioprotective effect of mesaconine was dependent on the activation of PINK1-induced mitophagy.

FRONTIERS IN PHARMACOLOGY (2023)

Article Endocrinology & Metabolism

Insulin induces insulin receptor degradation in the liver through EphB4

Xingfeng Liu, Kai Wang, Shaocong Hou, Qian Jiang, Chunxiao Ma, Qijin Zhao, Lijuan Kong, Jingwen Chen, Zhenhe Wang, Huabing Zhang, Tao Yuan, Yuxiu Li, Yi Huan, Zhufang Shen, Zhuowei Hu, Zhifeng Huang, Bing Cui, Pingping Li

Summary: The tyrosine kinase receptor EphB4 interacts with the insulin receptor to promote its endocytosis and degradation, leading to decreased insulin signaling and insulin resistance. Inhibition of EphB4 can improve insulin resistance and glucose intolerance.

NATURE METABOLISM (2022)

Article Pharmacology & Pharmacy

The cell cycle inhibitor P21 promotes the development of pulmonary fibrosis by suppressing lung alveolar regeneration

Xiaoxi Lv, Chang Liu, Shanshan Liu, Yunxuan Li, Wanyu Wang, Ke Li, Fang Hua, Bing Cui, Xiaowei Zhang, Jiaojiao Yu, Jinmei Yu, ZhuoWei Hu

Summary: The cell cycle inhibitor P21 plays a crucial role in the development of pulmonary fibrosis (PF) by promoting cell senescence and inhibiting lung alveolar epithelial cell differentiation. Elevated P21 expression in lung alveolar epithelial type 2 cells (AEC2s) induces cell cycle arrest and disrupts the P300-beta-catenin interaction, leading to impaired AEC2 differentiation. Additionally, senescent AEC2s activate myofibroblasts by releasing profibrotic cytokines. Knockdown of P21 restores lung alveolar regeneration in a mouse model of chronic PF.

ACTA PHARMACEUTICA SINICA B (2022)

Article Medicine, Research & Experimental

PML-RARα interaction with TRIB3 impedes PPARγ/RXR function and triggers dyslipidemia in acute promyelocytic leukemia

Ke Li, Feng Wang, Zhao-Na Yang, Bing Cui, Ping-Ping Li, Zhen-Yu Li, Zhuo-Wei Hu, Hong-Hu Zhu

THERANOSTICS (2020)

暂无数据