Calcium influx blocked by SK&amp;F 96365 modulates the LPS plus IFN-γ-induced inflammatory response in murine peritoneal macrophages

Ye, Yanxia; Huang, Xiuyan; Zhang, Yaxing; Lai, Xinqiang; Wu, Xiaoping; Zeng, Xiaofeng; Tang, Xiangao; Zeng, Yaoying

doi:10.1016/j.intimp.2011.12.011

Cited by 39 publications

(36 citation statements)

References 52 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…13) Briefly, astrocytes were seeded on a petri dish (MatTek, U.S.A.). The Ca 2+ indicator Fluo4-AM (2.5 µM) was gently mixed with an equal volume of pluronic F-127.…”

Section: )mentioning

confidence: 99%

Protective Effects of Ginsenoside Rg1 on Astrocytes and Cerebral Ischemic-Reperfusion Mice

Sun¹,

Lai²,

Huang³

et al. 2014

Biological & Pharmaceutical Bulletin

Self Cite

View full text Add to dashboard Cite

Ginsenoside Rg1 (Rg1), one of the active ingredients in Panax ginseng, has been known to regulate many cellular processes. The purpose of this study was to investigate the protective effects of Rg1 on apoptosis in mouse cultured astrocytes in vitro and a mouse model of cerebral ischemia and reperfusion in vivo. The cell apoptosis was measured by fluorescence microplate reader and xCELLigence system and the Ca 2 overload was recorded by confocal microscopy. The mitochondrial membrane potential and reactive oxygen species (ROS) were determined by flow cytometry. BALB/c mice were subjected to transient middle cerebral artery occlusion (MCAO) and randomly divided into four groups: Sham (sham-operated 0.9% saline), MCAO (MCAO 0.9% saline), Rg1-L (MCAO Rg1 20 mg/kg) and Rg1-H (MCAO Rg1 40 mg/kg). Neurological deficit scores, brain water content and infarct volume were evaluated at 24 h after reperfusion. The results showed that Rg1 significantly attenuated H 2 O 2 -induced apoptosis in astrocytes. Rg1 efficiently inhibited intracellular Ca 2 overload, loss of mitochondrial membrane potential, and ROS production in astrocytes. In vivo study, it was also observed that Rg1 markedly reduced the neurological deficit scores, brain edema, and infarct volume in the model mice. These results suggest that Rg1 possesses significant neuroprotective effects, which might be related to the prevention of astrocytes from apoptosis.

show abstract

“…13) Briefly, astrocytes were seeded on a petri dish (MatTek, U.S.A.). The Ca 2+ indicator Fluo4-AM (2.5 µM) was gently mixed with an equal volume of pluronic F-127.…”

Section: )mentioning

confidence: 99%

Protective Effects of Ginsenoside Rg1 on Astrocytes and Cerebral Ischemic-Reperfusion Mice

Sun¹,

Lai²,

Huang³

et al. 2014

Biological & Pharmaceutical Bulletin

Self Cite

View full text Add to dashboard Cite

show abstract

“…TAMs are alternatively activated by a variety of cytokines. Interferon‐γ (IFNγ) and IL‐12 have been shown to induce macrophage polarization to the M1‐like phenotype . Cytokines such as IL‐4, IL‐6, IL‐10, IL‐13, and prostaglandin E2 induce macrophage differentiation to the M2‐like phenotype .…”

Section: Introductionmentioning

confidence: 99%

PKCα in colon cancer cells promotes M1 macrophage polarization via MKK3/6‐P38 MAPK pathway

Cheng

Zhu

et al. 2018

Molecular Carcinogenesis

View full text Add to dashboard Cite

Tumor associated macrophages are potential targets of the immune therapy for patients with colon cancer. PKCα acts as a tumor suppressor in the intestine. However, the correlation between PKCα expressed in colon cancer cells and tumor associated macrophages polarization has never been detected. In the present study, the correlation between PKCα expression and level of M1 macrophages was evaluated in human colon cancer tissues. A xenograft mouse model of colon cancer cells with different PKCα expression level was constructed to evaluate the effect of PKCα on M1 macrophages polarization in vivo. Co-culture of colon cancer cells and differentiated macrophages was used to detect the potential interplay in vitro. PKCα regulated production of cytokines which correlated with macrophage polarization and the underlying mechanism was further explored. Our study showed that high PKCα expression in human colon cancer tissues correlated with better prognosis and high M1 macrophage content. PKCα expressed in colon cancer cells inhibited the growth of colon cancer in mice model. PKCα induced macrophages polarized to the M1-like phenotype both in vitro and in vivo. Mechanistically, PKCα targeted P38 via MKK3/6 to promote IL12 and GM-CSF expression which further enhanced M1-like macrophages polarization. In conclusion, this study provided evidence for the first time that PKCα in colon cancer cells play an anticancer action by inducing the polarization of tumor associated macrophages to M1-like phenotype in the tumor microenvironment. PKCα promoted IL12/GM-CSF-mediated M1 polarization through MKK3/6-P38 signaling pathway. Our investigation suggested that modulation of the PKCα signaling pathway might serve as a novel strategy for colon cancer therapy.

show abstract

“…IFN‐γ exposure has been reported to cause the elevation of intracellular Ca 2+ levels (Ye et al . ), and Ca 2+ ‐dependent cell death has been previously described in VC4.1 motoneuron cells (Smith et al . ).…”

Section: Discussionmentioning

confidence: 95%

Cross‐talk between IGF‐1 and estrogen receptors attenuates intracellular changes in ventral spinal cord 4.1 motoneuron cells because of interferon‐gamma exposure

Park

Nozaki

Smith

et al. 2013

Journal of Neurochemistry

View full text Add to dashboard Cite

Insulin-like growth factor-1 (IGF-1) is a neuroprotective growth factor that promotes neuronal survival by inhibition of apoptosis. In order to examine whether IGF-1 exerts cytoprotective effects against extracellular inflammatory stimulation, ventral spinal cord 4.1 (VSC4.1) motoneuron cells were treated with interferon-gamma (IFN-γ). Our data demonstrated apoptotic changes, increased calpain:calpastatin and Bax:Bcl-2 ratios, and expression of apoptosis related proteases (caspase-3 and −12) in motoneurons rendered by IFN-γ in a dose-dependent manner. Post-treatment with IGF-1 attenuated these changes. In addition, IGF-1 treatment of motoneurons exposed to IFN-γ decreased expression of inflammatory markers (cyclooxygenase-2 and nuclear factor-kappa B:inhibitor of kappa B ratio). Furthermore, IGF-1 attenuated the loss of expression of IGF-1 receptors (IGF-1Rα and IGF-1Rβ) and estrogen receptors (ERα and ERβ) induced by IFN-γ. To determine whether the protective effects of IGF-1 are associated with ERs, ERs antagonist ICI and selective siRNA targeted against ERα and ERβ were used in VSC4.1 motoneurons. Distinctive morphological changes were observed following siRNA knockdown of ERα and ERβ. In particular, apoptotic cell death assessed by TUNEL assay was enhanced in both ERα and ERβ-silenced VSC4.1 motoneurons following IFN-γ and IGF-1 exposure. These results suggest that IGF-1 protects motoneurons from inflammatory insult by a mechanism involving pivotal interactions with ERα and ERβ.

show abstract

Calcium influx blocked by SK&F 96365 modulates the LPS plus IFN-γ-induced inflammatory response in murine peritoneal macrophages

Cited by 39 publications

References 52 publications

Protective Effects of Ginsenoside Rg1 on Astrocytes and Cerebral Ischemic-Reperfusion Mice

Protective Effects of Ginsenoside Rg1 on Astrocytes and Cerebral Ischemic-Reperfusion Mice

PKCα in colon cancer cells promotes M1 macrophage polarization via MKK3/6‐P38 MAPK pathway

Cross‐talk between IGF‐1 and estrogen receptors attenuates intracellular changes in ventral spinal cord 4.1 motoneuron cells because of interferon‐gamma exposure

Contact Info

Product

Resources

About