Calbindin-D28K inhibits apoptosis in dopaminergic neurons by activation of the PI3-kinase-Akt signaling pathway

Sun, Shuang; Li, F.; Gao, Xiangyu; Zhu, Y.; Chen, J.; Zhu, Xia; Hu, Yuan; Gao, Dayong

doi:10.1016/j.neuroscience.2011.09.054

Cited by 33 publications

(31 citation statements)

References 33 publications

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“…CALB1 may also protect against apoptosis in dopaminergic neurons through activation of the phosphoinositide 3 (PI3) kinase-Akt signaling pathway (38). In the present study, the knockdown of CALB1 may have accelerated U2OS apoptosis via the activation of caspase-3 and/or by the inactivation of the PI3-kinase-Akt signaling pathway, which is dependent on the calcium binding activity of CALB1.…”

Section: Discussionmentioning

confidence: 56%

Downregulation of calbindin 1, a calcium-binding protein, reduces the proliferation of osteosarcoma cells

2017

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Abstract. Osteosarcoma is the most common type of primary malignant bone tumor and has a high propensity to metastasize to the lungs and bones. Calbindin 1 (CALB1) is a constituent Ca 2+ binding protein, which can prevent apoptotic death in several cell types induced through various pro-apoptotic signaling pathways. To investigate whether CALB1 is implicated in the tumor growth of human osteosarcoma, two different short hairpin RNAs (shRNAs) against CALB1 were used for CALB1-knockdown in osteosarcoma U2OS cells. The U2OS cells were divided into three groups: Two groups with CALB1 knockdown (CALB1-shRNA 1 and CALB1-shRNA 2) and one control group (Con-shRNA). Reverse transcription-quantitative polymerase chain reaction and western blot analysis confirmed that the CALB1-shRNA 1-and 2-infected cells exhibited significantly lower levels of CALB1 gene and protein expression compared with the Con-shRNA group. The proliferation and colony formation abilities were significantly inhibited in CALB1-deficient U2OS cells compared with the control, as measured using an MTT assay and crystal violet staining. Flow cytometry revealed that the number of CALB1-shRNA 2-injected cells was increased in the G 0 /G 1 and G 2 /M phases, but decreased in the S phase, compared with the control group. The assessment of apoptosis and necrosis using Annexin V/7-aminoactinomycin D demonstrated that there was a significantly higher percentage of necrotic, early apoptotic, and late apoptotic cells, but a significantly lower percentage of viable cells in U2OS cells with CALB1-knockdown compared with the control group. In conclusion, CALB1 contributes to protecting osteosarcoma cells from apoptosis and provides a potential novel target for gene therapy to treat patients with osteosarcoma.

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Section: Discussionmentioning

confidence: 56%

Downregulation of calbindin 1, a calcium-binding protein, reduces the proliferation of osteosarcoma cells

2017

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“…In this light, one of the key problem during weaning is to reduce apoptosis ratio. Apoptotic cell death-preventing properties of CB have been reported in relation to several cell types including PC12 cells (McMahon et al 1998), osteocytes and osteoblasts (Liu et al 2004), pancreatic β-cells (Rabinovitch et al 2001) and neurons as well (Sun et al 2011). Whether CB has a role in protecting epithelial cells from apoptotic cell death has not been reported yet, but higher expression of CB in NE cells after the lectin treatment may support this hypothesis.…”

Section: Discussionmentioning

confidence: 99%

Changes in expression of calbindin 28 kDa in the small intestine of red kidney bean (Phaseolus vulgaris) lectin-treated suckling piglets

Zacharko-Siembida¹,

Piedra²,

Arciszewski³

2013

Polish Journal of Veterinary Sciences

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Calbindin (CB) is a calcium binding protein playing a role in calcium uptake and anti-apoptotic cellular protection. The expression of CB was immunohistochemically studied in the small intestine of normal and red bean kidney lectin-treated suckling piglets. In the duodenum and jejunum (but not ileum) of lectin-treated animals overexpression of CB was noted in chromogranin A-immunoreactive (CgA-IR) neuroendocrine (NE) cells. In both control and experimental group a small population of CB-IR NE cells exhibited the presence of somatostatin (but not serotonin, histamine or CRF). After the lectin treatment, an increased (however not statistically significant) immunoreactivity to CB was found in a small subpopulation of neurons of outer submucous (but not inner submucous and myenteric) plexus. It is suggested that there is a functional interaction between lectin administration and CB-expression in the porcine small intestine. Future studies will be needed to clarify this processes.

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“…Interneurons comprise the majority of dorsal horn neurons, and certain subsets express calbindin [32,33], a protein that regulates the concentration of intracellular Ca 2+ . Therefore, calbindin is considered to be an intrinsic anti-excitotoxic agent [34,35,36]. In a previous in vitro study, calbindin-positive interneurons were preserved in the dorsal horn for up to 12 days, which was in strong contrast to motor neurons that were lost after a 3-day culture period [25].…”

Section: Discussionmentioning

confidence: 99%

“…We therefore considered the assessment of presumable Renshaw cells important. Unexpectedly, NMDA treatment vastly reduced the number of Chrna2 -expressing presumable Renshaw cells, although calbindin-positive interneurons should be more resistant to excitotoxic mechanisms [34,35,36,40,41]. The Chrna2 -expressing cells were no longer detectable, even under standard culture conditions (i.e., even in cultures not subjected to excitotoxic injury) after a 3-day in vitro incubation, while NeuN-positive cells in the ventral horn were rather well preserved.…”

Section: Discussionmentioning

confidence: 99%

Differential Neuroprotective Effects of Interleukin-1 Receptor Antagonist on Spinal Cord Neurons after Excitotoxic Injury

Schizas

Perry²,

Andersson

et al. 2017

Neuroimmunomodulation

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Secondary damage following spinal cord injury (SCI) induces neuronal damage through inflammatory and excitotoxic pathways. We hypothesized that the interleukin-1 receptor antagonist (IL1RA) protects neuronal populations and suppresses apoptosis and gliosis after injury. Spinal cord slice cultures (SCSCs) were subjected to excitotoxic injury with N-methyl-D-aspartate (NMDA) and treated with IL1RA. Immunohistochemistry for neuronal nuclei (NeuN), MacII, glial fibrillary acidic protein, and TdT-mediated dUTP nick end labelling stains were used to evaluate neuronal survival, glial activation, and apoptosis. Treatment with IL1RA significantly reduced the number of apoptotic cells in both NMDA-lesioned and unlesioned cultures. Experimental injury with NMDA reduced the number of NeuN-positive ventral horn neurons, and IL1RA treatment counteracted this loss 1 day after injury. However, IL1RA had no effect on the number of presumable Renshaw cells, identified by their selective expression of the cholinergic nicotinic α₂-receptor subunit (Chrna2). Activated microglial cells were more numerous in NMDA-lesioned cultures 1 day after injury, and IL1RA significantly reduced their numbers. We conclude that IL1RA modulates neuronal apoptosis and microglial activation in excitotoxically injured SCSCs. Renshaw cells were more susceptible to excitotoxic injury than other neurons and were not rescued by IL1RA treatment. Modulation of IL-1-mediated pathways may thus be effective in reducing excitotoxically induced neuronal damage after SCI, however only in specific neuronal populations, such as ventral horn neurons. These findings motivate further investigations of the possibility to antagonize inflammatory pathways after SCI.

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Calbindin-D28K inhibits apoptosis in dopaminergic neurons by activation of the PI3-kinase-Akt signaling pathway

Cited by 33 publications

References 33 publications

Downregulation of calbindin 1, a calcium-binding protein, reduces the proliferation of osteosarcoma cells

Downregulation of calbindin 1, a calcium-binding protein, reduces the proliferation of osteosarcoma cells

Changes in expression of calbindin 28 kDa in the small intestine of red kidney bean (Phaseolus vulgaris) lectin-treated suckling piglets

Differential Neuroprotective Effects of Interleukin-1 Receptor Antagonist on Spinal Cord Neurons after Excitotoxic Injury

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