Interleukin-22 protects rat PC12 pheochromocytoma cells from serum deprivation-induced cell death

Pan, Wenyan; Yang, Shengmei; Wu, Xiaoying; Wu, Jianfu; Ma, Jun; Yuan, Zengqiang; Shao, Meng

doi:10.1007/s11010-012-1430-8

Cited by 8 publications

(11 citation statements)

References 54 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This effect was mediated, at least in part, by a decrease of apoptosis. Supporting these findings, previous studies have shown that IL-22-treated rat pheochromocytoma cells exhibit a modest increased survival in serum-deprived conditions [ 59 ]. Some authors have found that IL-22 increased the proliferative function of keratinocytes [ 19 , 60 ] or colonic epithelial cells [ 42 ].…”

Section: Discussionsupporting

confidence: 68%

Interleukin-22 is increased in multiple sclerosis patients and targets astrocytes

Perriard¹,

Mathias²,

Enz

et al. 2015

J Neuroinflammation

View full text Add to dashboard Cite

BackgroundIncreasing evidences link T helper 17 (Th17) cells with multiple sclerosis (MS). In this context, interleukin-22 (IL-22), a Th17-linked cytokine, has been implicated in blood brain barrier breakdown and lymphocyte infiltration. Furthermore, polymorphism between MS patients and controls has been recently described in the gene coding for IL-22 binding protein (IL-22BP). Here, we aimed to better characterize IL-22 in the context of MS.MethodsIL-22 and IL-22BP expressions were assessed by ELISA and qPCR in the following compartments of MS patients and control subjects: (1) the serum, (2) the cerebrospinal fluid, and (3) immune cells of peripheral blood. Identification of the IL-22 receptor subunit, IL-22R1, was performed by immunohistochemistry and immunofluorescence in human brain tissues and human primary astrocytes. The role of IL-22 on human primary astrocytes was evaluated using 7-AAD and annexin V, markers of cell viability and apoptosis, respectively.ResultsIn a cohort of 141 MS patients and healthy control (HC) subjects, we found that serum levels of IL-22 were significantly higher in relapsing MS patients than in HC but also remitting and progressive MS patients. Monocytes and monocyte-derived dendritic cells contained an enhanced expression of mRNA coding for IL-22BP as compared to HC.Using immunohistochemistry and confocal microscopy, we found that IL-22 and its receptor were detected on astrocytes of brain tissues from both control subjects and MS patients, although in the latter, the expression was higher around blood vessels and in MS plaques.Cytometry-based functional assays revealed that addition of IL-22 improved the survival of human primary astrocytes. Furthermore, tumor necrosis factor α-treated astrocytes had a better long-term survival capacity upon IL-22 co-treatment. This protective effect of IL-22 seemed to be conferred, at least partially, by a decreased apoptosis.ConclusionsWe show that (1) there is a dysregulation in the expression of IL-22 and its antagonist, IL-22BP, in MS patients, (2) IL-22 targets specifically astrocytes in the human brain, and (3) this cytokine confers an increased survival of the latter cells.Electronic supplementary materialThe online version of this article (doi:10.1186/s12974-015-0335-3) contains supplementary material, which is available to authorized users.

show abstract

Section: Discussionsupporting

confidence: 68%

Interleukin-22 is increased in multiple sclerosis patients and targets astrocytes

Perriard¹,

Mathias²,

Enz

et al. 2015

J Neuroinflammation

View full text Add to dashboard Cite

show abstract

“…Our results demonstrate that the overexpression of Kv1.5 didn't significant inhibited survival after MPP + treatment in PC12, Kv1.5 gene knockdown was more sensitive for MPP + . Previously, accumulating evidence suggested that activation of the PI3K/Akt pathway inhibited MPP + induced PC12 apoptosis [28,29]. The salient feature of the data presented in this report was the finding that Kv1.5 involved in MPP + induced neurotoxicity.…”

Section: Discussionsupporting

confidence: 49%

Voltage-Gated Potassium Channel KV1.5 Protects against MPP+ Mediated Neurotoxicity in PC12 Cells

Fu²,

Han

et al. 2014

View full text Add to dashboard Cite

Background: Parkinson's disease (PD) is the second most common neurodegenerative disease and afflicts almost 1.8% of over 65-year-old group in the world. Epidemiological projections showed that the incidence of PD was increasing continuously each year, with a wider age range as well. A large number of studies indicated that voltage-gated potassium channel (Kv) played significant roles in cellular signaling in both excitable and non-excitable cells. What's more, Kv was also ubiquitously expressed in neurons and participated in signaling pathway in neurons. Kv1.5 (encoded by KCNA5) is an important voltage-gated K + channel, which is not only necessary for critical processes such as cell proliferation and apoptosis but ubiquitously expressed in neurons. Recent studies reported that PD clinical drugs could inhibit the expression of Kv1.5. To determine the mechanisms by which Kv1.5 protects against MPP + mediated neurotoxicity in PC12 cells. Materials and Methods: Knockdown of Kv1.5 model was established with pSINsi-hU6-Kv1.5 treated by the RNAi method in PC12. MTT, and Western Blot were used to detect the influence of Kv1.5 on PC12 proliferation, and the effect of Kv1.5 on PC12 apoptosis after MPP + treatment in vitro. Results: 1) Knockdown and overexpression of Kv1.5 participated in PC12 proliferation. Transiently over-expressed Kv1.5 could boost the survival rate of PC12, while transiently knockdown of Kv1.5 inhibited PC12 proliferation. 2) The effect of Kv1.5 on PC12 proliferation was through PI3K/Akt signaling pathway. Over-expressed Kv1.5 could induce the activation of Akt, and Bcl-2 expression in PC12; Knockdown of Kv1.5 in PC12 inhibited the activation of Akt, Bcl-2 expression, and promoted MAPK phosphorylation. 3) Over-expressed Kv1.5 could significantly prevent PC12 from apoptosis induced by MPP + via activating Akt pathway and increasing Bcl-2 expression; Knockdown of Kv1.5 was more sensitive than its control counterpart when treated with MPP + for 24 h. Conclusion: Kv1.5 could hinder MPP + neurotoxicity to PC12 by PI3K/Akt signaling pathway.

show abstract

“…In the case of IL22 , its expression was strongly induced by PACAP38 treatment at 24 h in both the ischemic and healthy penumbras but that was especially high in the ischemic penumbra. Although not much is known about the biological role of this cytokine in neuronal cells, a recent study using naïve PC12 cells suggested a role for IL22 in neurological processes, a first such report showing a neuroprotective function for this cytokine [ 31 ]. Another unrelated work on lung infection by the influenza A virus showed that IL22 limits lung inflammation and subsequent bacterial superinfections [ 32 ].…”

Section: Discussionmentioning

confidence: 99%

PACAP38 Differentially Effects Genes and CRMP2 Protein Expression in Ischemic Core and Penumbra Regions of Permanent Middle Cerebral Artery Occlusion Model Mice Brain

Hori

Nakamachi

Shibato

et al. 2014

IJMS

View full text Add to dashboard Cite

Pituitary adenylate-cyclase activating polypeptide (PACAP) has neuroprotective and axonal guidance functions, but the mechanisms behind such actions remain unclear. Previously we examined effects of PACAP (PACAP38, 1 pmol) injection intracerebroventrically in a mouse model of permanent middle cerebral artery occlusion (PMCAO) along with control saline (0.9% NaCl) injection. Transcriptomic and proteomic approaches using ischemic (ipsilateral) brain hemisphere revealed differentially regulated genes and proteins by PACAP38 at 6 and 24 h post-treatment. However, as the ischemic hemisphere consisted of infarct core, penumbra, and non-ischemic regions, specificity of expression and localization of these identified molecular factors remained incomplete. This led us to devise a new experimental strategy wherein, ischemic core and penumbra were carefully sampled and compared to the corresponding contralateral (healthy) core and penumbra regions at 6 and 24 h post PACAP38 or saline injections. Both reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting were used to examine targeted gene expressions and the collapsin response mediator protein 2 (CRMP2) protein profiles, respectively. Clear differences in expression of genes and CRMP2 protein abundance and degradation product/short isoform was observed between ischemic core and penumbra and also compared to the contralateral healthy tissues after PACAP38 or saline treatment. Results indicate the importance of region-specific analyses to further identify, localize and functionally analyse target molecular factors for clarifying the neuroprotective function of PACAP38.

show abstract

Interleukin-22 protects rat PC12 pheochromocytoma cells from serum deprivation-induced cell death

Cited by 8 publications

References 54 publications

Interleukin-22 is increased in multiple sclerosis patients and targets astrocytes

Interleukin-22 is increased in multiple sclerosis patients and targets astrocytes

Voltage-Gated Potassium Channel KV1.5 Protects against MPP+ Mediated Neurotoxicity in PC12 Cells

PACAP38 Differentially Effects Genes and CRMP2 Protein Expression in Ischemic Core and Penumbra Regions of Permanent Middle Cerebral Artery Occlusion Model Mice Brain

Contact Info

Product

Resources

About