Induction of Serum Amyloid A Genes Is Associated with Growth and Apoptosis of HC11 Mammary Epithelial Cells

Kho, Yoonjung; Kim, Sung‐Chan; Yoon, Byung Sun; Moon, Jung Hwan; Kim, Bona; Kwak, Sungwook; Woo, Jung-Hee; Oh, Sejong; Hong, Ki-Chang; Kim, Saehun; Kim, Hyunggee; You, Seungkwon; Choi, Youn Soo

doi:10.1271/bbb.70374

Cited by 19 publications

(15 citation statements)

References 47 publications

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“…Published data showed that SAA inhibits the proliferation of different types of cells, including lymphocytes, the mammary epithelial cell line HC11, bovine aortic endothelial cells, the human cervical adenocarcinoma HeLa cells, the human fetal lung fibroblast-like cell line MRC5, and the human amniotic epithelial cell line WISH [29][30][31][32]. In agreement with these findings, our results indicate that SAA also suppresses the growth of astrocytes.…”

Section: Discussionsupporting

confidence: 91%

“…The difference may be attributed to the utilization of signaling pathways. On one hand, SAA suppresses the growth of HC11 cells by increasing the activity of caspases [29] and inhibits the proliferation of amniotic cells through FPR2-dependent activation of ERK and p38 MAPK [32]. On the other hand, SAA can also reduce apoptosis of human neutrophils via a P2X7-sensitive pathway independent of FPR2 [33].…”

Section: Discussionmentioning

confidence: 99%

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Serum Amyloid A Differentially Activates Microglia and Astrocytes via the PI3K Pathway

Liu

et al. 2013

JAD

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Microglia and astrocytes in the brain play an important role in the development and progression of Alzheimer's disease (AD). Serum amyloid A (SAA) is a major acute-phase protein produced locally in the brain and colocalizes with senile plaques in AD patients. We investigated whether SAA plays a role in the development of AD. The viability of cultured primary microglia and astrocytes was measured by MTT; cell cycle and apoptosis analysis was also conducted. Cultured microglia and astrocytes were stimulated with 1 μM SAA for different periods of time (2, 4, 6, 12 h) or treated with 1 μM SAA with or without 15 min pretreatment of MAPK or PI3K inhibitors. Total RNA was extracted for qPCR analysis. SAA induced morphological changes of primary microglia but not astrocytes. Interestingly, SAA increased the viability of microglia by inhibiting their apoptosis and reduced the viability of astrocytes by inducing G1 cell cycle arresting. SAA treatment increased the mRNA levels of IL-6, TNF-α, IL12p40, IL23p19, and IL-10, with higher potency in microglia than in astrocytes. However, SAA induced more iNOS mRNA in astrocytes than in microglia. SAA induced these cytokines and iNOS expression by activating the PI3K pathway in both glial cells, but selectively activated the JNK pathway in microglia and the NF-κB pathway in astrocytes. These results suggest that SAA can stimulate a different reactive phenotype in microglia and astrocytes, and SAA regulates cell viability differently in these two glial cells in part through the PI3K pathway.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 99%

Serum Amyloid A Differentially Activates Microglia and Astrocytes via the PI3K Pathway

Liu

et al. 2013

JAD

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“…the caspase 3 activity in HC11 mammary gland epithelial cells 27) . Despite activation of the downstream executioner caspase 3, no activation was detected for the upstream initiator caspases 8 and 9.…”

Section: ----------------Bay11-7082---------------mentioning

confidence: 98%

“…The effects of apoptosis on plaque stability can eventually lead to plaque rupture and thrombosis 1) . Moreover, SAA has been reported to cause apoptosis via caspase 3 activation in mammalian cell lines 27,28) . Taking together the association between SAA and atherosclerosis as well as the contribution of NF-κB and apoptosis to the pathogenesis of atherosclerosis, we aimed to determine whether SAA contributes to the onset of atherosclerosis via inflammatory and apoptotic pathways.…”

Section: Quantitative Real-time Pcrmentioning

confidence: 99%

The Atherogenic Effects of Serum Amyloid A are Potentially Mediated via Inflammation and Apoptosis

Tan

Ooi

Shen

et al. 2014

JAT

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“…All PCR products in this study were tested to ensure that the number of PCR cycles was in the linear range. These values were analyzed and normalized as previously described (Kho et al, 2008).…”

Section: Rt-pcrmentioning

confidence: 99%

Differentiation of human labia minora dermis-derived fibroblasts into insulin-producing cells

et al. 2012

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Recent evidence has suggested that human skin fibroblasts may represent a novel source of therapeutic stem cells. In this study, we report a 3-stage method to induce the differentiation of skin fibroblasts into insulin-producing cells (IPCs). In stage 1, we establish the isolation, expansion and characterization of mesenchymal stem cells from human labia minora dermis-derived fibroblasts (hLMDFs) (stage 1: MSC expansion). hLMDFs express the typical mesenchymal stem cell marker proteins and can differentiate into adipocytes, osteoblasts, chondrocytes or muscle cells. In stage 2, DMEM/F12 serum-free medium with ITS mix (insulin, transferrin, and selenite) is used to induce differentiation of hLMDFs into endoderm-like cells, as determined by the expression of the endoderm markers Sox17, Foxa2, and PDX1 (stage 2: mesenchymal-endoderm transition). In stage 3, cells in the mesenchymal-endoderm transition stage are treated with nicotinamide in order to further differentiate into self-assembled, 3-dimensional islet cell-like clusters that express multiple genes related to pancreatic β-cell development and function (stage 3: IPC). We also found that the transplantation of IPCs can normalize blood glucose levels and rescue glucose homeostasis in streptozotocin-induced diabetic mice. These results indicate that hLMDFs have the capacity to differentiate into functionally competent IPCs and represent a potential cell-based treatment for diabetes mellitus.

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Induction of Serum Amyloid A Genes Is Associated with Growth and Apoptosis of HC11 Mammary Epithelial Cells

Cited by 19 publications

References 47 publications

Serum Amyloid A Differentially Activates Microglia and Astrocytes via the PI3K Pathway

Serum Amyloid A Differentially Activates Microglia and Astrocytes via the PI3K Pathway

The Atherogenic Effects of Serum Amyloid A are Potentially Mediated via Inflammation and Apoptosis

Differentiation of human labia minora dermis-derived fibroblasts into insulin-producing cells

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