Serum amyloid A (SAA)-induced remodeling of CSF-HDL

Miida, Takashi; Yamada, Toshiyuki; Seino, Utako; Itô, Masayuki; Fueki, Yuriko; Takahashi, Akihiro; Kosuge, Keiichiro; Soda, Satoshi; Hanyu, Osamu; Obayashi, Konen; Miyazaki, Osamu; Okada, Masahiko

doi:10.1016/j.bbalip.2006.03.013

Cited by 43 publications

(35 citation statements)

References 52 publications

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“…In a broad sense, the return to homeostasis is essential to prevent uncontrolled tissue damage. So, it is difficult to interpret the biological significance and impact on disease progression of persistently elevated levels of SAA in some chronic diseases [28][29][30]. The intriguing positive correlation that exists between elevated serum levels of SAA and coronary artery disease [31], and the presence of SAA in human atherosclerotic lesions [32], suggest a role of SAA in the genesis and progression of chronic diseases.…”

Section: Discussionmentioning

confidence: 98%

Serum amyloid A induces CCL20 secretion in mononuclear cells through MAPK (p38 and ERK1/2) signaling pathways

Sandri¹,

Hatanaka²,

Franco³

et al. 2008

Immunology Letters

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Section: Discussionmentioning

confidence: 98%

Serum amyloid A induces CCL20 secretion in mononuclear cells through MAPK (p38 and ERK1/2) signaling pathways

Sandri¹,

Hatanaka²,

Franco³

et al. 2008

Immunology Letters

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“…To examine the effects of LCAT inhibition on SI-HDL production, HDL in SI lymph perfusates collected using the in situ perfusion technique from WT mice with and without the presence of DTNB in the perfusion buffer was separated by native twodimensional gel electrophoresis as described previously ( 41,42 ). Fresh SI lymph perfusates were run on an agarose gel (0.75%) and then on a 2% to 25% polyacrylamide gel at 0°C at 100 V for 20 h. Fractionated HDL was electroblotted to a nitrocellulose sheet at 0°C and detected with the following antibodies.…”

Section: Two-dimensional Gel Electrophoresismentioning

confidence: 99%

Selective evaluation of high density lipoprotein from mouse small intestine by an in situ perfusion technique

Yamaguchi

Zhang

Tomonaga

et al. 2014

Journal of Lipid Research

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HDL is unquestionably a major antiatherogenic factor worldwide, regardless of sex, race, and age ( 1, 2 ). Therefore, an increase in HDL levels has been an important goal that guides the development of novel therapies for atherosclerotic cardiovascular diseases ( 3 ) because it was reported that plasma HDL cholesterol (HDL-C) levels were reduced in patients with ischemic heart disease and stroke ( 4, 5 ). Strategies for raising HDL are now available. Because remarkable progress has been made in our understanding of the molecular mechanism of HDL production, enhanced production is one of the major strategies for raising HDL.ABCA1, mutations of which are the genetic cause of Tangier disease and genetic HDL defi ciency, is one of the Abstract The small intestine (SI) is the second-greatest source of HDL in mice. However, the selective evaluation of SI-derived HDL (SI-HDL) has been diffi cult because even the origin of HDL obtained in vivo from the intestinal lymph duct of anesthetized rodents is doubtful. To shed light on this question, we have developed a novel in situ perfusion technique using surgically isolated mouse SI, with which the possible fi ltration of plasma HDL into the SI lymph duct can be prevented. With the developed method, we studied the characteristics of and mechanism for the production and regulation of SI-HDL. Nascent HDL particles were detected in SI lymph perfusates in WT mice, but not in ABCA1 KO mice. SI-HDL had a high protein content and was smaller than plasma HDL. SI-HDL was rich in TG and apo AIV compared with HDL in liver perfusates. SI-HDL was increased by high-fat diets and reduced in apo E KO mice. In conclusion, with our in situ perfusion model that enables the selective evaluation of SI-HDL, we demonstrated that ABCA1 plays an important role in intestinal HDL production, and SI-HDL is small, dense, rich in apo AIV, and regulated by nutritional and genetic factors.

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“…No SAA expression was detected in normal brain: however, SAA was found in the brains of patients with AD [18]. In cerebrospinal fluid (CSF), SAA concentration is much higher in AD subjects than in normal controls [19]. SAA has also been found to colocalize with A␤ deposits based on immunocytochemical analysis in AD brain [20].…”

Section: Introductionmentioning

confidence: 96%

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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Serum amyloid A (SAA)-induced remodeling of CSF-HDL

Cited by 43 publications

References 52 publications

Serum amyloid A induces CCL20 secretion in mononuclear cells through MAPK (p38 and ERK1/2) signaling pathways

Serum amyloid A induces CCL20 secretion in mononuclear cells through MAPK (p38 and ERK1/2) signaling pathways

Selective evaluation of high density lipoprotein from mouse small intestine by an in situ perfusion technique

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

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