Lipopolysaccharide increases resistin gene expression in vivo and in vitro

Lu, Shao‐Chun; Shieh, Wei-Yeong; Chen, Chia-Ying; Hsu, Shu-Shong; Chen, Huiling

doi:10.1016/s0014-5793(02)03450-6

Cited by 142 publications

(132 citation statements)

References 27 publications

(35 reference statements)

Supporting

Mentioning

119

Contrasting

Unclassified

Order By: Relevance

“…Some pro-inflammatory agents, such as tumor necrosis factor-alpha (Fasshauer et al, 2001), interleukin-6 (Kaser et al, 2003) and lipopolysaccharide (Lu et al, 2002), can regulate resistin gene expression. Other studies have also shown the regulation of pro-inflammatory cytokine expression by resistin (Bokarewa et al, 2005;Silswal et al, 2005;Pang and Le, 2006).…”

Section: Discussionmentioning

confidence: 99%

Plasma resistin, associated with single nucleotide polymorphism -420, is correlated with C-reactive protein in Chinese Han patients with spontaneous basal ganglia hemorrhage

Dong¹,

Du²,

Yu³

et al. 2012

Genet. Mol. Res.

View full text Add to dashboard Cite

ABSTRACT.We examined a possible relationship -420C>G SNP of the resistin gene with plasma resistin and C-reactive protein concentrations in intracerebral hemorrhage. Three hundred and fortyfour Chinese Han patients with intracerebral hemorrhage and 344 age-and gender-matched healthy controls were included in our study. Plasma resistin and C-reactive concentrations were measured and SNP -420C>G was genotyped. The genotype frequencies in controls and patients were not significantly different (P = 0.672). Plasma resistin and C-reactive protein levels were significantly different between the SNP -420C>G genotypes, even after adjustment for age, gender and body mass index. The common homozygote (C-C) had the lowest resistin and C-reactive protein plasma concentrations; the plasma resistin and C-reactive protein concentrations in the heterozygote (C-G) and the rare allele homozygote (G-G) did not differ significantly. Plasma resistin levels were significantly associated with plasma C-reactive protein level. We conclude that SNP -420C>G of the resistin gene could be involved in the inflammatory component of intracerebral hemorrhage through enhanced production of resistin.

show abstract

Section: Discussionmentioning

confidence: 99%

Plasma resistin, associated with single nucleotide polymorphism -420, is correlated with C-reactive protein in Chinese Han patients with spontaneous basal ganglia hemorrhage

Dong¹,

Du²,

Yu³

et al. 2012

Genet. Mol. Res.

View full text Add to dashboard Cite

show abstract

“…Placental leptin mRNA production is up-regulated by TNF-and IL-6 (Chardonnens et al 1999, Soh et al 2000, Cameo et al 2003, Nuamah et al 2004, and although there is little information available on the regulation of resistin and adiponectin within intrauterine tissues, resistin expression is up-regulated by LPS and suppressed by TNF- (Lu et al 2002, Shojima et al 2002, Kaser et al 2003, and adiponectin gene expression and secretion is inhibited by TNF- (Kappes & Loffler 2000, Halleux et al 2001) and IL-6 . In this study, there was no effect of LPS or proinflammatory cytokines on the release of leptin, resistin and adiponectin from gestational and maternal tissues.…”

Section: Discussionmentioning

confidence: 99%

Release and regulation of leptin, resistin and adiponectin from human placenta, fetal membranes, and maternal adipose tissue and skeletal muscle from normal and gestational diabetes mellitus-complicated pregnancies

Lappas

Yee²,

Permezel³

et al. 2005

Journal of Endocrinology

230

184

View full text Add to dashboard Cite

The aim of this study was to determine the release and regulation of leptin, resistin and adiponectin from human placenta and fetal membranes, and maternal subcutaneous adipose tissue and skeletal muscle obtained from normal and gestational diabetes mellitus (GDM)-complicated pregnancies at the time of Cesarean section. Tissue explants were incubated in the absence (basal control) or presence of 10 µg/ml lipopolysaccharide (LPS), 10, 20 or 40 ng/ml tumor necrosis factor-(TNF-), interleukin (IL)-6 and IL-8, 1 µM phorbol myristate acetate, 10, 20 and 40 mM glucose, 0·1, 1 and 10 µM insulin and 0·1 1 and 10 µM dexamethasone, progesterone and estrogen. After an 18-h incubation, the medium was collected and the release of leptin, resistin and adiponectin was quantified by ELISA. Human gestational tissues and maternal tissues released immunoreactive leptin, resistin and adiponectin; however, there was no difference in the release of either resistin or adiponectin between normal pregnant women and women with gestational diabetes. The release of leptin was significantly higher in placenta, amnion and choriodecidua obtained from normal pregnant women compared with women with GDM. However, in maternal tissues, the situation was reversed, with adipose tissue and skeletal muscle obtained from women with GDM releasing significantly greater amounts of leptin. In adipose tissue and skeletal muscle the release of leptin was significantly greater in insulin-controlled GDM compared with diet-controlled GDM, and leptin release from adipose tissue was significantly correlated with maternal body mass index. In all tissues tested, there was no effect of incubation with LPS, IL-6, IL-8 or TNF-on leptin, resistin or adiponectin release. PMA significantly increased the release of resistin from placenta and adipose tissue. Insulin increased placental resistin release, whereas the hormones dexamethasone, progesterone and estrogen significantly decreased placental resistin release. The data presented in this study demonstrate that dysregulation of leptin metabolism and/or function in the placenta may be implicated in the pathogenesis of GDM. Furthermore, resistin release is greatly affected by a variety of inflammatory mediators and hormones.

show abstract

“…In contrast to mice, only a low level of expression of resistin has been found in mature adipocytes in humans [24][25][26][27]. In humans, resistin is highly expressed in the bone marrow compared to other tissues [28], but it is also present in trophoblastic cells of placenta, pancreas, primary cell leukemia, synovial fluid, synovial tissue, and circulating blood [22,24,[28][29][30][31][32][33][34]. The particular cells that express resistin in white adipose tissue are monocytes and macrophages [26,28,35].…”

Section: Sites Of Resistin Productionmentioning

confidence: 99%

The role of resistin as a regulator of inflammation: Implications for various human pathologies

Filková

Haluzı́k

Šenolt

2009

Clinical Immunology

375

297

View full text Add to dashboard Cite

Lipopolysaccharide increases resistin gene expression in vivo and in vitro

Cited by 142 publications

References 27 publications

Plasma resistin, associated with single nucleotide polymorphism -420, is correlated with C-reactive protein in Chinese Han patients with spontaneous basal ganglia hemorrhage

Plasma resistin, associated with single nucleotide polymorphism -420, is correlated with C-reactive protein in Chinese Han patients with spontaneous basal ganglia hemorrhage

Release and regulation of leptin, resistin and adiponectin from human placenta, fetal membranes, and maternal adipose tissue and skeletal muscle from normal and gestational diabetes mellitus-complicated pregnancies

The role of resistin as a regulator of inflammation: Implications for various human pathologies

Contact Info

Product

Resources

About