Store lyophilized Acrp30 Mouse at -20°C. Aliquot the product after reconstitution to avoid repeated freezing/thawing cycles. Reconstituted Acrp30 Mouse can be stored at 4°C for a limited period of time; it does not show any change after two weeks at 4°C.

Synonyme

30 kDa adipocyte complement related protein, 30 kDa adipocyte complement-related protein, ACDC, Adipocyte, Adipocyte C1q and collagen domain containing protein, Adipocyte complement related 30 kDa protein, Adipocyte complement related protein of 30 kDa, Adipocyte complement-related 30 kDa protein, adipocyte-specific secretory protein, Adiponectin, Adiponectin precursor, adiponectin, C1Q and collagen domain containing, Adipoq, Adipose most abundant gene transcript 1, Adipose most abundant gene transcript 1 protein, Adipose specific collagen like factor, ADIPO_HUMAN, ADIPQTL1, ADPN, APM 1, apM-1, APM1, C1q and collagen domain-containing protein, GBP28, Gelatin binding protein , Gelatin binding protein 28, Gelatin-binding protein

Haftungsausschluss

Dieses Produkt ist nur für Forschungszwecke bestimmt. Es ist nicht für diagnostische oder therapeutische Zwecke bestimmt.

Produktreferenzen (1)

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(3)

Evidence that adiponectin receptor 1 activation exacerbates ischemic neuronal death.

Verweise: Acrp30 Mouse, Trimeric (A61371)

Abstrakt:

BACKGROUND:

Adiponectin is a hormone produced in and released from adipose cells, which has been shown to have anti-diabetic and anti-inflammatory actions in peripheral cells. Two cell surface adiponectin receptors (ADRs) mediate the majority of the known biological actions of adiponectin. Thus far, ADR expression in the brain has been demonstrated in the arcuate and the paraventricular nucleus of hypothalamus, where its activation affects food intake. Recent findings suggest that levels of circulating adiponectin increase after an ischemic stroke, but the role of adiponectin receptor activation in stroke pathogenesis and its functional outcome is unclear.

METHODS:

Ischemic stroke was induced in C57BL/6 mice by middle cerebral artery occlusion (MCAO) for 1 h, followed by reperfusion. Primary cortical neuronal cultures were established from individual embryonic neocortex. For glucose deprivation (GD), cultured neurons were incubated in glucose-free Locke's medium for 6, 12 or 24 h. For combined oxygen and glucose deprivation (OGD), neurons were incubated in glucose-free Locke's medium in an oxygen-free chamber with 95% N2/5% CO2 atmosphere for either 3, 6, 9, 12 or 24 h. Primary neurons and brain tissues were analysed for Adiponectin and ADRs using reverse transcriptase polymerase chain reaction (RT-PCR), immunoblot and immunochemistry methods.

RESULTS:

Cortical neurons express ADR1 and ADR2, and that the levels of ADR1 are increased in neurons in response to in vitro or in vivo ischemic conditions. Neurons treated with either globular or trimeric adiponectin exhibited increased vulnerability to oxygen and glucose deprivation which was associated with increased activation of a pro-apoptotic signaling cascade involving p38 mitogen-activated protein kinase (p38MAPK) and AMP-activated protein kinase (AMPK).

CONCLUSIONS:

This study reveals a novel pathogenic role for adiponectin and adiponectin receptor activation in ischemic stroke. We show that cortical neurons express ADRs and reveal a pro-apoptotic role for ADR1 activation in neurons, which may render them vulnerable to ischemic death.

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