Previous Page  7 / 20 Next Page
Information
Show Menu
Previous Page 7 / 20 Next Page
Page Background

Notes:

Page 57

Parkinsons 2016

December 05-07, 2016

Volume 6 Issue 6(Suppl)

J Alzheimers Dis Parkinsonism

ISSN: 2161-0460 JADP, an open access journal

conferenceseries

.com

December 05-07, 2016 Phoenix, USA

2

nd

International Conference on

Parkinson’s Disease & Movement Disorders

Junxia Xie et al., J Alzheimers Dis Parkinsonism 2016, 6:6(Suppl)

http://dx.doi.org/10.4172/2161-0460.C1.025

Differences in vulnerability of neurons and astrocytes to hemeoxygenase-1 modulation: Implications for

mitochondrial ferritin

Junxia Xie, Xiaojun Yu, Ning Song and Jun Wang

Qingdao University, China

I

nduction of the antioxidant enzyme hemeoxygenase-1 (HO-1) was observed in both astrocytes and neurons in the

substantianigra of patients with Parkinson’s disease (PD). In the current study, we investigated whether HO-1 behaves

differently between neurons and astrocytes under the condition of neurotoxicity related to PD. The results showed a time-

dependent HO-1 upregulation in primary cultured ventral mesencephalon (VM) neurons and astrocytes treated with the

mitochondria complex I inhibitor 1-methyl-4-phenylpyridinium (MPP+) or recombinant α-synuclein. However, HO-1

upregulation appeared much later in neurons than in astrocytes. The HO-1 inhibitor zinc protoporphyrin (ZnPP) aggravated

MPP+- or α-synuclein-induced oxidative damage in both astrocytes and neurons, indicating that this HO-1 response was

cytoprotective. For neurons, the HO-1 activator cobalt protoporphyrin IX (CoPPIX) exerted protective effects against MPP+

or α-synuclein during moderate HO-1 upregulation, but it aggravated damage at the peak of the HO-1 response. For astrocytes,

CoPPIX always showed protective effects. Higher basal and CoPPIX-inducedmitochondrial ferritin (MtFt) levels were detected

in astrocytes. Lentivirus-mediated MtFt overexpression rescued the neuronal damage induced by CoPPIX, indicating that a

large MtFt buffering capacity contributes to pronounced HO-1 tolerance in astrocytes. Such findings suggest that astrocyte-

targeted HO-1 interventions have potential as a novel pharmacological treatment strategy in PD.

Biography

Junxia Xie is Taishan scholar Distinguished Professor. She is currently the Director of Shandong Provincial Collaborative Innovation Center for Neurodegenerative

Disorders and Excellent Innovative Team of Shandong Province. She is the Vice-President of Qingdao University, Chinese Association of Physiological Sciences

as well as Chinese Neuroscience Society. She has 7 projects from the NSFC, including 2 key projects and participates in National 973 Project. She has published

150 articles up to now.

jxiaxie@public.qd.sd.cn