ISSN: 2161-0460

Journal of Alzheimers Disease & Parkinsonism
Open Access

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Research Article

Vascular Remodelling is Impaired in Parkinson Disease

Panzao Yang1,2,3, Henry Waldvogel2,4, Clinton Turner2,5, Richard Faull2,4, Mike Dragunow1,2 and Jian Guan1,2*

1Department of Pharmacology and Clinical Pharmacology, Faculty of Medical and Health Sciences, University of Auckland, New Zealand

2Centre for Brain Research, Faculty of Medical and Health Sciences, University of Auckland, New Zealand

3Liggins Institute, University of Auckland, New Zealand

4Department of Anatomy and Medical Imaging, Faculty of Medical and Health Sciences, University of Auckland, New Zealand

5Department of Anatomical Pathology, LabPlus, Auckland City Hospital Auckland, New Zealand

*Corresponding Author:
Jian Guan
Department of Pharmacology and Clinical Pharmacology
Faculty of Medical and Health Sciences, University of Auckland
Private Bag 92019, Auckland 1023, New Zealand
Tel: 006499236134
E-mail: j.guan@auckland.ac.nz

Received date: March 09, 2017; Accepted date: March 16, 2017; Published date: March 23, 2017

Citation: Yang P, Waldvogel H, Turner C, Faull R, Dragunow M, et al. (2017) Vascular Remodelling is Impaired in Parkinson Disease. J Alzheimers Dis Parkinsonism 7:313. doi:10.4172/2161-0460.1000313

Copyright: © 2017 Yang P, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Objective: We have previously reported vascular degeneration of human Parkinson disease (PD). In which we described degenerative pathology of endothelial cells and its association with increased string vessels in the grey matter of middle frontal gyrus (MFG). Growth factors, for example platelet-derived growth factor (PDGF), insulin-like growth factor-1 (IGF-1) and vascular endothelial growth factor (VEGF), involve in vascular remodelling by promoting cell proliferations and angiogenesis through capillary pericytes. Thus current study examined the hypothesis whether vascular degeneration in human PD is associated with impairment of vascular remodelling. Methods: Using tissue microarray method we conducted immuno histochemical staining in the grey matter of MFG of human PD (n=17) and age-matched control cases (n=17). The expression of PDGF receptor-beta, proliferating cell nuclear antigen and phosphorylation of IGF-1 receptor in capillaries, IGF binding protein-2 and VEGF were evaluated using automated image analysis software. Results: PDGF receptor-beta was specifically expressed in the pericytes which formed capillary morphology. Compared to the age-matched control cases, there were significant decrease in PDGF receptor-beta positive capillaries (p<0.05; p<0.01), proliferating vascular cells (p<0.05) and VEGF (p<0.05) in the PD cases. There no difference in phosphorylation of IGF-1 receptors, expressed in the capillaries between the groups. We found a significant increase in IGF binding protein-2, expressed in the astrocytes of PD when compared to the control cases (p<0.05). Interestingly the levels of phosphorylated IGF receptors in the capillaries were significantly correlated with the numbers of pericytes and proliferating cells in capillaries (p=0.001). Conclusion: Impaired PDGF function in the pericytes, reduced cell proliferation and VEGF suggested that the ability of vascular remodelling is impaired in PD. The maintained IGF-1 function appeared to be ineffective to retain vascular remodelling process in PD. The up-regulation of IGF binding protein-2 may suggest a role for autocrine/ paracrine of IGF-1 in PD.

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