Contribution of Vascular Cells to Neointimal Formation

There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

Abstract

The de-differentiation and proliferation of smooth muscle cells (SMCs) are widely accepted as the major contributor to vascular remodeling. However, recent studies indicate that vascular stem cells (VSCs) also play an important role, but their relative contribution remains to be elucidated. In this study, we used genetic lineage tracing approach to further investigate the contribution of SMCs and VSCs to neointimal thickening in response to endothelium denudation injury or artery ligation. In vitro and in vivo analysis of MYH11-cre/Rosa-loxP-RFP mouse artery showed that SMCs proliferated at a much slower rate than non-SMCs. Upon denudation or ligation injury, two distinct types of neointima were identified: Type-I neointimal cells mainly involved SMCs, while Type II mainly involved non-SMCs. Using Sox10-cre/Rosa-loxP-LacZ mice, we found that Sox10 ⁺ cells were one of the cell sources in neointima. In addition, lineage tracing using Tie2-cre/Rosa-LoxP-RFP showed that endothelial cells also contributed to the neointimal formation, but rarely transdifferentiated into mesenchymal lineages. These results provide a novel insight into the contribution of vascular cells to neointima formation, and have significant impact on the development of more effective therapies that target specific vascular cell types.

Related collections

Most cited references 17

Record: found
Abstract: found
Article: not found

SOX10 maintains multipotency and inhibits neuronal differentiation of neural crest stem cells.

W L Lo, Jaesang Kim, Emma-Louise Dormand … (2003)

The mechanisms that establish and maintain the multipotency of stem cells are poorly understood. In neural crest stem cells (NCSCs), the HMG-box factor SOX10 preserves not only glial, but surprisingly, also neuronal potential from extinction by lineage commitment signals. The latter function is reflected in the requirement of SOX10 in vivo for induction of MASH1 and PHOX2B, two neurogenic transcription factors. Simultaneously, SOX10 inhibits or delays overt neuronal differentiation, both in vitro and in vivo. However, this activity requires a higher Sox10 gene dosage than does the maintenance of neurogenic potential. The opponent functions of SOX10 to maintain neural lineage potentials, while simultaneously serving to inhibit or delay neuronal differentiation, suggest that it functions in stem or progenitor cell maintenance, in addition to its established role in peripheral gliogenesis.

0 comments Cited 133 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

The cephalic neural crest provides pericytes and smooth muscle cells to all blood vessels of the face and forebrain.

G Couly, Heather Etchevers, C Vincent-Delorme … (2001)

Most connective tissues in the head develop from neural crest cells (NCCs), an embryonic cell population present only in vertebrates. We show that NCC-derived pericytes and smooth muscle cells are distributed in a sharply circumscribed sector of the vasculature of the avian embryo. As NCCs detach from the neural folds that correspond to the future posterior diencephalon, mesencephalon and rhombencephalon, they migrate between the ectoderm and the neuroepithelium into the anterior/ventral head, encountering mesoderm-derived endothelial precursors. Together, these two cell populations build a vascular tree rooted at the departure of the aorta from the heart and ramified into the capillary plexi that irrigate the forebrain meninges, retinal choroids and all facial structures, before returning to the heart. NCCs ensheath each aortic arch-derived vessel, providing every component except the endothelial cells. Within the meninges, capillaries with pericytes of diencephalic and mesencephalic neural fold origin supply the forebrain, while capillaries with pericytes of mesodermal origin supply the rest of the central nervous system, in a mutually exclusive manner. The two types of head vasculature contact at a few defined points, including the anastomotic vessels of the circle of Willis, immediately ventral to the forebrain/midbrain boundary. Over the course of evolution, the vertebrate subphylum may have exploited the exceptionally broad range of developmental potentialities and the plasticity of NCCs in head remodelling that resulted in the growth of the forebrain.

0 comments Cited 125 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

Differentiation of Multipotent Vascular Stem Cells Contributes to Vascular Diseases

Zhenyu Tang, Aijun Wang, Falei Yuan … (2012)

It is generally accepted that the de-differentiation of smooth muscle cells (SMCs) from contractile to proliferative/synthetic phenotype has an important role during vascular remodeling and diseases. Here we provide evidence that challenges this theory. We identify a new type of multipotent vascular stem cell (MVSC) in blood vessel wall. MVSCs express markers including Sox17, Sox10 and S100β, are cloneable, have telomerase activity, and can differentiate into neural cells and mesenchymal stem cell (MSC)-like cells that subsequently differentiate into SMCs. On the other hand, we use lineage tracing with smooth muscle myosin heavy chain as a marker to show that MVSCs and proliferative or synthetic SMCs do not arise from the de-differentiation of mature SMCs. Upon vascular injuries, MVSCs, instead of SMCs, become proliferative, and MVSCs can differentiate into SMCs and chondrogenic cells, thus contributing to vascular remodeling and neointimal hyperplasia. These findings support a new hypothesis that the differentiation of MVSCs, rather than the de-differentiation of SMCs, contributes to vascular remodeling and diseases.

0 comments Cited 93 times – based on 0 reviews      Review now

Bookmark

All references

Author and article information

Contributors

Francis Miller Jr.: Role: Editor

Journal

Journal ID (nlm-ta): PLoS One

Journal ID (iso-abbrev): PLoS ONE

Journal ID (publisher-id): plos

Journal ID (pmc): plosone

Title: PLoS ONE

Publisher: Public Library of Science (San Francisco, CA USA )

ISSN (Electronic): 1932-6203

Publication date (Electronic): 6 January 2017

Publication date Collection: 2017

Volume: 12

Issue: 1

Electronic Location Identifier: e0168914

Affiliations

[1 ]Department of Neurology, Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China

[2 ]Med-X Research Institute and School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, China

[3 ]Department of Bioengineering, University of California, Berkeley, California, United States of America

[4 ]Department of Bioengineering, University of California, Los Angeles, California, United States of America

[5 ]Department of Medicine, University of California, Los Angeles, California, United States of America

[6 ]Department of Bioengineering, Chong Qing University, Chongqing, China

Duke University, UNITED STATES

Author notes

Competing Interests: The authors have declared that no competing interests exist.

Conceptualization: FY.
Formal analysis: FY ZZ LY.
Funding acquisition: GYY SL.
Methodology: FY DW KX JW ZZ LY.
Project administration: FY DW GYY SL.
Resources: GYY SL.
Supervision: GYY SL.
Validation: GYY SL.
Writing – original draft: FY DW.
Writing – review & editing: GYY SL.

* E-mail: gyyang0626@ 123456163.com (GYY); songli@ 123456ucla.edu (SL)

Article

Publisher ID: PONE-D-16-31010

DOI: 10.1371/journal.pone.0168914

PMC ID: 5218548

PubMed ID: 28060852

SO-VID: 0126ac84-fdb9-4c99-bdb2-a884b6b63de3

License:

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.

History

Date received : 3 August 2016

Date accepted : 8 December 2016

Page count

Figures: 5, Tables: 0, Pages: 11

Funding

Funded by: funder-id http://dx.doi.org/10.13039/100000002, National Institutes of Health;

Award ID: HL771213, HL121450, EB012240

Award Recipient : Song Li

Funded by: funder-id http://dx.doi.org/10.13039/501100001809, National Natural Science Foundation of China;

Award ID: #81428014

Award Recipient : Song Li

Funded by: funder-id http://dx.doi.org/10.13039/501100001809, National Natural Science Foundation of China;

Award ID: #81428014, # 81471178