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Updated: May 9, 2026

A High Output Method to Isolate Cerebral Pericytes from Mouse
Published on: January 14, 2020
Recruitment and retention: factors that affect pericyte migration
Kristina Y Aguilera1, Rolf A Brekken
1Division of Surgical Oncology, Department of Surgery, Hamon Center for Therapeutic Oncology Research, University of Texas Southwestern Medical Center, 6000 Harry Hines Blvd, Dallas, TX, 75390-8593, USA.
Insights
Secreted protein acidic and rich in cysteine (SPARC) may regulate pericyte migration, influencing vascular development and cancer progression. Understanding SPARC
Area of Science:
- Vascular biology
- Cell biology
- Oncology
Background:
- Pericytes are essential for blood vessel formation and implicated in cancer.
- Pericyte migration and differentiation mechanisms are not fully understood.
- Several signaling pathways regulate pericyte recruitment to new vessels.
Purpose of the Study:
- To review factors influencing pericyte migration.
- To explore the potential role of secreted protein acidic and rich in cysteine (SPARC) in pericyte recruitment.
- To discuss pericyte roles in pathological conditions, particularly cancer.
Main Methods:
- Literature review of pericyte migration mechanisms.
- Analysis of signaling pathways involved in pericyte recruitment.
- Discussion of SPARC's potential influence on these pathways.
Main Results:
- Multiple factors like PDGF/PDGFR-β, S1P/EDG1, Ang/TIE2, TGF-β/ALK, Sem-3A/Npn, and MMPs regulate pericyte migration.
- SPARC is identified as a factor potentially modulating these pericyte recruitment pathways.
- Pericyte inhibition in tumors and recruitment in pathology are discussed.
Conclusions:
- SPARC may offer an additional regulatory layer for vascular support cell recruitment.
- Understanding SPARC's role could impact therapeutic strategies targeting tumor angiogenesis.
- Further research is needed to elucidate SPARC's precise mechanisms in pericyte regulation.
Abstract:
Pericytes are critical for vascular morphogenesis and contribute to several pathologies, including cancer development and progression. The mechanisms governing pericyte migration and differentiation are complex and have not been fully established. Current literature suggests that platelet-derived growth factor/platelet-derived growth factor receptor-β, sphingosine 1-phosphate/endothelial differentiation gene-1, angiopoietin-1/tyrosine kinase with immunoglobulin-like and EGF-like domains 2, angiopoietin-2/tyrosine kinase with immunoglobulin-like and EGF-like domains 2, transforming growth factor β/activin receptor-like kinase 1, transforming growth factor β/activin receptor-like kinase 5, Semaphorin-3A/Neuropilin, and matrix metalloproteinase activity regulate the recruitment of pericytes to nascent vessels. Interestingly, many of these pathways are directly affected by secreted protein acidic and rich in cysteine (SPARC). Here, we summarize the function of these factors in pericyte migration and discuss if and how SPARC might influence these activities and thus provide an additional layer of control for the recruitment of vascular support cells. Additionally, the consequences of targeted inhibition of pericytes in tumors and the current understanding of pericyte recruitment in pathological environments are discussed.
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