期刊
CELLULAR AND MOLECULAR LIFE SCIENCES
卷 68, 期 19, 页码 3165-3173出版社
SPRINGER BASEL AG
DOI: 10.1007/s00018-011-0781-8
关键词
SPARC/osteonectin; TGF-beta; Angiogenesis; Extracellular matrix
资金
- NIH, NCI [R01CA118240]
- NIGMS [T32 GM008203]
- NIDCR [P20RR017696]
- NIHLB [094517]
- Veteran's Administration
SPARC is a matricellular protein, able to modulate cell/ECM interactions and influence cell responses to growth factors, and therefore is particularly attuned to contribute to physiological processes involving changes in ECM and cell mobilization. Indeed, the list of biological processes affected by SPARC includes wound healing, tumor progression, bone formation, fibrosis, and angiogenesis. The process of angiogenesis is complex and involves a number of cellular processes such as endothelial cell proliferation, migration, ECM degradation, and synthesis, as well as pericyte recruitment to stabilize nascent vessels. In this review, we will summarize current results that explore the function of SPARC in the regulation of angiogenic events with a particular emphasis on the modulation of growth factor activity by SPARC in the context of blood vessel formation. The primary function of SPARC in angiogenesis remains unclear, as SPARC activity in some circumstances promotes angiogenesis and in others is more consistent with an anti-angiogenic activity. Undoubtedly, the mercurial nature of SPARC belies a redundancy of functional proteins in angiogenesis as well as cell-type-specific activities that alter signal transduction events in response to unique cellular milieus. Nonetheless, the investigation of cellular mechanisms that define functional activities of SPARC continue to contribute novel and exciting paradigms to vascular biology.
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