PMID- 8915187
OWN - NLM
STAT- MEDLINE
DCOM- 19961204
LR  - 20220316
IS  - 0008-6363 (Print)
IS  - 0008-6363 (Linking)
VI  - 32
IP  - 4
DP  - 1996 Oct
TI  - Pericytes in the microvasculature.
PG  - 687-98
AB  - Pericytes, also known as Rouget cells or mural cells, are associated abluminally 
      with all vascular capillaries and post-capillary venules. Differences in pericyte 
      morphology and distribution among vascular beds suggest tissue-specific 
      functions. Based on their location and their complement of muscle cytoskeletal 
      proteins, pericytes have been proposed to play a role in the regulation of blood 
      flow. In vitro studies demonstrating the contractile ability of pericytes support 
      this concept. Pericytes have also been suggested to be oligopotential and have 
      been reported to differentiate into adipocytes, osteoblasts and phagocytes. The 
      mechanisms involved in vessel formation have yet to be elucidated but 
      observations indicate that the primordial endothelium can recruit 
      undifferentiated mesenchymal cells and direct their differentiation into 
      pericytes in microvessels, and smooth muscle cells in large vessels. 
      Communication between endothelial cells and pericytes, or their precursors, may 
      take many forms. Soluble factors such as platelet-derived growth factor and 
      transforming growth factors-beta are likely to be involved. In addition, physical 
      contact mediated by cell adhesion molecules, integrins and gap junctions appear 
      to contribute to the control of vascular growth and function. Development of 
      culture methods has allowed some functions of pericytes to be directly examined. 
      Co-culture of pericytes with endothelial cells leads to the activation of 
      transforming growth factor-beta, which in turn influences the growth and 
      differentiation of the vascular cells. Finally, the pericyte has been implicated 
      in the development of a variety of pathologies including hypertension, multiple 
      sclerosis, diabetic microangiopathy and tumor vascularization.
FAU - Hirschi, K K
AU  - Hirschi KK
AD  - Children's Hospital, Department of Pathology, Harvard Medical School, Boston, MA 
      02115, USA.
FAU - D'Amore, P A
AU  - D'Amore PA
LA  - eng
GR  - CA45548/CA/NCI NIH HHS/United States
GR  - EY05318/EY/NEI NIH HHS/United States
GR  - HL09037/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PT  - Review
PL  - England
TA  - Cardiovasc Res
JT  - Cardiovascular research
JID - 0077427
RN  - 0 (Growth Substances)
SB  - IM
MH  - Animals
MH  - Endothelium, Vascular/metabolism
MH  - Growth Substances/metabolism
MH  - Humans
MH  - Microcirculation/*cytology/metabolism
MH  - Neovascularization, Pathologic
MH  - Neovascularization, Physiologic
MH  - Oligodendroglia/metabolism/*physiology
MH  - Rats
MH  - Regional Blood Flow
RF  - 144
EDAT- 1996/10/01 00:00
MHDA- 1996/10/01 00:01
CRDT- 1996/10/01 00:00
PHST- 1996/10/01 00:00 [pubmed]
PHST- 1996/10/01 00:01 [medline]
PHST- 1996/10/01 00:00 [entrez]
AID - 0008636396000636 [pii]
PST - ppublish
SO  - Cardiovasc Res. 1996 Oct;32(4):687-98.