PMID- 16955051
OWN - NLM
STAT- MEDLINE
DCOM- 20060928
LR  - 20071114
IS  - 1524-4040 (Electronic)
IS  - 0148-396X (Linking)
VI  - 59
IP  - 3
DP  - 2006 Sep
TI  - Expression of hypoxia-inducible factor-1 and vascular endothelial growth factor 
      in response to venous hypertension.
PG  - 687-96; discussion 687-96
AB  - OBJECTIVE: Experimentally, a fistula created surgically between the carotid 
      artery and jugular vein, together with occlusion of venous sinuses, generate 
      venous hypertension, which can induce dural arteriovenous fistula formation 
      intracranially in rats. Our aim was to study the effect of nonischemic venous 
      hypertension on the elaboration of the angiogenic signal, hypoxia-inducible 
      factor-1 (HIF-1), and its downstream signal, vascular endothelial growth factor 
      (VEGF). METHODS: Sixty rats were exposed to venous hypertension for periods 
      ranging from 4 hours to 3 weeks. Western blot analysis, transbinding assays, 
      enzyme-linked immunosorbent assays, and immunohistochemistry quantified HIF-1 and 
      VEGF expression in brain. Forty-eight control rats underwent similar surgical 
      procedures without creating venous hypertension. Cerebral blood flow was measured 
      at baseline, after surgery, and before sacrifice. RESULTS: Venous hypertension 
      did not impair cerebral blood flow. Relative to controls, HIF-1 expression 
      increased fivefold in response to venous hypertension (P < 0.005), with peak 
      expression 1 day later localized to endothelial cells in venules next to the 
      sagittal sinus. VEGF expression also increased threefold in response to venous 
      hypertension (P < 0.05), with peak expression 7 days later localized to 
      parasagittal astrocytes. HIF-1 and VEGF were minimally expressed in rat normal 
      venous pressures. CONCLUSION: In this model, venous hypertension stimulates 
      angiogenesis by a mechanism other than ischemia. HIF-1 expression may result from 
      dilation of parasagittal veins and endothelial deformation. HIF-1 and VEGF seem 
      to be molecular agents that convert venous hypertension into intracellular 
      signals and angiogenesis activity.
FAU - Zhu, Yiqian
AU  - Zhu Y
AD  - Center for Cerebrovascular Research, and Department of Anesthesia and 
      Perioperative Care, University of California, San Francisco 94143-0112, USA.
FAU - Lawton, Michael T
AU  - Lawton MT
FAU - Du, Rose
AU  - Du R
FAU - Shwe, Yamin
AU  - Shwe Y
FAU - Chen, Yongmei
AU  - Chen Y
FAU - Shen, Fanxia
AU  - Shen F
FAU - Young, William L
AU  - Young WL
FAU - Yang, Guo-Yuan
AU  - Yang GY
LA  - eng
GR  - K08 K08 NS02220/NS/NINDS NIH HHS/United States
GR  - P01 NS044155/NS/NINDS NIH HHS/United States
GR  - R01 NS27713/NS/NINDS NIH HHS/United States
GR  - R21 NS45123/NS/NINDS NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PL  - United States
TA  - Neurosurgery
JT  - Neurosurgery
JID - 7802914
RN  - 0 (Hypoxia-Inducible Factor 1)
RN  - 0 (Vascular Endothelial Growth Factors)
SB  - IM
MH  - Animals
MH  - Gene Expression Regulation/*physiology
MH  - Hypertension/genetics/*metabolism
MH  - Hypoxia-Inducible Factor 1/*biosynthesis/genetics
MH  - Jugular Veins/metabolism/pathology
MH  - Male
MH  - Neovascularization, Pathologic/genetics/*metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Vascular Endothelial Growth Factors/*biosynthesis/genetics
EDAT- 2006/09/07 09:00
MHDA- 2006/09/29 09:00
CRDT- 2006/09/07 09:00
PHST- 2006/09/07 09:00 [pubmed]
PHST- 2006/09/29 09:00 [medline]
PHST- 2006/09/07 09:00 [entrez]
AID - 00006123-200609000-00022 [pii]
AID - 10.1227/01.NEU.0000228962.68204.CF [doi]
PST - ppublish
SO  - Neurosurgery. 2006 Sep;59(3):687-96; discussion 687-96. doi: 
      10.1227/01.NEU.0000228962.68204.CF.