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Adriana Tajonar Growth Factors

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Growth Factors



Adriana Tajonar

Clinical Group

5.22 J

Outline



 Endothelium: function and restenosis

 Definition of growth factors and their

importance

 FGF

 VEGF

 Conclusions

 Questions



04/08/2003

Endothelial cells (ECs)



 Form the linings of the

blood vessels



 Capable of suiting local

requirements by

adjusting their number

and arrangement







04/08/2003

Van Belle, et. al., RPI website

Endothelial cells (ECs)





 Play crucial part in regulating vessel function

and structure by signaling the surrounding

connective tissue and smooth muscle

 Maintain a non-adhesive luminal surface and

contribute to fluidity of the blood





04/08/2003 Van Belle, et. al.

Proliferation of endothelial cells



 New ECs are generated by simple

duplication of existing ones

 ECs proliferate and migrate to cover exposed

surface to repair damage to blood vessel

(e.g. denuded vessel)

 ECs turn over very slowly with cell lifetime

– couple of months (liver and lungs)

– years (brain and muscle)

04/08/2003 B. Alberts, et. al.

Endothelium-derived substances control

Vascular Smooth Muscle Cells (VSMCs)



 Relaxing factors:

- Prostacyclin

- Endothelium-derived relaxing factor (EDRF) = Nitric oxide

 Contracting factors:

- Vasoconstrictor metabolites of arachidonic acid

- Endothelin-1

 Induced by stimuli as angiotensin II, catecholamines, FGFs, or

thrombin

 Inhibited by NO and prostacyclin





Van Belle, et. al.

04/08/2003

Growth inhibitory effect on VSMCs



 Molecules that stimulate VSMC proliferation

- Endothelin

- PDGF

- Angiotensin

 Molecules that inhibit VSMC growth

- Heparin and heparin sulfate glycosaminoglycans

 Prevent VSMCs from entering S phase

 Protect against thrombus formation

- EDRF-NO

 Increases cGMP  depresses incorporation of 3H-thymidine in

DNA in VSMCs

 Inhibit platelet adhesion

Van Belle, et. al.

04/08/2003

Endothelialization after arterial injury



 ECs from areas of intact endothelium enter

replication cycle to restore endothelial continuity

– Limited reendothelialization within one month of balloon

angioplasty

– Extensive reendothelialization between 1 and 5 months

after PTCA

 Growth factors for ECs play significant role in

process

 Neoendothelium’s function remains abnormal for

weeks after the reendothelialization has been

completed

Van Belle, et. al.

04/08/2003

Definition of Growth Factors (GFs)



 Natural chemical messengers

 Proteins that can control

– Growth

– Proliferation

– Differentiation

– Survival

– Function of different types of cells

 Trigger biochemical cascade

The Cooperative Research Centre for Cellular Growth Factors

04/08/2003

Relevance of GFs



 Act as local mediators at very low

concentrations (~10-9 – 10-11 M)



 Responses to them are slow (on the order of

hours) but quicker than without GFs



 Results in changes in gene expression or

protein activity

B. Alberts, et. al.

04/08/2003

Growth Factors in stents?!



 Artery deprived of endothelium after stent

implantation

 Restenosis: reparative process involving

division of smooth muscle cells and

production of extracellular matrix

 Solution: Reendothelialization



Van Belle, et. al.

04/08/2003

Fibroblast Growth Factor (FGF)



 Stimulates both ECs and VSMCs

 Synthesized and stored by ECs and VSMCs

 Has increased stimulation of ECs of denuded

arteries

 Achieves total EC regrowth within 10 weeks

 Can lead to functional changes at the endothelial

level

 Has an unclear effect on neointimal thickening

 Problem: also stimulates VSMCs

Van Belle, et. al.

04/08/2003

Vascular Endothelial Growth Factor

(VEGF)



 Promotes angiogenesis

 Triggers proliferation of vascular endothelial

cells only

 Regulates blood vessel growth to match the

needs of the tissue

 Controlled through

– changes in the stability of its mRNA

– rate of transcription



04/08/2003 Van Belle, et. al., B. Alberts

Response of ECs to VEGF



 EC proliferation increases in dose dependent

manner

 Gene expression observed as early as 36 hours

post-transfection of phVEGF165, and persisting for

two weeks

 Near complete reendothelialization by 7 days among

VEGF-transfected arteries

 Recovery of normal endothelium-dependent

responses within a week

 Diminished neointimal thickening

 Decrease in cases of thrombotic occlusion

04/08/2003 Van Belle, et. al.

Artery cross-sections









Effect of local delivery of rhVEGF 165 on intimal hyperplasia. (A)

4 weeks post stent implantation with local delivery of rhVEGF. (B)

Control group (no rhVEGF)

04/08/2003

E. Van Belle et. al.

Chemical pathway:

Reception of signal









04/08/2003 Berg, Stryer et. al.

Chemical pathway:

Signal transduction









04/08/2003

B. Alberts, et. al.

Why is VEGF our “ideal growth

factor”?



 It acts on endothelial cells SELECTIVELY

 Extremely important potential advantage over

FGF

 EC reestablish endothelium

 Restenosis avoided!

 Can be delivered as a protein or by local

gene transfer of gene encoding (which is the

optimal form?  production group)

04/08/2003

Conclusions



 Accelerated endothelialization may prevent

thrombus formation and intimal growth at the

site of stent implantation

 GF cause accelerated endothelial regrowth,

minimize endothelial dysfunction, and

interfere with intimal growth

 VEGF’s selectivity is important advantage

over FGF

04/08/2003

Future work



 Which genes are activated by the VEGF

cascade



 Search if information is available from the

1998 clinical trial







04/08/2003

References

 Van Belle E, Bauters C, Asahara T, Isner JM. Endothelial regrowth after arterial injury: from vascular

repair to therapeutics. Cardiovascular Research 1998; 54-61.

 Alberts B., et al. Molecular Biology of the Cell, 4th Edition, 2002, Garland Science; 871-887, 1090-

1091,1279-1282.

 Kliche S, Waltenberger J. VEGF Receptor Signaling and Endothelial Function. Life 2001; 61-63.

 Van Belle E, Maillard L, Tio FO, Isner JM. Accelerated Endothelialization by Local Delivery of

Recombinant Human Vascular Endothelial Growth Factor Reduces In-Stent Intimal Formation. Biochem

Biophys Res Comm 1997; 311-315

 Berg JM, Tymoczko JL, Stryer L, Biochemistry, 5th Edition, 2001, W.H. Freeman and Co.; 415

 Van Belle E, Tio FO, Couffinhal T, Maillard L, Passeri J, Isner JM. Time course, impact of local catheter

delivery, feasibility of recombinant protein administration, and response to cytokine expedition. Circulation

1997; 438-448.

 Schneider DB, Dichek DA. Intravascular Stent Endothelialization: A goal worth pursuing? Circulation 1997;

308-310.

 Hombach B, Waltenberger J, Voisard R, Hoher M. Recurrent stenosis following coronary angioplasty.

Clinical, cell, biological, and molecular aspects. Z Kardiol, 1995; Abstract

 Isner JM. Vascular endothelial growth factor: gene therapy and therapeutic angiogenesis. Cardiosource

(www.cardiosource.com)

 http://bio.bio.rpi.edu/Parsons/index.html





04/08/2003

04/08/2003



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