Basic Fibroblast Growth Factor Stimulates Angiogenesis in the Hindlimb of Hyperglycemic Rats

Stark, James M.; Baffour, Richard; Garb, Jane; Kaufman, Jeffrey L.; Berman, Joel; Rhee, Sang Won; Norris, Marc A.; Friedmann, Paul

doi:10.1006/jsre.1998.5392

Cited by 23 publications

(24 citation statements)

References 32 publications

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“…VSMC migration is stimulated by growth factors such as bFGF or platelet-derived growth factor (23,30,34,38). Previous experiments could not identify a significant quantity of bFGF in MIF (40).…”

Section: Discussionmentioning

confidence: 99%

Haptoglobin expression and activity during coronary collateralization

Lohr

Warltier²,

Chilian³

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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Coronary collateral development relies on the coordinated secretion of growth factors. However, alone they are insufficient for permanent collateral growth. We utilized proteomics to identify other important proteins in the extracellular environment that could facilitate collateralization. Chronically instrumented dogs developed coronary collaterals by the repetitive occlusion method. Subendocardial (0.19 Ϯ 0.04, 0.27 Ϯ 0.06, 0.48 Ϯ 0.10, and 0.81 Ϯ 0.11 ml ⅐ min Ϫ1 ⅐ g Ϫ1 on days 1, 7, 14, and 21, respectively) and subepicardial (0.14 Ϯ 0.01, 0.36 Ϯ 0.06, 0.51 Ϯ 0.07, and 0.71 Ϯ 0.08 ml ⅐ min Ϫ1 ⅐ g Ϫ1 on days 1, 7, 14, and 21, respectively) blood flow increased in animals subjected to repetitive occlusion. Sham animals exhibited no changes in blood flow. Myocardial interstitial fluid (MIF) from both groups was analyzed by two-dimensional electrophoresis with matrix-assisted laser desorption/ionization time-of-flight identification. The acute-phase protein haptoglobin was identified in the group subjected to repetitive occlusion. ELISA of MIF showed haptoglobin to be elevated at all time points of collateral development compared with sham, with maximal production on day 7. Purified haptoglobin dose dependently stimulated endothelial cells to form tubes and vascular smooth muscle cells to migrate. Purified haptoglobin did not stimulate proliferation of either cell type. The relative contribution of haptoglobin to the chemotactic properties of MIF was tested using a neutralizing antibody. Neutralized MIF could not stimulate smooth muscle cells to migrate at any time during collateral development. Endothelial cell tube formation was inhibited after the midpoint of collateralization. Therefore, the acute-phase protein haptoglobin plays a critical role during coronary collateralization.angiogenesis; coronary circulation; inflammation; proteins CORONARY ARTERY DISEASE is characterized by plaque deposition, which ultimately reduces blood flow and leads to the pathophysiological sequelae of ischemic heart disease. Clinical data demonstrate that development of the coronary collateral circulation can ameliorate complications of coronary disease. Perez-Castellano et al. (33) associated reduced patient mortality from myocardial infarction with the extent of collateral development. Coronary collaterals can also reduce infarct size, preserve myocardial architecture, and improve cardiac function (5, 19).Coronary collaterals are preexisting arterial anastomoses between coronary arteries. These vessels cannot conduct blood flow sufficient to prevent ischemia in the event of coronary occlusion because of their small caliber and high resistance in their native state (10). However, collaterals can dramatically increase in diameter and muscularity when stimulated (10). Vascular endothelial growth factor (VEGF) has been identified as important in collateralization, and administration of VEGF or transfection in vivo enhances angiogenesis and collateral growth in many models (4,23,24,26). Basic fibroblast growth factor (bFGF), a mitog...

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Section: Discussionmentioning

confidence: 99%

Haptoglobin expression and activity during coronary collateralization

Lohr

Warltier²,

Chilian³

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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show abstract

“…In in vitro studies, the induction of proliferation activities by bFGF in various types of cells, including vascular cells (10,11,16), and the antiapoptotic action of bFGF on neural cells (14) have been reported. In in vivo studies, the effects of bFGF have been investigated in the fields of central and peripheral nervous systems (27)(28)(29)(30), skin (17), bone (18,19), heart (22,23), and vasculatures (20,21), and beneficial effects have been reported both experimentally and clinically. In addition to these effects, bFGF induces NO production through endothelial NO synthase activation, resulting in vasodilation (12,13,38).…”

Section: Discussionmentioning

confidence: 99%

“…With recent advances in molecular biology, bFGF has been recognized as a multifunctional growth factor that stimulates angiogenesis, acts as a vasodilatator (12,13), has antiapoptotic effects (14,15), and induces proliferation in various kinds of cells (10,11,16). Actually, the effects of bFGF have been investigated in the field of wound healing (17), bone regeneration (18,19), acute ischemic models (20,21), and myocardial infarction (22,23), both experimentally and clinically. The half-life time of bFGF is relatively short (24), and cross-linked gelatin hydrogel (CGH) has been used to maintain the bioactivity of locally administered bFGF for an extended period (25,26).…”

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confidence: 99%

Effects of Basic Fibroblast Growth Factor on Experimental Diabetic Neuropathy in Rats

et al. 2006

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Basic fibroblast growth factor (bFGF) stimulates angiogenesis and induces neural cell regeneration. We investigated the effects of bFGF on diabetic neuropathy in streptozotocin-induced diabetic rats. Diabetic rats were treated with human recombinant bFGF as follows: 1) intravenous administration, 2) intramuscular injection into thigh and soleus muscles with cross-linked gelatin hydrogel (CGH), and 3) intramuscular injection with saline. Ten or 30 days later, the motor nerve conduction velocity (MNCV) of the sciatic-tibial and caudal nerves, sensitivity to mechanical stimuli, sciatic nerve blood flow (SNBF), and retinal blood flow (RBF) were measured. Delayed MNCV in the sciatic-tibial and caudal nerves, hypoalgesia, and reduced SNBF in diabetic rats were all ameliorated by intravenous administration of bFGF after 10, but not 30, days. Intramuscular injection of bFGF with CGH also improved sciatic-tibial MNCV, hypoalgesia, and SNBF after 10 and 30 days, but caudal MNCV was not improved. However, intramuscular injection of bFGF with saline had no significant effects. bFGF did not significantly alter RBF in either normal or diabetic rats. These observations suggest that bFGF could have therapeutic value for diabetic neuropathy and that CGH could play important roles as a carrier of bFGF.

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“…The ischemic hindlimb model was created in diabetic rats (n ϭ 17) 12 wk after STZ injection and age-matched nondiabetic rats (n ϭ 17) as previously reported (17,26). Briefly, animals were anesthetized and a skin incision was made in the left hindlimb.…”

Section: Animals and Experimental Diabetic Rat Model This Experimentmentioning

confidence: 99%

“…Moreover, it has been reported that loss of the modulatory role of the endothelium in diabetic patients leads to insufficiencies of the coronary and peripheral collateral vessels (1,7,21). Several treatments have been attempted to ameliorate tissue ischemia in diabetic animals, such as intramuscular adeno-VEGF gene transfer and the direct injection of exogenous basic FGF (bFGF) (21,26). However, because it is well known that diabetes predisposes to microvascular proliferative disease, these treatments might also increase the plasma levels of VEGF or bFGF, thereby accelerating microvascular proliferation with unfavorable consequences.…”

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confidence: 99%