Nerve growth factor induces angiogenic activity in a mouse model of hindlimb ischemia

Turrini, Paolo; Gaetano, Carlo; Antonelli, Alessia; Capogrossi, Maurizio C.; Aloe, Luigi

doi:10.1016/s0304-3940(02)00090-3

Cited by 66 publications

(47 citation statements)

References 15 publications

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“…Ϫ20 and Ϫ10 min, 20 and 10 min before injection, respectively. Rabito et al, 1996) and can produce NGF (Turrini et al, 2002;Toti et al, 2003), myocytes themselves might produce NGF in this model. This point needs to be clarified.…”

Section: Discussionmentioning

confidence: 67%

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Bradykinin and Nerve Growth Factor Play Pivotal Roles in Muscular Mechanical Hyperalgesia after Exercise (Delayed-Onset Muscle Soreness)

Murase

Terazawa²,

Queme³

et al. 2010

J. Neurosci.

159

183

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Unaccustomed strenuous exercise that includes lengthening contraction (LC) often causes delayed-onset muscle soreness (DOMS), a kind of muscular mechanical hyperalgesia. The substances that induce this phenomenon are largely unknown. Peculiarly, DOMS is not perceived during and shortly after exercise, but rather is first perceived after ϳ1 d. Using B 2 bradykinin receptor antagonist HOE 140, we show here that bradykinin released during exercise plays a pivotal role in triggering the process that leads to muscular mechanical hyperalgesia. HOE 140 completely suppressed the development of muscular mechanical hyperalgesia when injected before LC, but when injected 2 d after LC failed to reverse mechanical hyperalgesia that had already developed. B 1 antagonist was ineffective, regardless of the timing of its injection. Upregulation of nerve growth factor (NGF) mRNA and protein occurred in exercised muscle over a comparable time course (12 h to 2 d after LC) for muscle mechanical hyperalgesia. Antibodies to NGF injected intramuscularly 2 d after exercise reversed muscle mechanical hyperalgesia. HOE 140 inhibited the upregulation of NGF. In contrast, shortening contraction or stretching induced neither mechanical hyperalgesia nor NGF upregulation. Bradykinin together with shortening contraction, but not bradykinin alone, reproduced lasting mechanical hyperalgesia. We also showed that rat NGF sensitized thin-fiber afferents to mechanical stimulation in the periphery after 10 -20 min. Thus, NGF upregulation through activation of B 2 bradykinin receptors is essential (though not satisfactory) to mechanical hyperalgesia after exercise. The present observations explain why DOMS occurs with a delay, and why lengthening contraction but not shortening contraction induces DOMS.

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Section: Discussionmentioning

confidence: 67%

“…NGF is produced in inflamed tissues and skeletal muscle after ischemia (Turrini et al, 2002) and nerve injury (Amano et al, 1991), and sensitizes nociceptors, resulting in hyperalgesia . It was also reported that intramuscular injection of NGF induced lasting tenderness (Svensson et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Bradykinin and Nerve Growth Factor Play Pivotal Roles in Muscular Mechanical Hyperalgesia after Exercise (Delayed-Onset Muscle Soreness)

Murase

Terazawa²,

Queme³

et al. 2010

J. Neurosci.

159

183

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“…Hematoxylin-eosin section preparation, 18 capillary density measurement, 19 and arteriolar length density assessment 18 were previously described. Necrotic muscle fibers were identified by morphology, differential eosin staining, and presence of infiltrating cells near the degenerating fibers on the whole section at ϫ400 magnification.…”

Section: Histology and Morphometric Analysismentioning

confidence: 99%

p66 ^ShcA Modulates Tissue Response to Hindlimb Ischemia

et al. 2004

Self Cite

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Background— Oxidative stress plays a pivotal role in ischemia and ischemia/reperfusion injury. Because p66 ShcA -null (p66 ShcA −/−) mice exhibit both lower levels of intracellular reactive oxygen species and increased resistance to cell death induced by oxidative stress, we investigated whether tissue damage that follows acute ischemia or ischemia/reperfusion was altered in p66 ShcA −/− mice. Methods and Results— Unilateral hindlimb ischemia was induced by femoral artery dissection, and ischemia/reperfusion was induced with an elastic tourniquet. Both procedures caused similar changes in blood perfusion in p66 ShcA wild-type (p66 ShcA wt) and p66 ShcA −/− mice. However, significant differences in tissue damage were found: p66 ShcA wt mice displayed marked capillary density decrease and muscle fiber necrosis. In contrast, in p66 ShcA −/− mice, minimal capillary density decrease and myofiber death were present. When apoptosis after ischemia was assayed, significantly lower levels of apoptotic endothelial cells and myofibers were found in p66 ShcA −/− mice. In agreement with these data, both satellite muscle cells and endothelial cells isolated from p66 ShcA −/− mice were resistant to apoptosis induced by simulated ischemia in vitro. Lower apoptosis levels after ischemia in p66 ShcA −/− cells correlated with decreased levels of oxidative stress both in vivo and in vitro. Conclusions— p66 ShcA plays a crucial role in the cell death pathways activated by acute ischemia and ischemia/reperfusion, indicating p66 ShcA as a potential therapeutic target for prevention and treatment of ischemic tissue damage.

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“…Nerve growth factor (NGF), which is well known as a neurotrophic factor, 13,14 has recently been recognized as an angiogenic factor in several tissues [15][16][17][18] and is reported to play an important regulatory role in pancreatic β-cell function. [19][20][21][22] We previously demonstrated that treatment of pancreatic islets with NGF improved their quality and viability.…”

Section: Introductionmentioning

confidence: 99%

Nerve growth factor is associated with islet graft failure following intraportal transplantation

Saito

Chan

Sakata

et al. 2012

Islets

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Nerve growth factor (NGF) has recently been recognized as an angiogenic factor with an important regulatory role in pancreatic b-cell function. We previously showed that treatment of pancreatic islets with NGF improved their quality and viability. Revascularization and survival of islets transplanted under the kidney capsule were improved by NGF. However, the usefulness of NGF in intraportal islet transplantation was not previously tested. To resolve this problem, we transplanted syngeneic islets (360 islet equivalents per recipient) cultured with or without NGF into the portal vein of streptozotocin-induced diabetic BALB/c mice. Analysis revealed that 44.4% (4/9) of control and 12.5% (1/8) of NGF-treated mice attained normoglycemia (# 200 mg/dL) (p = 0.195). NGF-treated islets led to worse graft function (area under the curve of intraperitoneal glucose tolerance tests (IPGTT) on post-operative day (POD) 30, control; 35,800 ± 3,960 min*mg/dl, NGF-treated; 47,900 ± 3,220 min*mg/dl: *p = 0.0348). NGF treatment of islets was also associated with increased graft failure [the percentage of TdT-mediated dUTP-biotin nick-end labeling (TUNEL)-positive and necrotic transplanted islets on POD 5, control; 23.8% (5/21), NGF-treated; 52.9% (9/17): p = 0.0650] following intraportal islet transplantation. Nonviable (TUNEL-positive and necrotic) islets in both groups expressed vascular endothelial growth factor (VEGF) and hypoxia-inducible factor-1a (HIF-1a). On the other hand, viable (TUNEL-negative and not necrotic) islets in both groups did not express VEGF and HIF-1a. In the present study, pre-transplant NGF treatment was associated with impaired survival and angiogenesis of intraportal islet grafts. The effect of NGF on islet transplantation may significantly vary according to the transplant site.

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Nerve growth factor induces angiogenic activity in a mouse model of hindlimb ischemia

Cited by 66 publications

References 15 publications

Bradykinin and Nerve Growth Factor Play Pivotal Roles in Muscular Mechanical Hyperalgesia after Exercise (Delayed-Onset Muscle Soreness)

Bradykinin and Nerve Growth Factor Play Pivotal Roles in Muscular Mechanical Hyperalgesia after Exercise (Delayed-Onset Muscle Soreness)

p66 ^ShcA Modulates Tissue Response to Hindlimb Ischemia

Nerve growth factor is associated with islet graft failure following intraportal transplantation

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Nerve growth factor induces angiogenic activity in a mouse model of hindlimb ischemia

Cited by 66 publications

References 15 publications

Bradykinin and Nerve Growth Factor Play Pivotal Roles in Muscular Mechanical Hyperalgesia after Exercise (Delayed-Onset Muscle Soreness)

Bradykinin and Nerve Growth Factor Play Pivotal Roles in Muscular Mechanical Hyperalgesia after Exercise (Delayed-Onset Muscle Soreness)

p66 ShcA Modulates Tissue Response to Hindlimb Ischemia

Nerve growth factor is associated with islet graft failure following intraportal transplantation

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Product

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About

p66 ^ShcA Modulates Tissue Response to Hindlimb Ischemia