QualificationsPost-Doctoral, University of Colorado Health Sciences Center, Rheumatology, 1990. M.D., Baylor College of Medicine, Medicine, 1983. B.Sc., Brooklyn College, City University of New York, Chemistry, 1979. Expertise and Research InterestsMy current research involves fibroblast growth factors (FGF's), which are well-described modifiers of angiogenesis, and endothelial cell proliferation. We are investigating these and other factors roles as neurotrophins in pain propagation.
From abstract: Fibroblast growth factor-2 is a polypeptide growth factor implicated in angiogenesis, osteogenesis, wound repair and neuronal survival. FGF-2 is expressed in sites of inflammation as well as being expressed in glial cells where it acts as an inducer of NGF. However, the precise role of FGF-2 in neuropathic and inflammatory pain is still poorly understood. This proposal will improve our understanding of the signals that lead to increased FGF-2 as well as the events that are regulated by FGF-2 in the context of both neuropathic and inflammatory pain through conduction of the following specific aims. Capsaicin treatment in adult SpNL and control rats will be used to determine the effect of C-fiber loss on FGF-2 immunoreactivity (IR) and mRNA expression and GFAP IR in spinal cord(SC) via laser capture microscopy (LCM) coupled with RT-PCR, ISH and IHC. To test if astrocyte reactivity leads or is required for increased FGF-2 expression, FGF-2 mRNA and protein levels in SC will be examined following inhibition of astrocyte reactivity in SPNL model. NGF mRNA and protein, GAP-43 (a marker of neuronal growth) and CGRP (a marker of afferent sensory fibers) IR will be examined following intrathecal (i.t.) administration of anti-FGF-2 neutralizing antibodies and/or FGF-2. The effect of inhibiting FGF-2 signaling via i.t. delivery of anti-FGF-2 neutralizing antibodies or delivery of FGF-2 will also be assessed behaviorally by assessing allodynia and hyperalgesia in the model. SC Substance P andPGE2 will be assessed by in vivo microdialysis in SpNL rats following delivery of either FGF-2 or anti-FGF-2 neutralizing antibodies. Finally, FGF-2 IR and mRNA expression will be similarly examined in the CFA model to allow us to better understand similarities and differences in signaling between these two models of chronic pain. From Another Abstract: Chronic pain conditions, which are estimated to affect 30% of the population in industrialized countries, are the culmination of a nociceptive cascade involving the participation of different cell types (glial cells, neurons) and a variety of molecules, which include neuropeptides, prostaglandins, cytokines, and excitatory amino acids. Nonetheless, in spite of the abundance of research aimed at elucidating the molecular mechanisms responsible for triggering, maintaining, and exacerbating pain, many questions still remain unanswered, and analgesic therapeutic options limited. Two accepted animal models that mimic neuropathic (NP) and inflammatory pain conditions are the L5-L6 spinal nerve ligation (SpNL), or Chung model, and the complete FreundÂ’s adjuvant-induced arthritis (CFA), respectively. Our investigation of several neurotrophic factors in the SpNL model has led to some important findings: First, fibroblast growth factor-2 (FGF-2) mRNA was up-regulated in NP L5-L6 dorsal root ganglia (DRG) and FGF-2 immunoreactivity (IR) was increased in reactive dorsal horn (DH) astrocytes. Furthermore, using laser capture microdissection (LCM) coupled with RT-PCR, we also observed an increase in ipsilateral DH FGF-2 mRNA. FGF-2 is a pleiotropic cytokine with neurotrophic and gliogenic properties. While its role in cellular responses to various physical injuries to the brain and spinal cord has been extensively investigated, there is a paucity of data regarding FGF-2 in the setting of chronic pain. This is in spite of a number of studies showing an increase in both FGF-2 mRNA and/or protein in sensory ganglia in different animal models of neuropathy (Ji, 1995; Grothe, 1997; DeLeo, 1997; preliminary results). Our preliminary results add to this body of evidence by further suggesting that FGF-2 participates in at least one of the events induced by nerve injury, that is, astrocyte reactivity. This event, in turn, appears to be a vital component of the development of hyperalgesia/allodynia (DeLeo et al, 1997, 2001; Coyle, 1998). In inflammatory disorders, FGF-2 is increased in the inflamed joints of rats with adjuvant-induced arthritis (Qu, 1994) and of humans with rheumatoid arthritis (Bucala, 1991; Remmers, 1991; Nakashima , 1994; Qu , 1995; Manabe , 1999), where it contributes to inflammation, synovial angiogenesis, pannus formation, and joint destruction (Yamashita et al., 2002). Unfortunately, a more detailed investigation into the central contribution of FGF-2 in inflammatory pain is lacking at present. Second, we have observed a significant increase in neuronal nerve growth factor (NGF) mRNA in ipsilateral L5-L6 DRG and DH by in situ hybridization (ISH) and LCM, respectively. Via immunohistochemistry, we have observed a decrease in NGF IR at 1-week post-ligation in the ipsilateral DH, with a significant recovery by 3-weeks to levels higher than in the contralateral side and in SHAM. These findings suggest that following nerve injury, which prevents the retrograde transport of NGF from the periphery (Raivich et al., 1991), novel signaling mechanisms are induced leading to newly synthesized NGF (Shen et al., 1999; Fukuoka et al., 2001; Oh et al., 2001). This newly produced NGF may be involved in the recovery of injured sensory fibers, as well as in the sprouting of non-injured nociceptive fibers (Romero et al., 2000; 2001) thereby contributing to the hyperalgesia observed in this model. Because FGF-2 has been shown to induce NGF synthesis in astrocytes, the early up-regulation of FGF-2 may be one of the mechanisms responsible for the increased NGF synthesis. Because NGF and astrocyte reactivity are associated with both SpNL and CFA models of pain (Bao et al., 2001; Coyle et al., 1998; Sweitzer et al., 2001; Pezet et al., 1999; 2001; appendix and preliminary results), comparing the contribution of FGF-2 to both NP pain (in the SpNL model) and inflammatory pain (CFA model) will improve our understanding of the mechanisms underlying nociception. Other ExpertiseAcademic Experience:
National Scientific Advisory Committee for American Federation for Aging Research 1996-1997 KeywordsCOS Keywords:Biochemistry, Cell Biology, Genetics, Growth Factors, Membranes, Molecular Biology, Molecular Chemistry.Additional Terms:Cell Biology, Membrane Biochemistry, Molecular Biology.Languages(Reading, Writing, Speaking)French: (Basic, Basic, Basic) Spanish: (Functional, Basic, Functional) MembershipsAmerican College of Physicians American College of Rheumatology Previous Positions1987-1990, University of Colorado Health Sciences Center, Research Fellow in Rheumatology 1986-1987, Columbia University College of Physicians and Surgeons, Clinical Fellow in Medicine Funding Received
Publications
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