BB14, a Nerve Growth Factor (NGF)-like peptide shown to be effective in reducing reactive astrogliosis and restoring synaptic homeostasis in a rat model of peripheral nerve injury

Cirillo, Giovanni; Colangelo, Anna Maria; Bianco, Mimma; Cavaliere, Carlo; Zaccaro, Laura; Sarmientos, Paolo; Alberghina, Lilia; Papa, Michèle

doi:10.1016/j.biotechadv.2011.05.008

Cited by 41 publications

(37 citation statements)

References 46 publications

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“…Reactive astrogliosis has been shown to correlate with the severity of peripheral nerve injury and increased GFAP expression, which is used as a marker of altered morphology and activity [44,46,49,50]. Microgliosis correlates with increased expression of CD11b and allograft inflammatory factor 1 (AIF1; also known as Iba-1) [46,51].…”

Section: Discussionmentioning

confidence: 99%

The nitroxyl donor, Angeli’s salt, reduces chronic constriction injury-induced neuropathic pain

Longhi-Balbinot

Rossaneis

Pinho‐Ribeiro

et al. 2016

Chemico-Biological Interactions

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Chronic pain is a major health problem worldwide. We have recently demonstrated the analgesic effect of the nitroxyl donor, Angeli’s salt (AS) in models of inflammatory pain. In the present study, the acute and chronic analgesic effects of AS was investigated in chronic constriction injury of the sciatic nerve (CCI)-induced neuropathic pain in mice. Acute (7th day after CCI) AS treatment (1 and 3 mg/kg; s.c.) reduced CCI-induced mechanical, but not thermal hyperalgesia. The acute analgesic effect of AS was prevented by treatment with 1H-[1,2, 4]oxadiazolo[4,3,-a]quinoxalin-1-one (ODQ, a soluble guanylate cyclase inhibitor), KT5823 (an inhibitor of protein kinase G [PKG]) or glibenclamide (GLB, an ATP-sensitive potassium channel blocker). Chronic (7–14 days after CCI) treatment with AS (3 mg/kg, s.c.) promoted a sustained reduction of CCI-induced mechanical and thermal hyperalgesia. Acute AS treatment reduced CCI-induced spinal cord allograft inflammatory factor 1 (known as Iba-1), interleukin-1β (IL-1β), and ST2 receptor mRNA expression. Chronic AS treatment reduced CCI-induced spinal cord glial fibrillary acidic protein (GFAP), Iba-1, IL-1β, tumor necrosis factor-α (TNF-α), interleukin-33 (IL-33) and ST2 mRNA expression. Chronic treatment with AS (3 mg/kg, s.c.) did not alter aspartate aminotransferase, alanine aminotransferase, urea or creatinine plasma levels. Together, these results suggest that the acute analgesic effect of AS depends on activating the cGMP/PKG/ATP-sensitive potassium channel signaling pathway. Moreover, chronic AS diminishes CCI-induced mechanical and thermal hyperalgesia by reducing the activation of spinal cord microglia and astrocytes, decreasing TNF-α, IL-1β and IL-33 cytokines expression. This spinal cord immune modulation was more prominent in the chronic treatment with AS. Thus, nitroxyl limits CCI-induced neuropathic pain by reducing spinal cord glial cells activation.

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Section: Discussionmentioning

confidence: 99%

The nitroxyl donor, Angeli’s salt, reduces chronic constriction injury-induced neuropathic pain

Longhi-Balbinot

Rossaneis

Pinho‐Ribeiro

et al. 2016

Chemico-Biological Interactions

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“…Consistent with the possibility that NGF modulates aspects of gliosis, Cirillo and colleges (2009) showed that NGF reduced the reactive astrocytosis associated with neuropathic pain. NGF also was able to restore glial and neuronal amino acid transporters (Cirillo et al, 2011). The potential outcome of NGF treatment on astrocytes may depend on the neurotrophin receptors expressed in a particular cellular context.…”

Section: Discussionmentioning

confidence: 99%

Nerve growth factor induces cell cycle arrest of astrocytes

Cragnolini

Volosin

Huang

et al. 2012

Developmental Neurobiology

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Neurotrophins can influence multiple cellular functions depending on the cellular context and the specific receptors they interact with. These neurotrophic factors have been extensively studied for their ability to support neuronal survival via Trk receptors, and to induce apoptosis via the p75NTR. However, the p75NTR is also detected on cell populations that do not undergo apoptosis in response to neurotrophins. In particular, we have detected p75NTR expression on astrocytes during development and after seizure-induced injury. In this study we the role of NGF in regulating astrocyte proliferation, and in influencing specific aspects of the cell cycle. We demonstrate that NGF prevents the induction of cyclins and their association with specific cyclin-dependent kinases, and thereby prevents progression through the G1 phase of the cell cycle. Since we have previously shown that p75NTR, but not TrkA, is expressed in astrocytes, these data suggest that activation of p75NTR promotes withdrawal of astrocytes from the cell cycle, which may have important consequences during development and after injury.

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“…SR101-specific labeling of spinal astroglia permits the analysis of density and distribution of astrocytes in vivo and their role in neurodegenerative disease [27, 28] or following spinal cord or nerve injury [11, 12, 29, 30]. Colabeling other spinal elements, such as blood vessels and neurons, enables morphological and functional study of gliosvascular plasticity and neuroglial network [31].…”

Section: Discussionmentioning

confidence: 99%

“…As we recently demonstrated [27, 29, 31], glial response and the consequent adaptive synaptic plasticity lead to the concept of noncell autonomous disease and phenotypic changes affecting astrocytes play a key role in the onset and progression of the disease. Thereby, the availability of a reproducible and steady technique facilitates the widespread application of this powerful tool in studies of the spinal cord disease in vivo .…”

Section: Discussionmentioning

confidence: 99%

Calcium Imaging of Living Astrocytes in the Mouse Spinal Cord following Sensory Stimulation

2012

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Astrocytic Ca2+ dynamics have been extensively studied in ex vivo models; however, the recent development of two-photon microscopy and astrocyte-specific labeling has allowed the study of Ca2+ signaling in living central nervous system. Ca2+ waves in astrocytes have been described in cultured cells and slice preparations, but evidence for astrocytic activation during sensory activity is lacking. There are currently few methods to image living spinal cord: breathing and heart-beating artifacts have impeded the widespread application of this technique. We here imaged the living spinal cord by two-photon microscopy in C57BL6/J mice. Through pressurized injection, we specifically loaded spinal astrocytes using the red fluorescent dye sulforhodamine 101 (SR101) and imaged astrocytic Ca2+ levels with Oregon-Green BAPTA-1 (OGB). Then, we studied astrocytic Ca2+ levels at rest and after right electrical hind paw stimulation. Sensory stimulation significantly increased astrocytic Ca2+ levels within the superficial dorsal horn of the spinal cord compared to rest. In conclusion, in vivo morphofunctional imaging of living astrocytes in spinal cord revealed that astrocytes actively participate to sensory stimulation.

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BB14, a Nerve Growth Factor (NGF)-like peptide shown to be effective in reducing reactive astrogliosis and restoring synaptic homeostasis in a rat model of peripheral nerve injury

Cited by 41 publications

References 46 publications

The nitroxyl donor, Angeli’s salt, reduces chronic constriction injury-induced neuropathic pain

The nitroxyl donor, Angeli’s salt, reduces chronic constriction injury-induced neuropathic pain

Nerve growth factor induces cell cycle arrest of astrocytes

Calcium Imaging of Living Astrocytes in the Mouse Spinal Cord following Sensory Stimulation

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