Neurotrophic factors attenuate neuronal nitric oxide synthase upregulation, microvascular permeability disturbances, edema formation and cell injury in the spinal cord following trauma: an experimental study using topical application of BDNF and IGF-1 in the rat

Sharma, Hari Shanker; Nyberg, Fred; Gordh, Torsten; Alm, P.; Westman, Jan

doi:10.1007/978-3-7091-6464-8_8

Cited by 12 publications

(24 citation statements)

References 84 publications

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“…5 D.c). The BSCB permeability to iodine and the increased water content in the T9 and T12 segment were significantly reduced ( [46,47,221] ; Fig. 7A).…”

Section: Neuroprotective Effects Of Neurotrophins In Scimentioning

confidence: 93%

“…However, the [1,47]. NGF = nerve growth factor, FGF = fibroblast growth factor, BDNF = brain derived neurotrophic factor, NT = neurotrophin, trk = tyrosine kinase, CNTF = ciliary neurotrophic factor, GDNF = glial derived neurotrophic factor, HBGF = heparin binding growth factor, TGF-β = transforming growth factor beta.…”

Section: Alteration In Neurotrophins Expression In Scimentioning

confidence: 98%

“…NGF = nerve growth factor, FGF = fibroblast growth factor, BDNF = brain derived neurotrophic factor, NT = neurotrophin, trk = tyrosine kinase, CNTF = ciliary neurotrophic factor, GDNF = glial derived neurotrophic factor, HBGF = heparin binding growth factor, TGF-β = transforming growth factor beta. [37,47]. NGF = nerve growth factor, FGF = fibroblast growth factor, BDNF = brain derived neurotrophic factor, NT = neurotrophin, trk = tyrosine kinase, CNTF = ciliary neurotrophic factor, GDNF = glial derived neurotrophic factor, HBGF = heparin binding growth factor, TGF-β = transforming growth factor beta, IL-6 = interleukin 6, LIF = leukaemia inhibitory factor.…”

Section: Alteration In Neurotrophins Expression In Scimentioning

confidence: 99%

“…The victims of SCI are generally young men of 20 to 30 years of age while only 20 to 30 % of cases involves women ( Table 1). Currently, no suitable therapeutic strategies are effective in improving the quality of life of SCI patients [see 28,29,37,[45][46][47][48]. Thus, exploration of new pharmacological avenues with possibility of regeneration of the damaged spinal cord axons is urgently needed.…”

Section: Clinical Cases Of Spinal Cord Injury Prevalence and Symptomsmentioning

confidence: 99%

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Pathophysiology of Blood-Spinal Cord Barrier in Traumatic Injury and Repair

Sharma¹

2005

CPD

157

218

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Blood-spinal cord barrier (BSCB) plays an important role in the regulation of the fluid microenvironment of the spinal cord. Trauma to the spinal cord impairs the BSCB permeability to proteins leading to vasogenic edema formation. Several endogenous neurochemical mediators and growth factors contribute to trauma induced BSCB disruption. Studies carried out in our laboratory suggest that those drugs and neurotrophic factors capable to attenuate the BSCB dysfunction following trauma are neuroprotective in nature. Whereas, agents that do not exert any influence on the BSCB disruption failed to reduce cell injury. These observations are in line with the idea that BSCB disruption plays an important role in the pathophysiology of spinal cord injuries. The probable mechanism(s) of trauma induced BSCB dysfunction and its contribution to cell injuries are discussed.

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“…5 D.c). The BSCB permeability to iodine and the increased water content in the T9 and T12 segment were significantly reduced ( [46,47,221] ; Fig. 7A).…”

Section: Neuroprotective Effects Of Neurotrophins In Scimentioning

confidence: 93%

Section: Alteration In Neurotrophins Expression In Scimentioning

confidence: 98%

Section: Alteration In Neurotrophins Expression In Scimentioning

confidence: 99%

Section: Clinical Cases Of Spinal Cord Injury Prevalence and Symptomsmentioning

confidence: 99%

See 2 more Smart Citations

Pathophysiology of Blood-Spinal Cord Barrier in Traumatic Injury and Repair

Sharma¹

2005

CPD

157

218

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“…Although, NO has been established as a biological mediator of clinical relevance, its role in motor dysfunction, disturbances in the blood-spinal cord barrier function, edema formation, and cell injury is still not well understood. Within the last few years, it has been shown that spinal cord hemisection, impact injury, or focal spinal cord trauma results in upregulation of nNOS expression [2][3][4][5][6][7][8][9][10][11][12][13]. Nitric oxide elevation occurring early after ischemia/trauma seems to be responsible for neurotoxicity [2,6].…”

Section: Introductionmentioning

confidence: 99%