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Smooth Muscle Growth in the Inflamed Intestine of the Rat
Published in William J. Snape, Stephen M. Collins, Effects of Immune Cells and Inflammation on Smooth Muscle and Enteric Nerves, 2020
M.G. Blennerhassett, S.M. Collins
The possibility that the nematode parasite directly elaborates a trophic factor is unlikely. The Tsp adults and larvae contact only the mucosa before entering the blood stream, and so are remote from the smooth muscle layers. The stimulation of mitosis was virtually absent in the distal ileum, which could be interpreted to show that trophic changes occur essentially only in the area of inflammation. Studies in situ show that the alterations in smooth muscle function are derived from the the immune system,24 suggesting the hypothesis that the trophic changes as well are mediated through the host immune system.
Fibroblast Growth Factors
Published in Martin Berry, Ann Logan, CNS Injuries: Cellular Responses and Pharmacological Strategies, 2019
Claudia Grothe, Christof Meisinger, Konstantin Weweker
It has also been shown that FGF-2 is able to rescue cells from cell death and stimulates transmitter metabolism of dopaminergic neurons,130–133 cholinergic septal neurons,134 and motoneurons.135–140 Although it has been shown that FGF-2 can act directly on neurons141 the neurotrophic effect of FGF-2 is indirect and is most likely mediated by glial cells.131 Nevertheless, FGF-2 has been applied successfully in a variety of different lesion models. Whereas the first of these studies directly applied FGF (injection, gel foams), recent studies have used the transplantation of genetically modified cells for trophic factor supply. It was demonstrated that exogenously applied FGF-2 undergoes receptor-mediated retrograde transport in various CNS neurons.138,142 Following fimbria-fornix transection, cholinergic septal neurons are rescued by FGF-2 which was injected or applied in a gel foam.143–146 In combination with the ganglioside GM1, FGF-2 can improve spatial memory deficits after partial fimbria transection.147
Oxidative Stress and Neurological Diseases: Is Glutathione Depletion a Common Factor?
Published in Christopher A. Shaw, Glutathione in the Nervous System, 2018
Jaswinder S. Bains, Christopher A. Shaw
The above data show that PKC regulates both NMDA and GSH receptor populations in human spinal cord, both of which are altered in the disease. PKC is itself greatly elevated in ALS spinal-cord tissue (Lanius et al. 1995). If so, why is one receptor population elevated while the other is decreased? Our very speculative working hypothesis is that the above changes are related via alterations in overall GSH status. A decline in GSH has two major consequences: loss of free radical scavenging and loss of GSH as neurotransmitter (see Pasqualotto et al., chapter 9, this volume). The first action leads to oxidative stress as discussed previously. The loss of GSH as neurotransmitter causes a decline in activity of target motor neurons (see Hjelle et al., Fig. 7, chapter 4, this volume). A combination of these events, along with the possibility of a diminished trophic factor release, culminates in motor-neuron death. Changes in NMDA and GSH receptor levels and in PKC reflect the compensatory events in the surviving cells. For the latter, increased activity of PKC on affected and survivor cells may generate more free radicals, further exacerbating the rate of neural degeneration (Robert 1996; Kuo et al. 1995).
High Correlation between Glaucoma Treatment with Topical Prostaglandin Analogs and BDNF Immunoreactivity in Human Retina
Published in Current Eye Research, 2021
Matthew M. Harper, Erin A. Boese, Randy H. Kardon, Johannes Ledolter, Markus H. Kuehn
Our current study had caveats that are important to note. First, this study was conducted with a small number of samples. Future studies to replicate this data and extend these findings to other cohorts and larger numbers of samples are necessary. Our current study was restricted to the analysis of BDNF and TrkB. It will be important to also to examine the expression of other trophic factors including ciliary neurotrophic factor (CNTF), nerve growth factor (NGF), neurotrophin-3 (NT-3), glial-derived neurotrophic factor (GDNF), and trophic factor receptors; in particular the p75 neurotrophin receptor (p75NTR) and the truncated TrkB receptor. Truncated TrkB and p75NTR each have the ability to modify BDNF-Trk signaling and in the case of p75NTR, to cause apoptosis.28 It will be important to analyze the distribution of the factors in the retina in each cell type as glial cells produce many trophic factors,29 and increased production by glial cells may be the reason that the overall expression does not differ between control and glaucoma tissue.
Corneal Cells: Fine-tuning Nerve Regeneration
Published in Current Eye Research, 2020
Bhavani S. Kowtharapu, Oliver Stachs
Corneal stromal keratocytes produce growth factors like hepatocyte growth factor (HGF), keratinocyte growth factor (KGF) and regulate the function of epithelial cells. In the cornea, HGF and KGF are the paracrine mediators of the corneal epithelial-stromal cell interactions159,160 and significantly increased HGF expression in keratocytes following epithelial injury contributes to modulate the wound healing response.161 Apart from its role in epithelial wound healing, HGF is acknowledged as neuroprotective162 and promote axonal regeneration of retinal ganglion cells during optic nerve damage.163,164 Furthermore, HGF trophic properties augment the growth and survival of sensory, motor and sympathetic neurons165,166 and thus functions as a trophic factor for damaged neurons. Given its neurotrophic and neuroprotective properties along with its increased expression following the epithelial injury, it may also be possible that stromal keratocyte derived HGF may also participate in supplementing the epithelial, stromal nerve function and regeneration during wound healing. Stromal keratocytes also produce NGF, GDNF, BDNF, NT-3 and NT-443,167 which are important for the neuronal survival, growth and regeneration.
The identification of small molecules that stimulate retinal pigment epithelial cells: potential novel therapeutic options for treating retinopathies
Published in Expert Opinion on Drug Discovery, 2019
Ana Artero-Castro, Stepan Popelka, Pavla Jendelova, Jan Motlik, Taras Ardan, Francisco Javier Rodriguez Jimenez, Slaven Erceg
Another small molecule drug candidate for the treatment of RPE malfunction is L-3,4-dihydroxyphenylalanine (L-DOPA). This compound is an intermediate of melanin synthesis in pigmented cells and is a highly selective ligand for an orphan G protein-coupled receptor (gene GPR143) [17]. The binding of L-DOPA to this receptor in RPE cells up-regulates the secretion of pigment epithelia-derived factor (PEDF) [17] and downregulates the secretion of VEGF [18]. This influence on trophic factor release is assumed to give protection from AMD progression. Indeed, a correlation between L-DOPA prescription and the delayed onset of either form of AMD has been found in a retrospective study [19]. A clinical study on the safety and efficacy of L-DOPA in AMD patients has recently been initiated (NCT03451500). Additionally, the physical and biological properties of the blood–retinal barrier (BRB) in vivo have to be taken into account in order to efficiently design small molecules for future therapy in humans [20,21]. The BRB features as well as the physical and dynamic factors of RPE cells could prevent or enable the efficient delivery, efficacy, and toxicity of compounds to the eye [20,21]. This problem could be circumvented by local, more direct delivery such as intravitreal administration, but this could produce more local side-effects such as pain at the site of injection [21].