Growth hormone and retinal ganglion cell function: QNR/D cells as an experimental model

Martínez-Moreno, Carlos G.; Andres, Alexis; Giterman, Daniel; Karpinski, Edward; Harvey, S.

doi:10.1016/j.ygcen.2013.10.016

Cited by 15 publications

(3 citation statements)

References 44 publications

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“…It remains unclear whether the partial recovery of function was due to increased RGC survival or axon regeneration induced by neurotrophic factors, but further studies would be needed to clarify these effects. Müller glia has been shown to produce ciliary neurotrophic factor (CNTF) [39], FGF‐2, brain‐derived neurotrophic factor (BDNF), and glial cell line‐derived neurotrophic factor [40], whereas RGCs have been shown to produce factors such as insulin growth factor and neurotrophin 3 [41], as well as BDNF [42]. Our suggestion that the improvement on the RGC function was due to a neurotrophic effect of the transplanted cells is supported by observations by others that BDNF and CNTF decrease RGC loss in animal models of optic nerve damage [43] and that overexpression of BDNF in the retina protects RGCs in a rat model of glaucoma [44].…”

Section: Discussionmentioning

confidence: 99%

Allogeneic Transplantation of Müller-Derived Retinal Ganglion Cells Improves Retinal Function in a Feline Model of Ganglion Cell Depletion

Becker

Eastlake

Jayaram

et al. 2015

Stem Cells Translational Medicine

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This study investigated the effect of allogeneic transplantation of feline Müller glia with the ability to differentiate into cells expressing retinal ganglion cell (RGC) markers, following ablation of RGCs by N-methyl-d-aspartate. The results suggest that Müller glia with stem cell characteristics have a neuroprotective ability that promotes partial recovery of impaired RGC function and indicate that cell attachment onto the retina may be necessary for transplanted cells to confer neuroprotection to the retina.

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Section: Discussionmentioning

confidence: 99%

Allogeneic Transplantation of Müller-Derived Retinal Ganglion Cells Improves Retinal Function in a Feline Model of Ganglion Cell Depletion

Becker

Eastlake

Jayaram

et al. 2015

Stem Cells Translational Medicine

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“…Avian retinal cells are the target of GH stimulation since the GH receptor (GHR) expression has been described there, particularly in neuroretinal and glial cells, in which axogenic and synaptogenic effects are well established [16,17,18,19,20]. It is also important to note that both GH and IGF-1 are neuroprotective factors that are also expressed in the retina [17], and their actions are mediated through signaling pathways such as JAK/STAT, IP3/Akt, MAPK, and Notch, which are activated during the neuroregenerative process [7,21,22,23].…”

Section: Introductionmentioning

confidence: 99%

Regenerative Effect of Growth Hormone (GH) in the Retina after Kainic Acid Excitotoxic Damage

Martínez-Moreno

Epardo

Balderas-Márquez

et al. 2019

IJMS

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In addition to its role as an endocrine messenger, growth hormone (GH) also acts as a neurotrophic factor in the central nervous system (CNS), whose effects are involved in neuroprotection, axonal growth, and synaptogenic modulation. An increasing amount of clinical evidence shows a beneficial effect of GH treatment in patients with brain trauma, stroke, spinal cord injury, impaired cognitive function, and neurodegenerative processes. In response to injury, Müller cells transdifferentiate into neural progenitors and proliferate, which constitutes an early regenerative process in the chicken retina. In this work, we studied the long-term protective effect of GH after causing severe excitotoxic damage in the retina. Thus, an acute neural injury was induced via the intravitreal injection of kainic acid (KA, 20 µg), which was followed by chronic administration of GH (10 injections [300 ng] over 21 days). Damage provoked a severe disruption of several retinal layers. However, in KA-damaged retinas treated with GH, we observed a significant restoration of the inner plexiform layer (IPL, 2.4-fold) and inner nuclear layer (INL, 1.5-fold) thickness and a general improvement of the retinal structure. In addition, we also observed an increase in the expression of several genes involved in important regenerative pathways, including: synaptogenic markers (DLG1, NRXN1, GAP43); glutamate receptor subunits (NR1 and GRIK4); pro-survival factors (BDNF, Bcl-2 and TNF-R2); and Notch signaling proteins (Notch1 and Hes5). Interestingly, Müller cell transdifferentiation markers (Sox2 and FGF2) were upregulated by this long-term chronic GH treatment. These results are consistent with a significant increase in the number of BrdU-positive cells observed in the KA-damaged retina, which was induced by GH administration. Our data suggest that GH is able to facilitate the early proliferative response of the injured retina and enhance the regeneration of neurite interconnections.

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“…Our findings also suggest that locally produced GH and factors are more effective in neural retinal development. This possibility is supported by the presence of GH immunoreactivity in the brain prior to the ontogeny of the pituitary gland and somatotroph differentiation, as has been demonstrated in the human and chicken brain ( 20 , 21 ). Vascularization of the retina normally starts at approximately 12 weeks of gestation, while pituitary somatotroph GH production has already begun and continues during fetal development, with little or no vascularization after birth ( 22 , 23 ).…”

Section: Discussionmentioning

confidence: 66%

Retinal Neural and Vascular Structure in Isolated Growth Hormone Deficiency Children and Evaluation of Growth Hormone Treatment Effect

Yüce

Yalçın

Bıdecı

et al. 2018

Jcrpe

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Objective:To evaluate neural and vascular retinal morphology of children with isolated growth hormone deficiency (GHD) and to determine any retinal changes due to GH treatment.Methods:Twenty-eight children with isolated GHD and 53 age-, gender- and body mass index-matched healthy volunteers were enrolled in this prospective study. The retinal nerve fibre layer (RNFL) and macular thickness (MT) were measured, as well as intraocular pressure (IOP). The number of retinal vascular branching points were calculated. Effect of GH treatment on the retina and IOP was evaluated after one year of treatment. Measurements were also made in the control group at baseline and following the initial examination. Pre- and post-treatment changes were compared. The findings were also compared with those of the controls. The correlation between ocular dimensions and insulin-like growth factor-I (IGF-1) levels were also analysed.Results: The number of branching points was significantly lower in GHD patients as compared with control subjects (15.11±2.67 and 19.70±3.37, respectively, p=0.05 for all comparisons). No statistically significant differences were found in mean RNFL, MT and IOP values between GHD patients and control subjects. GH treatment did not create any significant changes in the retinal vascularization or other retinal neural parameters and IOP either within the patient group or when compared with the control group. No correlations were observed between ocular dimensions and IGF-1 levels.Conclusion:Our findings suggest that isolated GHD may lead to decreased retinal vascularization. However, retinal neural growth and differentiation were not affected by GHD. These findings may be related to the fetal development process of pituitary somatotropic cells and the retina. Additionally, GH treatment did not cause any changes in retinal neural and vascular tissues.

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Growth hormone and retinal ganglion cell function: QNR/D cells as an experimental model

Cited by 15 publications

References 44 publications

Allogeneic Transplantation of Müller-Derived Retinal Ganglion Cells Improves Retinal Function in a Feline Model of Ganglion Cell Depletion

Allogeneic Transplantation of Müller-Derived Retinal Ganglion Cells Improves Retinal Function in a Feline Model of Ganglion Cell Depletion

Regenerative Effect of Growth Hormone (GH) in the Retina after Kainic Acid Excitotoxic Damage

Retinal Neural and Vascular Structure in Isolated Growth Hormone Deficiency Children and Evaluation of Growth Hormone Treatment Effect

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