scholarly journals Visually induced changes in cytokine production in the chick choroid

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Jody Ann Summers ◽  
Elizabeth Cano Martinez
Keyword(s):  
Gene Expression ◽  
Nitric Oxide ◽  
Nitric Oxide Donor ◽  
Visually Guided ◽  
Nitric Oxide Synthase Inhibitor ◽  
Ocular Growth ◽  
Gene And Protein Expression ◽  
Synthase Inhibitor ◽  
Induced Changes ◽  
Oxide Synthase

Postnatal ocular growth is regulated by a vision-dependent mechanism which acts to minimize refractive error through coordinated growth of the ocular tissues. Of great interest is the identification of the chemical signals that control visually-guided ocular growth. Here we provide evidence that the pro-inflammatory cytokine, Interleukin-6 (IL-6), may play a pivotal role in the control of ocular growth using a chicken model of myopia. Microarray, real time RT-qPCR, and ELISA analyses identified IL-6 upregulation in the choroids of chick eyes under two visual conditions that introduce myopic defocus and slow the rate of ocular elongation (recovery from induced myopia and compensation for positive lenses). Intraocular administration of atropine, an agent known to slow ocular elongation, also resulted in an increase in choroidal IL-6 gene expression. Nitric oxide appears to directly or indirectly upregulate choroidal IL-6 gene expression, as administration of the non-specific nitric oxide synthase inhibitor, L-NAME, inhibited choroidal IL-6 gene expression, and application of a nitric oxide donor stimulated IL-6 gene and protein expression in isolated chick choroids. Considering the pleiotropic nature of IL-6 and involvement in many biological processes, these results suggest that IL-6 may mediate many aspects of the choroidal response in the control of ocular growth.

scholarly journals Visually Induced Changes in Cytokine Production in the Chick Choroid

2021 ◽  
Author(s):  
Jody Ann Summers ◽  
Elizabeth Cano Martinez
Keyword(s):  
Gene Expression ◽  
Nitric Oxide ◽  
Nitric Oxide Donor ◽  
Visually Guided ◽  
Nitric Oxide Synthase Inhibitor ◽  
Ocular Growth ◽  
Gene And Protein Expression ◽  
Synthase Inhibitor ◽  
Induced Changes ◽  
Oxide Synthase

Postnatal ocular growth is regulated by a vision-dependent mechanism which acts to minimize refractive error through coordinated growth of the ocular tissues. Of great interest is the identification of the chemical signals that control visually-guided ocular growth. Here we provide evidence that the pro-inflammatory cytokine, Interleukin-6 (IL-6), may play a pivotal role in the control of ocular growth using a chicken model of myopia. Microarray, real time RT-qPCR, and ELISA analyses identified IL-6 upregulation in the choroids of chick eyes under two visual conditions that introduce myopic defocus and slow the rate of ocular elongation (recovery from induced myopia and compensation for positive lenses). Intraocular administration of atropine, an agent known to slow ocular elongation, also resulted in an increase in choroidal IL-6 gene expression. Nitric oxide appears to directly or indirectly upregulate choroidal IL-6 gene expression, as administration of the non-specific nitric oxide synthase inhibitor, L-NAME, inhibited choroidal IL-6 gene expression, and application of a nitric oxide donor stimulated IL-6 gene and protein expression in isolated chick choroids. Considering the pleiotropic nature of IL- 6 and involvement in many biological processes, these results suggest that IL-6 may mediate many aspects of the choroidal response in the control of ocular growth.

scholarly journals Effect of cross-linked hemoglobin transfusion on endothelial-dependent dilation in cat pial arterioles

1998 ◽  
Vol 275 (4) ◽  
pp. H1313-H1321 ◽  
Author(s):  
Yoshio Asano ◽  
Raymond C. Koehler ◽  
John A. Ulatowski ◽  
Richard J. Traystman ◽  
Enrico Bucci
Keyword(s):  
Nitric Oxide ◽  
Hemoglobin Concentration ◽  
Nitric Oxide Donor ◽  
Nitric Oxide Synthase Inhibitor ◽  
Cranial Window ◽  
Dilatory Response ◽  
Pial Arterioles ◽  
Synthase Inhibitor ◽  
Oxide Synthase ◽  
Arteriolar Diameter

We determined whether addition of hemoglobin to the plasma would inhibit endothelial-dependent dilation in brain where tight endothelial junctions limit hemoglobin extravasation. Pial arteriolar diameter was measured by intravital microscopy through closed cranial windows in anesthetized cats either without transfusion (hematocrit = 32%) or after exchange transfusion with an albumin or sebacyl-cross-linked human hemoglobin solution (hematocrit = 18%). Dilation of small, medium, and large arterioles to acetylcholine and ADP was not significantly altered by hemoglobin transfusion. The dilatory responses were inhibited by the nitric oxide synthase inhibitor N G-nitro-l-arginine, although significant dilation to 30 μM acetylcholine persisted in small arterioles in the control and albumin-transfused group but not in the hemoglobin-transfused group. The dilatory response to the nitric oxide donor 3-morpholinosydnonimine was unaffected by albumin or hemoglobin transfusion, but the response to nitroprusside was reduced by one-third after hemoglobin transfusion. When cross-linked hemoglobin was superfused through the cranial window, the acetylcholine response became inhibited at a hemoglobin concentration of 0.1 μM and was completely blocked at 10 μM. Because this concentration is substantially less than the 500 μM hemoglobin concentration in plasma after transfusion when there was no inhibition of the acetylcholine response, hemoglobin permeation of the blood-brain barrier was considered negligible. We conclude that exchange of red cell-based hemoglobin with plasma-based hemoglobin does not produce a more effective sink for endothelial-derived nitric oxide evoked by agonist receptor-mediated activation. Furthermore, decreased hematocrit does not affect agonist-evoked endothelial-dependent dilation.

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