scholarly journals Keratocyte Density Is Reduced and Related to Corneal Nerve Damage in Diabetic Neuropathy

2018 ◽  
Vol 59 (8) ◽  
pp. 3584 ◽  
Author(s):  
Alise Kalteniece ◽  
Maryam Ferdousi ◽  
Shazli Azmi ◽  
Andrew Marshall ◽  
Handrean Soran ◽  
...  
Keyword(s):  
Diabetic Neuropathy ◽  
Nerve Damage ◽  
Corneal Nerve ◽  
Keratocyte Density

scholarly journals Docosanoid signaling modulates corneal nerve regeneration: effect on tear secretion, wound healing, and neuropathic pain

2020 ◽  
pp. jlr.TR120000954 ◽  
Author(s):  
Thang L. Pham ◽  
Haydee E.P. Bazan
Keyword(s):  
Wound Healing ◽  
Neuropathic Pain ◽  
Nerve Regeneration ◽  
Contact Lenses ◽  
Therapeutic Option ◽  
Pigment Epithelium ◽  
Nerve Damage ◽  
Sensory Nerves ◽  
Tear Secretion ◽  
Corneal Nerve

The cornea is densely innervated, mainly by sensory nerves of the ophthalmic branch of the trigeminal ganglia (TG). These nerves  are important to maintain corneal homeostasis, and nerve damage can lead to a decrease in wound healing, an increase in corneal ulceration and dry eye disease (DED), and neuropathic pain. Pathologies, such as diabetes, aging, viral and bacterial infection, as well as  prolonged use of contact lenses and surgeries to correct vision can produce nerve damage. There are no effective therapies to alleviate DED (a multifunctional disease) and several clinical trials using ω-3 supplementation show unclear and sometimes negative results. Using animal models of corneal nerve damage, we show that treating corneas with pigment epithelium-derived factor (PEDF) plus docosahexaenoic acid (DHA) increases nerve regeneration, wound healing, and tear secretion. The mechanism involves the activation of a calcium-independent phospholipase A2 (iPLA2ζ) that releases the incorporated DHA from phospholipids and enhances the synthesis of docosanoids neuroprotectin D1 (NPD1) and a new resolvin stereoisomer  RvD6i. NPD1 stimulates the synthesis of brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF), and of semaphorin 7A (Sema7A).  RvD6i treatment of injured corneas modulates gene expression in the TG resulting in enhanced neurogenesis; decreased neuropathic pain and increased sensitivity. Taken together, these results represent a promising therapeutic option to re-establish the homeostasis of the cornea.

scholarly journals Effect of Inhibition or Deletion of Neutral Endopeptidase on Neuropathic Endpoints in High Fat Fed/Low Dose Streptozotocin-Treated Mice

2016 ◽  
Vol 75 (11) ◽  
pp. 1072-1080 ◽  
Author(s):  
Matthew S. Yorek ◽  
Alexander Obrosov ◽  
Bao Lu ◽  
Craig Gerard ◽  
Randy H. Kardon ◽  
...  
Keyword(s):  
Diabetic Neuropathy ◽  
Neutral Endopeptidase ◽  
Neural Function ◽  
High Fat ◽  
Multiple Endpoints ◽  
Active Peptides ◽  
Corneal Nerves ◽  
Intervention Protocol ◽  
Prevention Protocol ◽  
Corneal Nerve

Previously we demonstrated that a vasopeptidase inhibitor of angiotensin converting enzyme and neutral endopeptidase (NEP), a protease that degrades vaso- and neuro-active peptides, improves neural function in diabetic rodent models. The purpose of this study was to determine whether inhibition or deletion of NEP provides protection from neuropathy caused by diabetes with an emphasis on morphology of corneal nerves as a primary endpoint. Diabetes, modeling type 2, was induced in C57Bl/6J and NEP deficient mice through a combination of a high fat diet and streptozotocin. To inhibit NEP activity, diabetic C57Bl/6J mice were treated with candoxatril using a prevention or intervention protocol. Twelve weeks after the induction of diabetes in C57Bl/6J mice, the existence of diabetic neuropathy was determined through multiple endpoints including decrease in corneal nerves in the epithelium and sub-epithelium layer. Treatment of diabetic C57Bl/6J mice with candoxatril improved diabetic peripheral neuropathy and protected corneal nerve morphology with the prevention protocol being more efficacious than intervention. Unlike C57Bl/6J, mice deficient in NEP were protected from the development of neuropathologic alterations and loss of corneal nerves upon induction of diabetes. These studies suggest that NEP contributes to the development of diabetic neuropathy and may be a treatable target.

IN VIVO CONFOCAL MICROSCOPY FOR STUDYING CORNEAL DISEASES/CONDITIONS ASSOCIATED WITH CORNEAL NERVE DAMAGE AND OCULAR SURFACE DISEASE.

Cornea ◽  
2000 ◽  
Vol 19 (Supplement 2) ◽  
pp. S131
Author(s):  
T Tervo ◽  
T U Valle ◽  
J AO Moilanen ◽  
M E Rosenberg ◽  
I SJ Tuominen ◽  
...  
Keyword(s):  
Confocal Microscopy ◽  
Ocular Surface ◽  
Nerve Damage ◽  
Ocular Surface Disease ◽  
In Vivo Confocal Microscopy ◽  
Corneal Nerve

Exploring the optimal diagnostic threshold value of corneal nerve fibre length (CNFL) for diabetic neuropathy (DN) identification

2017 ◽  
Vol 41 (5) ◽  
pp. S62
Author(s):  
Leif E. Lovblom ◽  
Vera Bril ◽  
Andrej Orszag ◽  
Katie Edwards ◽  
Nicola Pritchard ◽  
...  
Keyword(s):  
Diabetic Neuropathy ◽  
Nerve Fibre ◽  
Fibre Length ◽  
Threshold Value ◽  
Diagnostic Threshold ◽  
Corneal Nerve

scholarly journals Diabetic Neuropathy Is Characterized by Progressive Corneal Nerve Fiber Loss in the Central and Inferior Whorl Regions

2020 ◽  
Vol 61 (3) ◽  
pp. 48 ◽  
Author(s):  
Maryam Ferdousi ◽  
Alise Kalteniece ◽  
Ioannis Petropoulos ◽  
Shazli Azmi ◽  
Shaishav Dhage ◽  
...  
Keyword(s):  
Diabetic Neuropathy ◽  
Nerve Fiber ◽  
Corneal Nerve
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