Scleral PERK and ATF6 as targets of myopic axial elongation of mouse eyes.
Shin-Ichi IkedaToshihide KuriharaXiaoyan JiangYukihiro MiwaDeokho LeeNaho SerizawaHeonuk JeongKiwako MoriYusaku KatadaHiromitsu KunimiNobuhiro OzawaChiho ShodaMari IbukiKazuno NegishiHidemasa ToriiMasayuki OhtaPublished in: Nature communications (2022)
Axial length is the primary determinant of eye size, and it is elongated in myopia. However, the underlying mechanism of the onset and progression of axial elongation remain unclear. Here, we show that endoplasmic reticulum (ER) stress in sclera is an essential regulator of axial elongation in myopia development through activation of both PERK and ATF6 axis followed by scleral collagen remodeling. Mice with lens-induced myopia (LIM) showed ER stress in sclera. Pharmacological interventions for ER stress could induce or inhibit myopia progression. LIM activated all IRE1, PERK and ATF6 axis, and pharmacological inhibition of both PERK and ATF6 suppressed myopia progression, which was confirmed by knocking down above two genes via CRISPR/Cas9 system. LIM dramatically changed the expression of scleral collagen genes responsible for ER stress. Furthermore, collagen fiber thinning and expression of dysregulated collagens in LIM were ameliorated by 4-PBA administration. We demonstrate that scleral ER stress and PERK/ATF6 pathway controls axial elongation during the myopia development in vivo model and 4-PBA eye drop is promising drug for myopia suppression/treatment.
Keyphrases
- endoplasmic reticulum stress
- endoplasmic reticulum
- optic nerve
- transcription factor
- crispr cas
- poor prognosis
- optical coherence tomography
- genome editing
- emergency department
- oxidative stress
- diabetic rats
- metabolic syndrome
- dna methylation
- tissue engineering
- adverse drug
- electronic health record
- replacement therapy
- bioinformatics analysis