Neuroprotective and Anti-Inflammatory Effects of SOCS1 Mimetic Peptides in Mouse Diabetic Retinopathy.
6 affiliations
- 1Department of Immunology, Ophthalmology, and ENT, Ramón Castroviejo Institute for Ophthalmic Research, Faculty of Optics and Optometry, Complutense University of Madrid, Madrid, Spain.
- 2Health Research Institute of the Hospital Clínico San Carlos, Madrid, Spain.
- 3Renal, Vascular and Diabetes Research Laboratory IIS-Fundación Jiménez Díaz, Spanish Biomedical Research Centre in Diabetes and Associated Metabolic Disorders, Universidad Autonoma de Madrid, Madrid, Spain.
- 4Health Science Faculty, University of Las Américas, Concepcion-Talcahuano, Chile.
- 5Department of Ophthalmology, University Hospital Fundación Jiménez Díaz, Madrid, Spain.
- 6Department of Cell Biology, Physiology and Immunology, Maimónides Biomedical Research Institute of Cordoba, UGC Nephrology, Hospital Universitario Reina Sofía, University of Córdoba, Córdoba, Spain.
Abstract
Purpose
To evaluate the therapeutic potential of a suppressor of cytokine signaling 1 (SOCS1) mimetic peptide (MiS1) via systemic administration in a mouse model of diabetic retinopathy (DR).Methods
Male db/db mice, a model of type 2 diabetes, were treated for 7 weeks with intraperitoneal injections of MiS1. In comparison, a group of animals received the Janus kinase (JAK)1/2 inhibitor baricitinib. Untreated diabetic db/db mice and non-diabetic db/m littermates served as controls. Retinal structure was assessed in vivo by optical coherence tomography. Retinal ganglion cell (RGC) survival (Brn3a+ cells) and Iba1-positive microglial activation (Iba1+ cells) were analyzed by immunohistochemistry in retinal wholemounts.Results
Untreated db/db mice exhibited retinal thinning, RGC loss, and marked Iba1+ microglial activation. Both MiS1 and baricitinib treatments significantly attenuated retinal thinning, with MiS1 preserving retinal thickness at levels comparable to those of nondiabetic controls. RGC numbers were partially preserved in both treated groups, although the increase compared with untreated db/db mice reached statistical significance only in baricitinib-treated animals. Both treatments improved microglial morphology, mainly by increasing arbor area, whereas their effects on Iba1+ cell numbers were layer and parameter dependent.Conclusions
Systemic administration of the SOCS1 mimetic peptide MiS1 showed a consistent protective profile on retinal thickness preservation and microglial remodeling in experimental DR. These findings support SOCS1-based therapies as a promising therapeutic strategy.
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BibTeX
@article{salobrargarcia2026neuroprotective,
title = {{Neuroprotective and Anti-Inflammatory Effects of SOCS1 Mimetic Peptides in Mouse Diabetic Retinopathy.}},
author = {Elena Salobrar-García and Lucas Opazo-Ríos and José A Matamoros and Lidia Sánchez-Puebla and José A Fernández-Albarral and Juan J Salazar and Raquel Castro and Manuel Soto-Catalán and Juan Antonio Moreno and Carmen Gómez-Guerrero and Sebastián Mas and Jesús Egido and Ana I Ramírez},
journal = {Investigative ophthalmology \& visual science},
year = {2026},
month = oct,
doi = {10.1167/iovs.67.12.21},
url = {https://europepmc.org/article/MED/42872951},
note = {CC BY-NC-ND},
}
RIS
TY - JOUR
TI - Neuroprotective and Anti-Inflammatory Effects of SOCS1 Mimetic Peptides in Mouse Diabetic Retinopathy.
AU - Elena Salobrar-García
AU - Lucas Opazo-Ríos
AU - José A Matamoros
AU - Lidia Sánchez-Puebla
AU - José A Fernández-Albarral
AU - Juan J Salazar
AU - Raquel Castro
AU - Manuel Soto-Catalán
AU - Juan Antonio Moreno
AU - Carmen Gómez-Guerrero
AU - Sebastián Mas
AU - Jesús Egido
AU - Ana I Ramírez
PY - 2026
DA - 2026/10/01
JO - Investigative ophthalmology & visual science
DO - 10.1167/iovs.67.12.21
UR - https://europepmc.org/article/MED/42872951
AB - Purpose To evaluate the therapeutic potential of a suppressor of cytokine signaling 1 (SOCS1) mimetic peptide (MiS1) via systemic administration in a mouse model of diabetic retinopathy (DR).Methods Male db/db mice, a model of type 2 diabetes, were treated for 7 weeks with intraperitoneal injections of MiS1. In comparison, a group of animals received the Janus kinase (JAK)1/2 inhibitor baricitinib. Untreated diabetic db/db mice and non-diabetic db/m littermates served as controls. Retinal structure was assessed in vivo by optical coherence tomography. Retinal ganglion cell (RGC) survival (Brn3a+ cells) and Iba1-positive microglial activation (Iba1+ cells) were analyzed by immunohistochemistry in retinal wholemounts.Results Untreated db/db mice exhibited retinal thinning, RGC loss, and marked Iba1+ microglial activation. Both MiS1 and baricitinib treatments significantly attenuated retinal thinning, with MiS1 preserving retinal thickness at levels comparable to those of nondiabetic controls. RGC numbers were partially preserved in both treated groups, although the increase compared with untreated db/db mice reached statistical significance only in baricitinib-treated animals. Both treatments improved microglial morphology, mainly by increasing arbor area, whereas their effects on Iba1+ cell numbers were layer and parameter dependent.Conclusions Systemic administration of the SOCS1 mimetic peptide MiS1 showed a consistent protective profile on retinal thickness preservation and microglial remodeling in experimental DR. These findings support SOCS1-based therapies as a promising therapeutic strategy.
SN - 0146-0404
SN - 1552-5783
ER -