Atropine reinstates inflammation-induced dysregulation of dopamine and its receptors in human scleral cells: Implications for myopia therapy
Shivapriya Shivakumar, Nithin Kiran, Rohit Shetty, Pradhyumna Hulsermane Krishnamurthy, Arkasubhra Ghosh, Vrushali Deshpande, Nallathambi JeyabalanPurpose:
Myopia is a complex refractive disorder and a leading cause of visual impairment worldwide. Inflammation plays a crucial role in the onset and progression of myopia. This study aimed to investigate the role of atropine in modulating inflammation-induced alterations in dopamine and its receptors in primary human scleral cells under
Methods:
Human primary scleral cells were exposed to long-term inflammatory conditions in the presence or absence of atropine or dopamine hydrochloride. Following treatment, gene and protein expressions were analyzed for inflammatory markers, dopamine receptors, and extracellular matrix (ECM) using quantitative polymerase chain reaction, immunoblotting, and immunofluorescence. Secretory cytokines and dopamine levels were measured using an automated enzyme-linked immunosorbent assay system.
Results:
In primary human scleral cells, atropine treatment increases the dopamine receptor expression. Prolonged inflammatory stimulation led to a marked reduction in dopamine and its receptor (D1–D2) expression, which was effectively restored following atropine treatment in scleral cells. Under inflammatory conditions, atropine significantly suppressed pro-inflammatory cytokines expression at both the transcript and protein levels and mitigated the inflammation-induced dysregulation of ECM genes.
Conclusion:
Our findings demonstrate atropine restores inflammation-induced dopaminergic and extracellular matrix dysregulation in human scleral cells, highlighting its dual anti-inflammatory and neuro-modulatory roles. The restoration of dopamine signaling and ECM balance underscores atropine’s potential as a therapeutic agent for myopia.