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Updated: Jun 17, 2026
Experimental Models for Study of Retinal Pigment Epithelial Physiology and Pathophysiology
Published on: November 6, 2010
TGF-beta2 in human retinal pigment epithelial cells: expression and secretion regulated by cholinergic signals in
Jia Tan1, Zhi-hong Deng, Shuang-zhen Liu
1Department of Ophthalmology, Xiangya Medical College, Central South University, Changsha, China.
Purpose:
To investigate the (i) effect(s) of cholinergics on the expression and secretion of transforming growth factor (TGF)-beta(2) in human retinal pigment epithelium (RPE) and (ii) mechanism of action of atropine in the treatment of myopia.
Materials And Methods:
The RPE cell line, D407, was (i) treated with carbachol (10 microM), (ii) treated with atropine (10 nM-100 microM), or (iii) pre-treated with atropine (10 nM-100 microM) and then exposed to carbachol (10 microM). A no-treatment group served as control. Expression of TGF-beta(2), after stimulation at different time points (2, 4, 8, 16, 24, and 48 hr), was measured by RT-PCR and Western blot analysis. Secretion of TGF-beta(2) was determined by ELISA.
Results:
Carbachol induced a time-dependent increase in the levels of TGF-beta(2) mRNA and protein in the cytoplasm (p < 0.001). ELISA assays showed a time-dependent increase in levels of TGF-beta(2) protein in the supernatant with carbachol treatment (p < 0.001). There was no change of TGF-beta(2) in the cytoplasm or supernatant with atropine alone (p > 0.05). The increased expression and secretion of TGF-beta(2) caused by carbachol were suppressed by atropine (in the range of 10 nM-100 microM) when compared to treatment with carbachol alone (p < 0.001). The stimulating effect of 10 microM carbachol was inhibited completely by 100 microM atropine.
Conclusions:
In RPE cells, atropine inhibits the expression and secretion of TGF-beta(2) by blocking the muscarinic acetylcholine receptor (mAChR), which may control the development of myopia.
